[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 297
1. Minniti G, Traish D, Ashley S, Gonsalves A, Brada M: Fractionated stereotactic conformal radiotherapy for secreting and nonsecreting pituitary adenomas. Clin Endocrinol (Oxf); 2006 May;64(5):542-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fractionated stereotactic conformal radiotherapy for secreting and nonsecreting pituitary adenomas.
  • OBJECTIVE: To assess the medium-term outcome in a cohort of patients with residual or recurrent pituitary adenoma treated with fractionated stereotactic conformal radiotherapy (SCRT).
  • PATIENTS AND METHODS: Ninety-two patients (median age 50 years) with a residual or recurrent nonfunctioning (67) or a secreting (25) pituitary adenoma were treated between 1995 and 2003.
  • Eighteen patients had a GH-secreting, five PRL-secreting and two an ACTH-secreting pituitary adenoma.
  • In secreting adenomas, hormone levels declined progressively, becoming normal in more than a third of patients with GH-secreting and PRL-secreting pituitary tumours.
  • Hypopituitarism was the most common long-term effect; 22% of patients had worsening of pituitary function.
  • CONCLUSION: SCRT as a high-precision technique of localized irradiation achieves tumour and hormone control of pituitary adenomas comparable with previously published data on the efficacy of conventional radiotherapy.
  • Despite the potential advantage of reducing the volume of normal brain irradiated, the theoretical benefit over conventional radiotherapy in terms of the reduction in long-term morbidity has not yet been demonstrated and requires longer follow-up.
  • Potential effect on long-term cognitive function has not been tested.
  • [MeSH-major] Adenoma / radiotherapy. Pituitary Neoplasms / radiotherapy. Radiotherapy, Conformal / methods
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Adult. Aged. Cohort Studies. Female. Growth Hormone / secretion. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / radiotherapy. Neoplasm, Residual / pathology. Neoplasm, Residual / radiotherapy. Prolactinoma / radiotherapy. Prolactinoma / secretion. Radiotherapy Dosage. Statistics, Nonparametric. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16649974.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9002-72-6 / Growth Hormone
  •  go-up   go-down


2. Cavagnini F, Scacchi M, Pecori Giraldi F: Hypopituitarism in Cushing's disease. J Endocrinol Invest; 2008 Sep;31(9 Suppl):44-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypopituitarism in Cushing's disease.
  • Impaired GH secretion usually accompanies Cushing's syndrome and a variable proportion of patients reportedly fail to recover normal GH secretion after successful treatment.
  • We prospectively studied 34 patients (27 females and 7 males, age range 21- 68 yr) formerly affected by Cushing's disease.
  • All patients had undergone transsphenoidal surgery with the removal of an ACTH-secreting adenoma.
  • Our experience has demonstrated a GHD in a high percentage of patients with Cushing's disease even after long-term remission of hypercortisolism obtained by surgery alone.
  • This finding is significant as it highlights that even the most favorable therapeutical course, i.e. remission achieved by surgery, is often accompanied by impaired GH release.
  • Assessment of GH secretion is therefore recommended in all patients cured from Cushing's disease, even if not submitted to radiotherapy.
  • [MeSH-major] Hypopituitarism / complications. Pituitary ACTH Hypersecretion / complications
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / complications. Adenoma / surgery. Adult. Aged. Female. Follow-Up Studies. Growth Disorders / epidemiology. Growth Disorders / etiology. Human Growth Hormone / blood. Human Growth Hormone / secretion. Humans. Male. Middle Aged. Prevalence. Young Adult

  • Genetic Alliance. consumer health - Hypopituitarism.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19020385.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
  •  go-up   go-down


3. Jane JA Jr: Management of pediatric sellar tumors. Pediatr Endocrinol Rev; 2008 Feb;5 Suppl 2:720-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Craniopharyngiomas and pituitary adenomas are the most common forms of sellar tumors in children.
  • First-line treatment usually consists of surgical resection of the tumor, although dopamine agonist therapy may be considered as first-line therapy in most patients with prolactin-secreting adenomas.
  • Transsphenoidal resection has become increasingly widespread and represents the mainstay of surgical therapy for pituitary adenomas and selected craniopharyngiomas.
  • [MeSH-major] Pituitary Neoplasms / therapy
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / epidemiology. Adenoma / therapy. Adolescent. Adult. Child. Craniopharyngioma / diagnosis. Craniopharyngioma / epidemiology. Craniopharyngioma / therapy. Female. Human Growth Hormone / secretion. Humans. Male. Pituitary ACTH Hypersecretion / therapy. Prolactinoma / therapy. Radiosurgery. Radiotherapy. Surgical Procedures, Operative / methods

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18317443.001).
  • [ISSN] 1565-4753
  • [Journal-full-title] Pediatric endocrinology reviews : PER
  • [ISO-abbreviation] Pediatr Endocrinol Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Israel
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
  • [Number-of-references] 57
  •  go-up   go-down


Advertisement
4. Gnjidić Z, Sajko T, Kudelić N, Malenica M, Vizner B, Vrkljan M, Hat J, Rumboldt Z: Reversible "brain atrophy" in patients with Cushing's disease. Coll Antropol; 2008 Dec;32(4):1165-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reversible "brain atrophy" in patients with Cushing's disease.
  • During the past 25 years, we came across 60 patients with corticotroph pituitary adenomas and Cushing's disease.
  • Neuroradiological examination showed prominent volume loss of the brain parenchyma, unexpected for the patient's age.
  • This "brain atrophy" appeared to regress after surgical removal of pituitary adenoma and normalization of cortisol level.
  • Observed difference between degree of "brain atrophy" in the Cushing's disease group and in the control group was statistically significant (p < 0.001).
  • The degree of "brain atrophy" correlated well with the duration of Cushing's disease.
  • Partial reversibility of "brain atrophy" was noticed during the 2nd, 3rd and 4th year after surgery and normalization of cortisol level.
  • Increased cortisol level is one of the causative factors in pathogenesis of "brain atrophy".
  • Loss of brain volume is at least partially reversible after normalization of cortisol levels.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Brain / pathology. Pituitary ACTH Hypersecretion / pathology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19149224.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Croatia
  •  go-up   go-down


5. Castinetti F, Morange I, Dufour H, Jaquet P, Conte-Devolx B, Girard N, Brue T: Desmopressin test during petrosal sinus sampling: a valuable tool to discriminate pituitary or ectopic ACTH-dependent Cushing's syndrome. Eur J Endocrinol; 2007 Sep;157(3):271-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Desmopressin test during petrosal sinus sampling: a valuable tool to discriminate pituitary or ectopic ACTH-dependent Cushing's syndrome.
  • Corticotropin-releasing hormone (CRH)-stimulated petrosal sinus sampling is currently the gold standard method for the differential diagnosis between pituitary and ectopic ACTH-dependent Cushing's syndrome.
  • PATIENTS AND METHODS: Forty-three patients had petrosal sinus sampling because of the lack of visible adenoma on magnetic resonance imaging (MRI) and/or because of discordant cortisol response to high-dose dexamethasone suppression test.
  • ACTH sampling was performed in an antecubital vein, right and left petrosal sinuses, then at each location 5 and 10 min after injection of desmopressin.
  • Diagnosis was based on the ACTH ratio between petrosal sinus and humeral vein ACTH after desmopressin test.
  • Diagnosis was confirmed after surgery.
  • RESULTS: Thirty-six patients had Cushing's disease (CD) and seven had ectopic ACTH secretion.
  • A ratio < or = 2 was found in the seven patients with ectopic ACTH secretion (specificity: 100%).
  • Sinus sampling was ineffective in determining the left or right localization of the adenoma (sensitivity = 50%).
  • CONCLUSION: Desmopressin test during petrosal sinus sampling is a safe and effective diagnostic procedure in ACTH-dependent Cushing's syndrome.

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17766708.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antidiuretic Agents; ENR1LLB0FP / Deamino Arginine Vasopressin
  •  go-up   go-down


6. Bocca G, Voorhoeve PG, de Delemarre-van Wall HA: [Cushing's syndrome in children]. Ned Tijdschr Geneeskd; 2006 Oct 28;150(43):2345-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cushing's syndrome in children].
  • In two girls, aged 13 and 16 years, Cushing's syndrome was diagnosed.
  • In addition, the first showed a decrease in linear growth and weight gain; a pituitary adenoma was found, which was surgically excised.
  • She had an adrenal adenoma, visible on MRI, which was excised during laparoscopy.
  • Cushing's syndrome is a rare disease in childhood.
  • Arriving at an aetiological diagnosis may be difficult and is based on the performance and interpretation of endocrinologic function and laboratory tests such as determination of the cortisol level in blood, saliva and urine, a dexamethasone-suppression test, and a corticotropin assay in blood drawn from the cerebral cavernous sinuses.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Cushing Syndrome / diagnosis. Hydrocortisone / blood
  • [MeSH-minor] Adolescent. Dexamethasone. Diagnosis, Differential. Female. Growth. Humans. Magnetic Resonance Imaging. Treatment Outcome. Weight Gain

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Ned Tijdschr Geneeskd. 2007 Mar 3;151(9):560; author reply 560-1 [17375397.001]
  • [CommentOn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2365-9 [17100127.001]
  • [CommentOn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2390-3 [17100132.001]
  • [CommentOn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2359-64 [17100126.001]
  • (PMID = 17100122.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] Case Reports; Comment; English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 7S5I7G3JQL / Dexamethasone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


7. Schmid C, Goede DL, Hauser RS, Brändle M: Increased prevalence of high Body Mass Index in patients presenting with pituitary tumours: severe obesity in patients with macroprolactinoma. Swiss Med Wkly; 2006 Apr 15;136(15-16):254-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased prevalence of high Body Mass Index in patients presenting with pituitary tumours: severe obesity in patients with macroprolactinoma.
  • As opposed to ACTH- and GH-secreting adenoma, the mechanism by which macroprolactinoma causes obesity has not been fully understood.
  • Having seen patients with both prolactinoma and obesity and more recent literature on brain dopamine, dopamine 2 receptors and obesity, we re-evaluated the potential relationship between prolactinoma and obesity.
  • METHODS: Data of patients with pituitary adenomas were collected retrospectively over a period of 20 years.
  • 399 patients with well-documented pituitary adenomas and information about pre-treatment body mass index (BMI), age, sex, and tumour type were analysed.
  • RESULTS: Elevated BMI (> or = 30 kg/m2) was observed in 8/36 patients (22.2%) with ACTH-producing tumours, in 15/70 (21.4%) with GH-producing tumours, in 25/100 (25%) with macroprolactinoma, in 8/81 (9.9%) with microprolactinoma, and in 18/105 (17.1%) with inactive macroadenomas.
  • Macroprolactinoma patients had a mean BMI value (27.5 +/- 7.7 kg/m2) similar to that of patients with Cushing's disease (27.2 +/- 5.9 kg/m2) and acromegaly (27.4 +/- 4.4 kg/m2) and on average a significantly higher BMI value compared to that of patients with inactive macroadenomas (25.8 +/- 4.4 kg/m2) (95% CI 1.2, 4.4; p-value <0.001).
  • CONCLUSIONS: Average BMI in macroprolactinoma patients is significantly higher than BMI in patients with inactive adenomas.
  • [MeSH-major] Obesity / etiology. Pituitary Neoplasms / complications. Prolactinoma / complications
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / complications. Adolescent. Adult. Body Mass Index. Female. Growth Hormone-Secreting Pituitary Adenoma / complications. Humans. Male. Middle Aged. Retrospective Studies

  • Genetic Alliance. consumer health - Obesity.
  • MedlinePlus Health Information. consumer health - Obesity.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16708311.001).
  • [ISSN] 1424-7860
  • [Journal-full-title] Swiss medical weekly
  • [ISO-abbreviation] Swiss Med Wkly
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


8. Lad SP, Patil CG, Laws ER Jr, Katznelson L: The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease. Neurosurg Focus; 2007;23(3):E2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease.
  • Cushing's syndrome can present a complex problem of differential diagnosis.
  • Of cases in which hypercortisolemia results from an adrenocorticotropic hormone (ACTH)-dependent process, approximately 80% are due to a pituitary adenoma (Cushing's disease [CD]), 10% are due to adrenal lesions, and the remaining 10% are secondary to ectopic ACTH secretion.
  • For patients with CD, surgical removal of the pituitary adenoma is the treatment of choice.
  • Thus, localization of the source of ACTH secretion is critical in guiding timely treatment decisions.
  • Inferior petrosal sinus sampling (IPSS) is considered to be the gold standard for confirming the origin of ACTH secretion in patients with Cushing's syndrome.
  • A number of other techniques are discussed including sampling from the cavernous sinus, the jugular vein, and multiple sites to aid the diagnosis and lateralization of ACTH-producing pituitary adenomas.
  • [MeSH-major] Petrosal Sinus Sampling / methods. Pituitary ACTH Hypersecretion / diagnosis

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17961020.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 46
  •  go-up   go-down


9. Moriarty M, Hoe F: Cushing disease in a toddler: not all obese children are just fat. Curr Opin Pediatr; 2009 Aug;21(4):548-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing disease in a toddler: not all obese children are just fat.
  • Cushing disease is exceedingly rare in children, especially in those under the age of 2 years.
  • Her diagnosis was delayed; however, she was successfully treated by surgical excision of the microadenoma.
  • Review of this case, as well as a handful of other cases of infantile Cushing disease in the literature, suggests that features such as hypertension and slowed linear growth, which are rare in nutritional causes of obesity in infants, can help identify this rare, but life-threatening, illness among an increasing number of overweight infants.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Cushing Syndrome / etiology. Hypertension / etiology. Obesity, Morbid / etiology
  • [MeSH-minor] Craniotomy. Dissection. Female. Humans. Infant. Pituitary Gland / pathology. Pituitary Gland / surgery

  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19521241.001).
  • [ISSN] 1531-698X
  • [Journal-full-title] Current opinion in pediatrics
  • [ISO-abbreviation] Curr. Opin. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


10. Barlier A, Vanbellinghen JF, Daly AF, Silvy M, Jaffrain-Rea ML, Trouillas J, Tamagno G, Cazabat L, Bours V, Brue T, Enjalbert A, Beckers A: Mutations in the aryl hydrocarbon receptor interacting protein gene are not highly prevalent among subjects with sporadic pituitary adenomas. J Clin Endocrinol Metab; 2007 May;92(5):1952-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutations in the aryl hydrocarbon receptor interacting protein gene are not highly prevalent among subjects with sporadic pituitary adenomas.
  • CONTEXT: Limited screening suggests that three germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene are not involved in sporadic pituitary tumorigenesis.
  • Multiple novel mutations of this gene have since been identified in familial isolated pituitary adenoma cohorts.
  • OBJECTIVE: The objective of the study was to undertake full AIP coding sequence screening to assess for the presence of germline and somatic mutations in European Union subjects with sporadic pituitary tumors.
  • Multiplex ligation-dependent probe amplification was used to screen separate sporadic pituitary tumor tissue samples for discrete and extensive deletions or mutations of the AIP gene.
  • RESULTS: In 107 patients [prolactinomas (n =49), nonfunctioning tumors (n = 29), somatotropinomas (n = 26), ACTH-secreting tumors (n = 2), TSH-secreting tumors (n = 1)], no germline mutations of AIP were demonstrated.
  • Among a group of 41 tumor samples from other subjects, a novel AIP mutation (R22X) was found in one sample in which the corresponding allele was deleted; follow-up screening of the patient demonstrated a germline R22X AIP mutation.
  • CONCLUSIONS: AIP mutations do not appear to play a prominent role in sporadic pituitary tumorigenesis in this population of European subjects.
  • [MeSH-major] Adenoma / genetics. Mutation / genetics. Pituitary Neoplasms / genetics. Proteins / genetics
  • [MeSH-minor] Adult. DNA, Neoplasm / genetics. Female. Gene Frequency. Genotype. Humans. Intracellular Signaling Peptides and Proteins. Male. Middle Aged. Multiple Endocrine Neoplasia Type 1 / genetics. Polymorphism, Genetic / genetics

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • ORBi (University of Liege). Free full Text at ORBi .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • SciCrunch. Clinical Genomic Database: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Endocrinol Metab. 2007 May;92(5):1617-9 [17483376.001]
  • (PMID = 17299063.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proteins; 0 / aryl hydrocarbon receptor-interacting protein
  •  go-up   go-down


11. Alzahrani AS, Farhat R, Al-Arifi A, Al-Kahtani N, Kanaan I, Abouzied M: The diagnostic value of fused positron emission tomography/computed tomography in the localization of adrenocorticotropin-secreting pituitary adenoma in Cushing's disease. Pituitary; 2009;12(4):309-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The diagnostic value of fused positron emission tomography/computed tomography in the localization of adrenocorticotropin-secreting pituitary adenoma in Cushing's disease.
  • Despite the high resolution of magnetic resonance imaging (MRI) of the pituitary gland, up to 40% of cases of Cushing's disease (CD) have normal MRI.
  • Objective of this study is to explore the diagnostic potential of PET-CT for localization of adrenocorticotropin-secreting pituitary adenomas in CD.
  • PET-CT was performed in 12 cases with de novo (7 cases) or persistent CD (5 cases) that were proven to have CD on biochemical, radiological and/or histopathological findings.
  • PET-CT was positive in 7 of the 12 cases of CD (58%) showing a focal area of uptake in the pituitary gland.
  • If these findings are confirmed in larger studies, PET-CT might become an important diagnostic technique, especially when the more invasive and technically demanding procedure of IPSS is not available or inconclusive.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Pituitary ACTH Hypersecretion / pathology. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Pituitary Gland / metabolism. Pituitary Gland / pathology

  • MedlinePlus Health Information. consumer health - CT Scans.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Nucl Med. 2002 Mar;27(3):176-8 [11852303.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2214-21 [15126544.001]
  • [Cites] N Engl J Med. 1991 Sep 26;325(13):897-905 [1652686.001]
  • [Cites] AJR Am J Roentgenol. 1994 Sep;163(3):680-2 [8079867.001]
  • [Cites] Rinsho Hoshasen. 1990 Mar;35(3):407-10 [2161060.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Apr;64(4):371-4 [16584507.001]
  • [Cites] Ann Intern Med. 1994 May 15;120(10):817-20 [8154641.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):418-22 [8106630.001]
  • [Cites] J Nucl Med. 2001 May;42(5 Suppl):1S-93S [11483694.001]
  • [Cites] Lancet. 2006 May 13;367(9522):1605-17 [16698415.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jun;82(6):1780-5 [9177382.001]
  • [Cites] Neurosurgery. 1991 Jun;28(6):826-33 [2067604.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):440-8 [10022398.001]
  • [Cites] J Clin Endocrinol Metab. 2008 May;93(5):1526-40 [18334580.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 Sep;39(3):307-13 [8222293.001]
  • [Cites] AJNR Am J Neuroradiol. 2000 Apr;21(4):690-6 [10782779.001]
  • [Cites] Radiology. 1990 Oct;177(1):39-44 [2399336.001]
  • (PMID = 19387839.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


12. Assimakopoulou M, Zolota V, Chondrogianni C, Gatzounis G, Varakis J: p75 and TrkC neurotrophin receptors demonstrate a different immunoreactivity profile in comparison to TrkA and TrkB receptors in human normal pituitary gland and adenomas. Neuroendocrinology; 2008;88(2):127-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p75 and TrkC neurotrophin receptors demonstrate a different immunoreactivity profile in comparison to TrkA and TrkB receptors in human normal pituitary gland and adenomas.
  • TrkA and TrkB receptors have been previously detected in numerous endocrine cells in human anterior pituitary and adenomas.
  • METHODS: Semi-serial paraffin-embedded sections of 5 human normal pituitaries and 30 adenomas were immunostained using specific antibodies.
  • RESULTS: Expression of p75(NTR) receptor was demonstrated in the intricate capillary and reticulin network in the anterior pituitary and in the pericapillary tissue and pituicytes in the posterior lobe. p75(NTR) immunoreactivity was absent from all adenomas.
  • In normal anterior pituitary, a few scattered cells showed weak TrkC immunoreactivity in contrast to a high percentage of endocrine cells distributed throughout the pars distalis and pars intermedia which exhibited strong TrkA and/or intermediate TrkB immunoreactivity.
  • Double immunohistochemistry demonstrated TrkA immunoreactivity in more than 80% of lactotropes and 70% of corticotropes and to a lesser extent in other cell types.
  • Furthermore, in the majority of adenomas, independently of type, sex and age, a high percentage of TrkA- and/or TrkB-positive cells was detected.
  • Interestingly, TrkC expression appeared to be increased in some adenomas compared to normal pituitary.
  • CONCLUSION: The above findings support a potential role of all neurotrophins, through their different receptors, in pituitary functions.
  • [MeSH-major] Adenoma / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Receptor, Nerve Growth Factor / metabolism. Receptor, trkA / metabolism. Receptor, trkB / metabolism. Receptor, trkC / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Female. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Humans. Immunohistochemistry. Male. Middle Aged. Prolactinoma / metabolism. Prolactinoma / pathology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18319596.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Receptor, Nerve Growth Factor; EC 2.7.10.1 / Receptor, trkA; EC 2.7.10.1 / Receptor, trkB; EC 2.7.10.1 / Receptor, trkC
  •  go-up   go-down


13. Pisarek H, Pawlikowski M, Kunert-Radek J, Radek M: Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies. Endokrynol Pol; 2009 Jul-Aug;60(4):240-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies.
  • BACKGROUND: The highly variable expression of SSTR subtypes in pituitary adenomas (PA) may partially explain why the subgroup of somatotropinomas or other adenomas do not respond to the therapeutic action of currently used long-acting somatostatin analogues like octreotide or lanreotide.
  • RESULTS: The pattern of SSTR immunostaining (estimated according to the percentage frequency of appearance) was in acromegaly: SSTR 5 > SSTR 1 > SSTR 2A = SSTR 3 > SSTR 2B, in prolactinomas: SSTR 2B = SSTR 3 = SSTR 5 > SSTR 1 = SSTR 2A, in gonadotropinomas: SSTR 3 > SSTR 2B > SSTR 1 = SSTR 2A > SSTR 5, in corticotropinomas: SSTR 2A > SSTR 1 = SSTR 3 > SSTR 5 > SSTR 2B.
  • In PA immunonegative for pituitary hormones, we noticed only a weak staining of all receptor subtypes including SSTR 4.
  • In plurihormonal adenomas with positive GH phenotype the staining pattern was: SSTR 5 > SSTR 1 = SSTR 2B and in plurihormonal PA with negative GH phenotype: SSTR 1 = SSTR 5 > SSTR 2A = SSTR 2B = SSTR 3.
  • In plurihormonal adenoma with ACTH immunopositivity, the staining pattern was: SSTR = SSTR 2A = SSTR 3 = SSTR 5.
  • SSTR 1 and SSTR 5 were the most frequent subtypes of somatostatin receptor in plurihormonal adenomas without ACTH expression.
  • Apart from applying SSTR 2 and SSTR 5-preferring octreotide and lanreotide - newly synthesized multiligand analogues, such as SOM 230, KE 108, or other SST selective analogues, may represent a further useful approach for the treatment, especially in cases other than somatotropinoma or thyrotropinoma.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Somatostatin / metabolism

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19753537.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Peptides, Cyclic; 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


14. Karavitaki N, Scheithauer BW, Watt J, Ansorge O, Moschopoulos M, Llaguno AV, Wass JA: Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma. Pituitary; 2008;11(3):317-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma.
  • Most contributions include a pituitary adenoma or a cyst/cystic tumor, particularly a Rathke cleft cyst.
  • The association of craniopharyngioma with an adenoma is particularly rare.
  • Among reported cases, some have included secondary prolactin cell hyperplasia due to pituitary stalk section effect.
  • Herein, we report two collision lesions, including a gonadotroph adenoma with adamantinomatous craniopharyngioma and a corticotroph adenoma with Rathke's cleft cyst.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Central Nervous System Cysts / complications. Corticotrophs / pathology. Craniopharyngioma / complications. Gonadotrophs / pathology. Pituitary Neoplasms / complications. Sella Turcica / pathology

  • Genetic Alliance. consumer health - Craniopharyngioma.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] No Shinkei Geka. 2005 Aug;33(8):797-803 [16095210.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1986 Nov;49(11):1305-7 [3794737.001]
  • [Cites] No To Shinkei. 1969 Dec;21(12):1326-9 [5395295.001]
  • [Cites] Arch Pathol. 1970 Nov;90(5):444-50 [5476241.001]
  • [Cites] Am J Clin Pathol. 2003 Nov;120(5):732-6 [14608900.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1959 Feb;12(2):199-205 [13633216.001]
  • [Cites] Am J Pathol. 2002 Dec;161(6):1997-2001 [12466115.001]
  • [Cites] Arch Pathol Lab Med. 1994 May;118(5):562-5 [8192565.001]
  • [Cites] Arch Dis Child. 1987 Oct;62(10):1077-8 [2823728.001]
  • [Cites] Endocr Rev. 2006 Jun;27(4):371-97 [16543382.001]
  • [Cites] J Pathol. 2004 Jul;203(3):814-21 [15221941.001]
  • [Cites] JAMA. 1978 Aug 4;240(5):471-3 [660898.001]
  • [Cites] J Neurosurg. 1966 Aug;25(2):199-204 [5296495.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):798-827 [9861546.001]
  • [Cites] Intern Med J. 2004 Sep-Oct;34(9-10):573-6 [15482272.001]
  • [Cites] Cancer. 1978 Jan;41(1):337-43 [626939.001]
  • [Cites] No Shinkei Geka. 1984 Jun;12(7):833-8 [6483092.001]
  • [Cites] Anat Rec. 1951 Feb;109(2):217-31 [14811058.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1983;399(1):49-59 [6299000.001]
  • [Cites] Acta Neuropathol. 2005 Jun;109(6):589-97 [15891929.001]
  • [Cites] No Shinkei Geka. 1987 Dec;15(12):1313-8 [3448501.001]
  • [Cites] Mayo Clin Proc. 1989 Sep;64(9):1077-84 [2811485.001]
  • [Cites] No Shinkei Geka. 1986 Mar;14 (3 Suppl):435-40 [3703147.001]
  • [Cites] Endocrinology. 2002 Nov;143(11):4429-36 [12399440.001]
  • [Cites] Neuroradiology. 2001 Sep;43(9):755-9 [11594426.001]
  • [Cites] Endocr Pathol. 2001 Summer;12(2):125-36 [11579678.001]
  • [Cites] J Neurosurg. 2004 Jan;100(1):33-40 [14743909.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1983 Nov;56(5):502-11 [6196702.001]
  • [Cites] Surg Neurol. 1989 May;31(5):381-6 [2711312.001]
  • [Cites] J Neurosurg. 2003 Jan;98(1):162-4 [12546365.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1975 Aug;38(8):782-6 [1185198.001]
  • [Cites] Neurosurgery. 1987 Sep;21(3):371-7 [3670583.001]
  • [Cites] J Neurosurg. 1966 Jan;24(1):77-81 [5903300.001]
  • [Cites] Neurosurgery. 1985 Oct;17(4):657-9 [4058703.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Apr;62(4):397-409 [15807869.001]
  • [Cites] J Pathol. 1971 Mar;103(3):185-7 [5567175.001]
  • [Cites] Br J Neurosurg. 1995;9(1):51-5 [7786427.001]
  • [Cites] J Neurooncol. 2005 Jul;73(3):205-9 [15980970.001]
  • [Cites] Cancer. 1972 Feb;29(2):423-30 [5013542.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jul;82(7):2357-62 [9215319.001]
  • [Cites] Pediatr Neurosurg. 1994;21 Suppl 1:2-10 [7841074.001]
  • [Cites] J Neurosurg. 1994 Jun;80(6):1018-25 [8189257.001]
  • [Cites] J Neurosurg. 1998 Oct;89(4):547-51 [9761047.001]
  • [Cites] No Shinkei Geka. 1987 Sep;15(9):999-1003 [3320806.001]
  • [Cites] Zh Vopr Neirokhir Im N N Burdenko. 1981 Nov-Dec;(6):52-4 [7336839.001]
  • [Cites] J Neurosurg. 2005 Apr;102(3 Suppl):318-21 [15881759.001]
  • [Cites] J Pathol Bacteriol. 1955 Jan-Apr;69(1-2):141-5 [13243181.001]
  • [Cites] Arch Pathol. 1960 Sep;70:293-9 [13850582.001]
  • [Cites] Cancer. 1976 Apr;37(4):1944-52 [1260697.001]
  • [Cites] Neurosurgery. 2000 Feb;46(2):291-302; discussion 302-5 [10690718.001]
  • [Cites] Cancer Genet Cytogenet. 1992 Mar;59(1):12-9 [1313329.001]
  • [Cites] Surg Neurol. 1994 Aug;42(2):112-6 [8091286.001]
  • [Cites] Cancer Genet Cytogenet. 1992 Jun;60(2):212-3 [1606570.001]
  • [Cites] Pituitary. 2004;7(1):39-44 [15638297.001]
  • [Cites] Endocr Pathol. 2002 Summer;13(2):157-65 [12165665.001]
  • [Cites] Intern Med. 1997 Feb;36(2):107-12 [9099592.001]
  • [Cites] Acta Neuropathol. 1992;83(2):211-5 [1557952.001]
  • [Cites] J Neurosurg. 1988 Oct;69(4):620-3 [3418397.001]
  • [Cites] Neurosci Lett. 2001 Sep 7;310(1):5-8 [11524144.001]
  • [Cites] Neurol Med Chir (Tokyo). 1993 Sep;33(9):643-50 [7505406.001]
  • (PMID = 17917812.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 65
  •  go-up   go-down


15. Suárez-Llanos JP, Fernández-Fernández E, Checa MR, Jara-Albarrán A: Response of ACTH to octreotide in a probable corticotropic adenoma associated with Addison's disease. Neuro Endocrinol Lett; 2007 Oct;28(5):549-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Response of ACTH to octreotide in a probable corticotropic adenoma associated with Addison's disease.
  • BACKGROUND: Our patient was a 65-year-old woman previously diagnosed with Addison's disease.
  • She presented an empty sella turcica and, at the age of 47, was discovered to have autonomous hypersecretion of adrenocorticotropic hormone (ACTH), suggesting a corticotropic adenoma secondary to Addison's disease, with a lack of response to high levels of dexamethasone.
  • She maintained high ACTH levels despite corticosteroid treatment.
  • RESULTS: Thirty minutes after the corticotropic-releasing-hormone (CRH) stimulation test, baseline ACTH levels (1 063 pg/ml) increased to 1530, the other values lying between 1 020-862.
  • After octreotide infusion, baseline ACTH (1 212 pg/ml) was 946-643-1 630-4 600-1 730 at 30-60-90-120-180 minutes.
  • The following month, with octreotide treatment, serum ACTH levels were 454-768-1233-429 pg/ml each week.
  • DISCUSSION: Octreotide acts mainly on somatostatin type 2 receptors (SSTR2) and has no effect in Cushing's syndrome, although a suppressor effect in some ACTH ectopic hypersecretions and in Nelson's syndrome has been demonstrated.
  • It has been observed that SSTR5 appear more frequently than SSTR2 in corticotropic adenomas and corticosteroids downregulate octreotide sensitivity.
  • CONCLUSIONS: Octreotide did not suppress secretion of ACTH in suspected corticotropic adenoma.
  • Newer somatostatin analogues, acting mainly on SSTR5, may be able to control ACTH hypersecretion in cases such as this.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenocorticotropic Hormone / drug effects. Antineoplastic Agents, Hormonal / therapeutic use. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Addison's Disease.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17984930.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9002-60-2 / Adrenocorticotropic Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


16. Penezić Z, Zarković M, Vujović S, Ivović M, Beleslin B, Ciric J, Drezgić M: [The value of corticotropin-releasing hormone (CRH) test for differential diagnosis of Cushing's syndrome]. Srp Arh Celok Lek; 2007 Jan-Feb;135(1-2):31-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The value of corticotropin-releasing hormone (CRH) test for differential diagnosis of Cushing's syndrome].
  • INTRODUCTION: Diagnosis and differential diagnosis of Cushing's syndrome (CS) remain considerable challenge in endocrinology.
  • Following the CRH administration, the majority of patients with ACTH secreting pituitary adenoma show a significant rise of plasma cortisol and ACTH, whereas those with ectopic ACTH secretion characteristically do not.
  • OBJECTIVE: The aim of our study was to assess the value of CRF test for differential diagnosis of CS using the ROC (receiver operating characteristic) curve method.
  • ACTH secreting pituitary adenoma was found in 18, ectopic ACTH secretion in 3 and cortisol secreting adrenal adenoma in 9 of all patients with CS.
  • Cortisol and ACTH were determined -15.0, 15, 30, 45, 60, 90 and 120 min. after i.v. administration of 100 microg of ovine CRH.
  • Cortisol and ACTH were determined by commercial RIA.
  • Due to small number, the patients with ectopic ACTH secretion were excluded from test evaluation by ROC curve method.
  • Consequently, basal ACTH was (100.9 +/- 85.0 vs. 138.0 +/- 123.7 vs. 4.8 +/- 4.3 pg/mL) and maximal stimulated ACTH (203.8 +/- 160.1 vs. 288.0 +/- 189.5 vs. 7.4 +/- 9.2 pg/mL).
  • For ACTH, determination area under ROC curve was 0.637 +/- 0.142 (CI 95% 0.359-0.916).
  • For ACTH increase cut-off level of 30%, test sensitivity was 70%, with specificity of 57%.
  • CONCLUSION: Determination of cortisol and ACTH levels in CRH test remains reliable tool in differential diagnosis of Cushing's syndrome.
  • [MeSH-major] Corticotropin-Releasing Hormone. Cushing Syndrome / diagnosis
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Adrenocorticotropic Hormone / blood. Adult. Diagnosis, Differential. Female. Humans. Hydrocortisone / blood. Male. ROC Curve. Sensitivity and Specificity

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17503565.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia and Montenegro
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


17. Ronchi CL, Ferrante E, Rizzo E, Giavoli C, Verrua E, Bergamaschi S, Lania AG, Beck-Peccoz P, Spada A: Long-term basal and dynamic evaluation of hypothalamic-pituitary-adrenal (HPA) axis in acromegalic patients. Clin Endocrinol (Oxf); 2008 Oct;69(4):608-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term basal and dynamic evaluation of hypothalamic-pituitary-adrenal (HPA) axis in acromegalic patients.
  • OBJECTIVE: Long-term effects of trans-naso-sphenoidal surgery (TNS) or long-acting somatostatin analogs (SSA) on the function of hypothalamic-pituitary-adrenal (HPA) axis have been poorly investigated.
  • Aim of this study was to evaluate HPA axis integrity during the follow-up in patients with GH-secreting pituitary adenomas and preserved HPA function post-TNS or prior SSA.
  • MEASUREMENTS: HPA function was studied by morning circulating cortisol and ACTH levels, 24-h urinary free cortisol (UFC) and cortisol response to low-dose short Synacthen test (LDSST, 1 microg) with a peak > 500 nmol/l as cut-off for normal function.
  • RESULTS: Serum basal cortisol, ACTH and UFC levels were in the normal range and did not significantly change over time.
  • No significant correlations between HPA axis deterioration and follow-up duration, serum GH/IGF-I levels, occurrence of other pituitary deficiencies, presence of secondary empty sella, changes in tumour or residual volume were observed.
  • [MeSH-major] Acromegaly / physiopathology. Hypothalamo-Hypophyseal System / physiology. Pituitary-Adrenal System / physiology
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / metabolism. Adenoma / physiopathology. Adrenocorticotropic Hormone / blood. Adrenocorticotropic Hormone / metabolism. Adult. Aged. Basal Metabolism / physiology. Delayed-Action Preparations. Disease Progression. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Hydrocortisone / metabolism. Male. Middle Aged. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / physiopathology. Retrospective Studies. Somatostatin / administration & dosage. Somatostatin / analogs & derivatives. Time Factors

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18410544.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Delayed-Action Preparations; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


18. Benoit I, Drui D, Chaillous L, Dupas B, Mosnier JF, Charbonnel B, Cariou B: A corticotroph pituitary adenoma as the initial presentation of familial glucocorticoid deficiency. Eur J Endocrinol; 2009 Jul;161(1):195-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A corticotroph pituitary adenoma as the initial presentation of familial glucocorticoid deficiency.
  • CONTEXT; Familial glucocorticoid deficiency (FGD) is a rare autosomal recessive ACTH-resistance syndrome characterized by glucocorticoid deficiency in the absence of mineralocorticoid deficiency.
  • Here, we report the case of a young woman with a corticotroph pituitary adenoma as the initial presentation of FGD.
  • CASE REPORT: A 15-year-old girl was referred to our institution for a 16 mm pituitary adenoma associated with glucocorticoid deficiency.
  • DNA sequencing did not identify mutations in either the melanocortin 2 receptor (MC2R) or the MC2R accessory protein genes, indicating type 3 FGD.
  • Despite adequate glucocorticoid replacement, plasma ACTH levels remained increased and pituitary magnetic resonance imaging (MRI) showed a progression of the tumour size resulting in optic chiasm compression with intra-tumoural haemorrhaging.
  • The histomorphological analysis identified a well-individualized pituitary adenoma immunoreactive for ACTH.
  • The proband's sister also exhibited type 3 FGD associated with pituitary hyperplasia upon MRI.
  • CONCLUSION: This case highlights the relationship between FGD and hyperplasia of ACTH-producing cells, potentially leading to histologically proven pituitary corticotroph adenomas.
  • This observation raises the question of the pituitary MRI's significance in the follow-up of FGD.

  • Genetic Alliance. consumer health - Glucocorticoid Deficiency, Familial.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • MedlinePlus Health Information. consumer health - Steroids.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19423561.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucocorticoids; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


19. Sinha S, Sharma BS: Giant pituitary adenomas--an enigma revisited. Microsurgical treatment strategies and outcome in a series of 250 patients. Br J Neurosurg; 2010 Feb;24(1):31-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Giant pituitary adenomas--an enigma revisited. Microsurgical treatment strategies and outcome in a series of 250 patients.
  • BACKGROUND: Giant pituitary adenomas (> 4 cm) are a surgical challenge.
  • METHODS: Two hundred and fifty patients with giant pituitary adenomas were managed surgically at our center over last 13 years.
  • Among functioning adenomas, 63 patients (25.4%) had prolactinomas and 45 patients (18%) had GH-secreting adenomas; while 3 patients each had LH and ACTH- secreting adenomas.
  • The maximum tumor diameter varied from 4 to 10.5 cm, with mean diameter of 5.4 cm.
  • 23 patients (9.2%) underwent re-exploration either because of postoperative apoplexy or residual tumor.
  • Overall, near total (>90%) tumor excision could be achieved in 74%, with improved vision in 53% and good outcome in 75% patients.
  • CONCLUSIONS: The main goal of surgical treatment of giant pituitary adenoma is maximum possible tumor extirpation with minimal side effects, which can be achieved by careful preoperative planning of operative approach, based on directions of tumor extensions and invasiveness.
  • Maximal surgical removal of giant adenomas offers best chances to control tumor growth when followed with adjuvant medical and radiation therapies.
  • [MeSH-major] Adenoma / surgery. Microsurgery / methods. Pituitary Neoplasms / surgery

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20158350.001).
  • [ISSN] 1360-046X
  • [Journal-full-title] British journal of neurosurgery
  • [ISO-abbreviation] Br J Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


20. Smith PW, Turza KC, Carter CO, Vance ML, Laws ER, Hanks JB: Bilateral adrenalectomy for refractory Cushing disease: a safe and definitive therapy. J Am Coll Surg; 2009 Jun;208(6):1059-64
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral adrenalectomy for refractory Cushing disease: a safe and definitive therapy.
  • BACKGROUND: Refractory Cushing disease (CD) is associated with considerable morbidity and mortality.
  • Elevated serum ACTH (> 200 ng/mL) was present during followup in 33% (13 of 40).
  • There are persistent fatigue and QOL deficits that are not ameliorated by laparoscopic compared with open resection.
  • [MeSH-major] Adrenalectomy / methods. Pituitary ACTH Hypersecretion / surgery
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Adult. Aged. Female. Humans. Male. Middle Aged. Retrospective Studies. Treatment Outcome. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19476892.001).
  • [ISSN] 1879-1190
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


21. Hanson JM, Mol JA, Meij BP: Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas. Domest Anim Endocrinol; 2010 May;38(4):260-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas.
  • Leukemia inhibitory factor (LIF) is a pleiotropic cytokine of the IL-6 family that activates the hypothalamic-pituitary-adrenal axis and promotes corticotrope cell differentiation during development.
  • The aim of this study was to investigate the expression of LIF and its receptor (LIFR) in the canine pituitary gland and in corticotrope adenomas, and to perform a mutation analysis of LIFR.
  • Using immunohistochemistry, immunofluorescence, and quantitative expression analysis, LIF and LIFR expression were studied in pituitary glands of control dogs and in specimens of corticotrope adenoma tissue collected through hypophysectomy in dogs with pituitary-dependent hypercortisolism (PDH, Cushing's disease).
  • In the control pituitary tissues and corticotrope adenomas, there was a low magnitude of LIF expression.
  • The LIFR, however, was highly expressed and co-localized with ACTH(1-24) expression.
  • Cytoplasmatic immunoreactivity of LIFR was preserved in corticotrope adenomas and adjacent nontumorous cells of pars intermedia.
  • Surprisingly, nuclear to perinuclear immunoreactivity for LIFR was present in nontumorous pituitary cells of the pars distalis in 10 of 12 tissue specimens from PDH dogs.
  • These data show that LIFR is highly co-expressed with adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) in the canine pituitary gland and in corticotrope adenomas.
  • Nuclear immunoreactivity for LIFR in nontumorous cells of the pars distalis may indicate the presence of a corticotrope adenoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Dog Diseases / metabolism. Leukemia Inhibitory Factor / analysis. Pituitary Gland / chemistry. Pituitary Neoplasms / veterinary. Receptors, OSM-LIF / analysis
  • [MeSH-minor] Animals. Cell Nucleus / chemistry. Cosyntropin / analysis. Cytoplasm / chemistry. DNA, Complementary / analysis. Dogs. Female. Fluorescent Antibody Technique. Immunohistochemistry. Male. Mutation. Polymerase Chain Reaction. Sequence Analysis, DNA. alpha-MSH / analysis

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Cosyntropin .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20036483.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Leukemia Inhibitory Factor; 0 / Receptors, OSM-LIF; 16960-16-0 / Cosyntropin; 581-05-5 / alpha-MSH
  •  go-up   go-down


22. Psaras T, Honegger J, Buslei R, Saeger W, Klein D, Capper D, Meyermann R, Mittelbronn M: Atypical type II silent corticotrophic adenoma developing into Cushing's disease upon second recurrence. Exp Clin Endocrinol Diabetes; 2007 Oct;115(9):610-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical type II silent corticotrophic adenoma developing into Cushing's disease upon second recurrence.
  • Herein, we report the case of a 73-year old male patient who presented with two recurrences of a pituitary adenoma within a period of 15 years.
  • The first tumor resection 15 years ago revealed a non-functioning pituitary macroadenoma.
  • 11 years later, the first recurrence of the tumor was reoperated.
  • Throughout the early course of the disease, he suffered from secondary adrenal insufficiency and required replacement therapy with hydrocortisone.
  • Currently, he presented with the second recurrence and clinical examination revealed signs of Cushing's disease.
  • A retrospective analysis of all histological and immunohistochemical slides rendered an adenoma exhibiting chromophobia, ACTH-positivity and features of atypia such as elevated p53 and Ki67 expression as well as nuclear polymorphism.
  • According to the revised WHO classification it was classified as atypical type II silent corticotroph adenoma at the time of the first and second surgery.
  • The specimen removed during the recent surgery displayed the same histological features and was classified as corticotroph adenoma.
  • The combination of an atypical type II adenoma and the switch in the hormone status to an endocrinologically active adenoma makes this case exceedingly rare.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Neoplasm Recurrence, Local / pathology. Pituitary ACTH Hypersecretion / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Aged. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Tumor Suppressor Protein p53 / metabolism

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17943697.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


23. Yawar A, Zuberi LM, Haque N: Cushing's disease and pregnancy: case report and literature review. Endocr Pract; 2007 May-Jun;13(3):296-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's disease and pregnancy: case report and literature review.
  • OBJECTIVE: To describe a patient with untreated Cushing's disease who had 2 spontaneous pregnancies that resulted in healthy babies on both occasions.
  • METHODS: We present a case report with clinical, laboratory, and imaging data and discuss the literature pertaining to pregnancy in patients with Cushing's syndrome.
  • RESULTS: A 28-year-old woman came to our endocrinology clinic with a 1-year history of symptoms and signs of Cushing's syndrome.
  • An elevated 24-hour urinary cortisol excretion and an unsuppressed 1-mg overnight dexamethasone test confirmed the diagnosis.
  • Further work-up subsequently showed 2 elevated 24-hour urinary cortisol values, loss of diurnal variation, and an elevated corticotropin level.
  • Magnetic resonance imaging of the pituitary showed normal findings.
  • Investigations showed increased 24-hour urinary cortisol excretion and serum corticotropin levels.
  • Repeated magnetic resonance imaging disclosed a microadenoma on the right side of the pituitary.
  • Unstimulated inferior petrosal sinus sampling showed a gradient to the right; thus, the presence of pituitary-dependent Cushing's disease was confirmed.
  • CONCLUSION: Our case demonstrates that patients with pituitary-dependent Cushing's disease are more likely to have spontaneous pregnancies with favorable outcomes than are patients with Cushing's syndrome due to other causes.
  • Our patient, despite having Cushing's disease for more than 7 years, had 2 uneventful pregnancies that produced normal healthy children, without exacerbation of her disease during pregnancy.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / complications. Pregnancy Complications

  • Genetic Alliance. consumer health - Pregnancy.
  • MedlinePlus Health Information. consumer health - Health Problems in Pregnancy.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17599863.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 18
  •  go-up   go-down


24. Alexandraki KI, Grossman AB: Medical therapy of Cushing's disease: where are we now? Front Horm Res; 2010;38:165-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical therapy of Cushing's disease: where are we now?
  • The goals of ideal medical therapy for Cushing's disease should be to target the aetiology of the disorder, and thus surgery is the current 'gold standard' treatment.
  • However, no effective drug that directly and effectively targets the adrenocorticotropin-secreting pituitary adenoma has been found to date, and treatments to control the hypercortisolaemic state by adrenal-based therapy are frequently used.
  • Inhibitors of adrenal steroidogenesis, adrenolytic agents, compounds with neuromodulatory properties, and ligands of different nuclear hormone receptors involved in hypothalamo-pituitary regulation currently used have been reviewed.
  • The somatostatin analogue pasireotide and the dopamine agonist cabergoline, as well as their combination, show some therapeutic promise, while retinoic acid analogues should be further investigated in the pituitary-targeted medical therapy of Cushing's disease.
  • Since a percentage of patients treated with surgery are not cured, or improve and subsequently relapse, there is an urgent need for effective medical therapies for this disorder.
  • [MeSH-major] Pituitary ACTH Hypersecretion / drug therapy

  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. MITOTANE .
  • Hazardous Substances Data Bank. METYRAPONE .
  • Hazardous Substances Data Bank. KETOCONAZOLE .
  • Hazardous Substances Data Bank. MIFEPRISTONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20616508.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dopamine Agonists; 320T6RNW1F / Mifepristone; 51110-01-1 / Somatostatin; 78E4J5IB5J / Mitotane; R9400W927I / Ketoconazole; WI4X0X7BPJ / Hydrocortisone; ZS9KD92H6V / Metyrapone
  • [Number-of-references] 50
  •  go-up   go-down


25. de Bruin C, Feelders RA, Waaijers AM, van Koetsveld PM, Sprij-Mooij DM, Lamberts SW, Hofland LJ: Differential regulation of human dopamine D2 and somatostatin receptor subtype expression by glucocorticoids in vitro. J Mol Endocrinol; 2009 Jan;42(1):47-56
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Dopamine agonists (DA) and somatostatin (SS) analogues have been proposed in the treatment of ACTH-producing neuro-endocrine tumours that cause Cushing's syndrome.
  • In this study, we investigated the effects of the GC dexamethasone (DEX) on D(2) and sst expression in three human neuro-endocrine cell lines: BON (carcinoid) and TT (medullary thyroid carcinoma) versus DMS (small cell lung cancer), which is severely GC resistant.
  • In DMS, DEX did not cause significant changes in the expression of these receptor subtypes.
  • In conclusion, we show that GCs selectively down-regulate sst(2), but not D(2) and only to a minor degree sst(5) in human neuro-endocrine BON and TT cells.
  • This mechanism may also be responsible for the low expression of sst(2) in corticotroph adenomas and underwrite the current interest in sst(5) and D(2) as possible therapeutic targets for a medical treatment of Cushing's disease.
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / metabolism. Cell Line. Cell Proliferation. DNA Fragmentation. Dexamethasone / metabolism. Dopamine / metabolism. Hormone Antagonists / metabolism. Humans. Mifepristone / metabolism. Octreotide / metabolism. RNA, Messenger / metabolism. Radioligand Assay. Somatostatin / metabolism

  • MedlinePlus Health Information. consumer health - Steroids.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. DOPAMINE .
  • Hazardous Substances Data Bank. MIFEPRISTONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18852217.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Glucocorticoids; 0 / Hormone Antagonists; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 320T6RNW1F / Mifepristone; 51110-01-1 / Somatostatin; 7S5I7G3JQL / Dexamethasone; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
  •  go-up   go-down


26. Iino K, Oki Y, Yamashita M, Matsushita F, Hayashi C, Yogo K, Nishizawa S, Yamada S, Maekawa M, Sasano H, Nakamura H: Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma. J Clin Endocrinol Metab; 2010 Aug;95(8):4003-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma.
  • CONTEXT: Methods for preoperative diagnosis of prohormone convertase 2 (PC2)-positive ACTH-producing pituitary adenomas (APPAs) have not been established.
  • Also, their characteristics are not evident.
  • OBJECTIVE: This study was designed to understand the meaning of plasma alphaMSH levels and the role of cell proliferation-signaling molecules in PC2-positive APPAs.
  • RESULTS: Nine adenomas (47.4%) were immunopositive for PC2 and were large and invasive in nature.
  • Eight adenomas (42.1%) were immunopositive for both PC2 and p-Akt, and seven others (36.8%) were immunonegative for both, suggesting significant coexpression of PC2 and p-Akt in tumors.
  • Quantitative RT-PCR revealed that PC2 expression is associated with phosphorylation of Akt but not with its gene expression.
  • Most APPAs expressed receptor tyrosine kinases, but membrane-bound receptors could not be identified.
  • CONCLUSIONS: Our study suggests that PC2 expression and Akt phosphorylation are related at the molecular level, resulting in a change in cell cycle and an increase in pituitary adenoma size.
  • An elevation of plasma alphaMSH could conjecture the activation of the phosphatidylinositol 3/Akt cascade in PC2-positive APPAs and may become a valuable clinical marker of tumor growth in Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Proprotein Convertase 2 / metabolism. alpha-MSH / blood

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20501680.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 581-05-5 / alpha-MSH; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.21.94 / Proprotein Convertase 2
  •  go-up   go-down


27. Brito J, Sáez L, Lemp M, Liberman C, Michelsen H, Araya AV: [Immunohistochemistry for pituitary hormones and Ki-67 in growth hormone producing pituitary adenomas]. Rev Med Chil; 2008 Jul;136(7):831-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Immunohistochemistry for pituitary hormones and Ki-67 in growth hormone producing pituitary adenomas].
  • [Transliterated title] Evaluación por inmunohistoquímica de la expresión de hormonas hipofisiarias y del marcador de proliferación celular Ki-67 en tejido de adenomas causantes de acromegalia.
  • BACKGROUND: Growth hormone (GH) producing adenomas, frequently express several hormones.
  • AIM: To measure the immunohistochemical hormone expression in pituitary adenomas, excised from patients with acromegaly.
  • To determine if the plurihormonal condition of these adenomas is associated with a higher proliferative capacity, assessed through the expression of Ki-67.
  • MATERIAL AND METHODS: Forty one paraffin embedded surgical samples of pituitary adenomas from patients with acromegalia were studied.
  • Immunohistochemistry for GH, prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH), adrenocorticotropin (ACTH) and for the expression of Ki-67 was carried out.
  • CONCLUSIONS: Half of GH producing pituitary adenomas are plurihormonal.
  • There are no differences in the expression of Ki-67 between mono and plurihormonal adenomas.
  • [MeSH-major] Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Human Growth Hormone / metabolism. Ki-67 Antigen / metabolism. Neoplasm Proteins / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Acromegaly / physiopathology. Acromegaly / surgery. Adrenocorticotropic Hormone / analysis. Adult. Aged. Female. Follicle Stimulating Hormone / analysis. Humans. Immunohistochemistry. Male. Middle Aged. Prolactin / analysis. Proliferating Cell Nuclear Antigen / analysis. Statistics, Nonparametric. Thyrotropin / analysis

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • Hazardous Substances Data Bank. MENOTROPINS .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18949157.001).
  • [ISSN] 0034-9887
  • [Journal-full-title] Revista médica de Chile
  • [ISO-abbreviation] Rev Med Chil
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Chile
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / Proliferating Cell Nuclear Antigen; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
  •  go-up   go-down


28. Giacomini D, Haedo M, Gerez J, Druker J, Páez-Pereda M, Labeur M, Stalla GK, Arzt E: Differential gene expression in models of pituitary prolactin-producing tumoral cells. Horm Res; 2009 Apr;71 Suppl 2:88-94
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression in models of pituitary prolactin-producing tumoral cells.
  • Although several genes and signalling pathways have been identified as important effectors in the development of pituitary tumours, our understanding of pituitary tumorigenesis remains incomplete and is the focus of much current research.
  • Use of the mRNA differential display technique in prolactinomas from D2-receptor knockout mice and in stable GH3 cell line clones with enhanced tumorigenicity in vivo has led to the identification of two genes that are involved in the pathogenic process--BMP-4 and RSUME.
  • In contrast, BMP-4 has an inhibitory role in corticotrophinomas.
  • RSUME (RWD-containing sumoylation enhancer) was identified from a transformed lactosomatotrophic cell line that had increased tumorigenic and angiogenic potential.
  • The differential expression and action of BMP-4 in prolactinomas and corticotrophinomas highlights the importance of studying a gene with contrasting actions in two cell lineages of the same organ in order to understand the pituitary transformation process.
  • Both BMP-4 and RSUME may be interesting targets for inhibiting steps involved in pituitary tumorigenesis.
  • [MeSH-major] Bone Morphogenetic Protein 4 / biosynthesis. Gene Expression Regulation, Neoplastic. Models, Biological. Neoplasm Proteins / biosynthesis. Prolactinoma / metabolism. Transcription Factors / biosynthesis
  • [MeSH-minor] Animals. Cell Hypoxia / genetics. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Signal Transduction / genetics

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407504.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Neoplasm Proteins; 0 / RSUME protein, human; 0 / Receptors, Dopamine D2; 0 / Transcription Factors
  • [Number-of-references] 56
  •  go-up   go-down


29. Winczyk K, Pawlikowski M: Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA. Folia Histochem Cytobiol; 2005;43(3):137-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA.
  • The occurrence of peroxisome proliferator-activated receptors gamma (PPARgamma) was investigated in 51 human pituitary adenomas and in 6 non-tumoral human pituitary tissue samples.
  • The mean percentage of cells with positive nuclear reaction was 3-fold higher in pituitary adenomas in comparison with non-tumoral pituitary tissues.
  • It was clearly stronger in pituitary adenomas than in non-tumoral pituitary tissues.
  • A slight, statistically insignificant tendency towards negative correlation between PPARgamma and PCNA was found in somatotropinomas, prolactinomas, corticotropinomas and gonadotropinomas.
  • On the other hand, in null cell adenomas and "silent" corticotropinomas, a strong positve correlation between the expression of PPARgamma and PCNA was observed.
  • The strong expression of PPARgamma in human pituitary adenomas and its possible involvement in control of cell proliferation in these tumors give a good reason for the attempts of their treatment with PPARgamma ligands.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16201313.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Proliferating Cell Nuclear Antigen
  •  go-up   go-down


30. Daly AF, Rixhon M, Adam C, Dempegioti A, Tichomirowa MA, Beckers A: High prevalence of pituitary adenomas: a cross-sectional study in the province of Liege, Belgium. J Clin Endocrinol Metab; 2006 Dec;91(12):4769-75
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High prevalence of pituitary adenomas: a cross-sectional study in the province of Liege, Belgium.
  • CONTEXT: Prevalence data are important for assessing the burden of disease on the health care system; data on pituitary adenoma prevalence are very scarce.
  • OBJECTIVE: The objective of the study was to measure the prevalence of clinically relevant pituitary adenomas in a well-defined population.
  • DESIGN: This was a cross-sectional, intensive, case-finding study performed in three regions of the province of Liège, Belgium, to measure pituitary adenoma prevalence as of September 30, 2005.
  • Medical practitioners in these districts were recruited, and patients with pituitary adenomas under their care were identified.
  • RESULTS: Sixty-eight patients with clinically relevant pituitary adenomas were identified in a population of 71,972 individuals; the mean (+/- sd) prevalence was 94 +/- 19.3 cases per 100,000 population (95% confidence interval, 72.2 to 115.8).
  • The group was 67.6% female and had a mean age at diagnosis of 40.3 yr; 42.6% had macroadenomas and 55.9% underwent surgery.
  • Prolactinomas comprised 66% of the group, with the rest having nonsecreting tumors (14.7%), somatotropinomas (13.2%), or Cushing's disease (5.9%); 20.6% had hypopituitarism.
  • CONCLUSION: The prevalence of pituitary adenomas in the study population (one case in 1064 individuals) was more than 3.5-5 times that previously reported.
  • This increased prevalence may have important implications when prioritizing funding for research and treatment of pituitary adenomas.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Belgium / epidemiology. Child. Cross-Sectional Studies. Female. Growth Hormone-Secreting Pituitary Adenoma / epidemiology. Growth Hormone-Secreting Pituitary Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / therapy. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / epidemiology. Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / therapy. Prevalence. Prolactinoma / epidemiology. Prolactinoma / pathology. Prolactinoma / therapy


31. Keil MF, Stratakis CA: Facial metrics in children with corticotrophin-producing pituitary adenomas suggest abnormalities in midface development. J Pediatr Endocrinol Metab; 2009 Jan;22(1):47-53
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Facial metrics in children with corticotrophin-producing pituitary adenomas suggest abnormalities in midface development.
  • BACKGROUND: Tumors of the hypothalamic-pituitary unit have been linked to genetic syndromes that are associated with midfacial abnormalities.
  • AIM: We hypothesized that mutations of genes that affect the development of the face (and consequently of the anterior pituitary) may be present in children with ACTH-producing pituitary adenomas, and if this is true then facial measurements would be different from those predicted by parental features.
  • METHODS: We studied 20 children with corticotropinomas and a control group and their parents.
  • RESULTS: Significant differences were seen between the children with pituitary adenomas and their parents for vertical facial height measures: nasal length (p < 0.001), lower facial height (p < 0.03) and overall facial height (p < 0.01).
  • CONCLUSION: We conclude that some of the indices of midline craniofacial development, in particular those affecting the vertical axis, are different in children with corticotroph adenomas producing ACTH.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Face / pathology. Maxillofacial Abnormalities / etiology. Maxillofacial Development / physiology

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Craniofac Surg. 2003 Jan;14(1):13-28 [12544216.001]
  • [Cites] Am J Med Genet. 2002 Sep 1;111(4):388-91 [12210297.001]
  • [Cites] Horm Res. 2003;60(4):168-73 [14530604.001]
  • [Cites] Am J Phys Anthropol. 1974 Nov;41(3):423-9 [4473903.001]
  • [Cites] Am J Med Genet. 1980;7(1):47-74 [7211952.001]
  • [Cites] Am J Med Genet. 1983 Mar;14(3):557-65 [6859106.001]
  • [Cites] J Craniofac Genet Dev Biol. 1985;5(3):229-38 [4044786.001]
  • [Cites] Clin Genet. 1993 Sep;44(3):129-38 [8275570.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Nov;79(5):1498-502 [7962349.001]
  • [Cites] Am J Med Genet. 1998 Oct 2;79(4):294-304 [9781911.001]
  • [Cites] Am J Phys Anthropol. 1953 Mar;11(1):121-40 [13040508.001]
  • [Cites] Horm Metab Res. 2005 Jun;37(6):347-54 [16001326.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Sep;90(9):5134-40 [15941871.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Jan;91(1):221-4 [16219718.001]
  • [Cites] Eur J Endocrinol. 2006 May;154(5):753-8 [16645024.001]
  • [Cites] J Endocrinol Invest. 2006 Mar;29(3):208-13 [16682832.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Sep;91(9):3316-23 [16787992.001]
  • [Cites] Genes Dev. 2006 Oct 15;20(20):2871-86 [17043312.001]
  • [Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R73-9 [17613551.001]
  • [Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R80-7 [17613552.001]
  • [Cites] Pediatrics. 2007 Sep;120(3):e575-86 [17698579.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Aug;85(8):2701-8 [10946868.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Dec;85(12):4556-61 [11134108.001]
  • [Cites] J Pediatr. 2001 Aug;139(2):215-9 [11487746.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):95-110 [11761437.001]
  • [Cites] Ann Med. 2002;34(3):179-91 [12173688.001]
  • [Cites] Front Neuroendocrinol. 2003 Apr;24(2):94-127 [12763000.001]
  • (PMID = 19344074.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00001595
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] Germany
  • [Other-IDs] NLM/ NIHMS310299; NLM/ PMC3143028
  •  go-up   go-down


32. Eljamel MS, Leese G, Moseley H: Intraoperative optical identification of pituitary adenomas. J Neurooncol; 2009 May;92(3):417-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intraoperative optical identification of pituitary adenomas.
  • INTRODUCTION: The main goals of transsphenoidal pituitary surgery are total removal of pituitary adenomas (PAs) and preservation of normal pituitary functions.
  • Achieving these goals is dependent upon the precise localisation of PAs during surgery, particularly secreting microadenomas.
  • After the dura of the floor of the sella was incised a laser probe was inserted into the pituitary gland to identify the ALA-induced protoporphyrin IX spectroscopy at 632 nm, using an optical biopsy system (OBS).
  • Once the adenoma was identified by the OBS it was exposed and examined by the PD system to detect fluorescence.
  • PATIENTS: Thirty consecutive patients were studied: 14 were non-functioning macroadenomas (NFA), 12 were secreting PAs and 4 pituitary cysts.
  • The secreting PAs were GH (2), ACTH (3), prolactin (2) and gonadotrophins (5).
  • Six were microadenomas (3 ACTH, 1 GH, 2 prolactin) and 20 were macroadenomas, of which 12 were invading macroadenomas.
  • CONCLUSION: Intraoperative optical identification of pituitary adenomas is a feasible and reliable way to localize pituitary adenomas during transsphenoidal surgery and it may lead to improved cure rate and preservation of normal pituitary functions.
  • [MeSH-major] Adenoma / pathology. Diagnostic Imaging / methods. Pituitary Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Diagnostic Imaging.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1991 Sep 26;325(13):897-905 [1652686.001]
  • [Cites] Neurosurgery. 2001 Oct;49(4):857-62; discussion 862-3 [11564246.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Aug;45(2):147-56 [8881446.001]
  • [Cites] Radiology. 1992 Oct;185(1):143-7 [1523298.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Nov;43(5):517-22 [8548933.001]
  • [Cites] J Neurosurg. 1986 May;64(5):713-9 [3701419.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] Surg Neurol. 2000 Mar;53(3):211-9 [10773251.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Sep;84(9):3401-2 [10487721.001]
  • [Cites] Lancet Oncol. 2006 May;7(5):392-401 [16648043.001]
  • [Cites] Acta Neurochir Suppl (Wien). 1991;53:72-6 [1803889.001]
  • [Cites] Clin Endocrinol (Oxf). 1988 Mar;28(3):289-95 [2844450.001]
  • [Cites] Br J Neurosurg. 1999 Aug;13(4):349-51 [10616559.001]
  • [Cites] Ann Intern Med. 1988 Sep 15;109(6):487-93 [2843068.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Sep;90(9):5134-40 [15941871.001]
  • [Cites] Endocr Pract. 1998 Nov-Dec;4(6):365-7 [15251709.001]
  • [Cites] Pituitary. 1999 Aug;2(2):117-22 [11081161.001]
  • [Cites] Technol Cancer Res Treat. 2003 Aug;2(4):303-9 [12892512.001]
  • [Cites] Radiother Oncol. 1999 Sep;52(3):233-7 [10580869.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):487-92 [10022405.001]
  • [Cites] Neuroradiology. 1998 Oct;40(10 ):651-5 [9833894.001]
  • [Cites] J Endocrinol Invest. 2000 Sep;23(8):542-4 [11021772.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):3752-63 [15292301.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jul;83(7):2291-5 [9661597.001]
  • [Cites] J Neurosurg. 1986 Dec;65(6):733-44 [3095506.001]
  • [Cites] J Neurosurg. 1998 Dec;89(6):927-32 [9833817.001]
  • [Cites] Neurol Neurochir Pol. 2004 May-Jun;38(3):201-7 [15354233.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):195-208 [11838791.001]
  • [Cites] AJNR Am J Neuroradiol. 2000 Apr;21(4):690-6 [10782779.001]
  • [Cites] Neurosurgery. 1995 Sep;37(3):541-5; discussion 545-6 [7501126.001]
  • (PMID = 19357967.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
  •  go-up   go-down


33. Liao CC, Lin SY, Lin HW, Chen KH, Chang LH, Chen ST, Wang J: Menstrual abnormalities in a woman with ACTH-dependent pituitary macroadenoma mimicking polycystic ovary syndrome. Taiwan J Obstet Gynecol; 2006 Jun;45(2):176-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Menstrual abnormalities in a woman with ACTH-dependent pituitary macroadenoma mimicking polycystic ovary syndrome.
  • OBJECTIVE: Here, we present a case of ACTH-dependent pituitary macroadenoma (Cushing's disease) resulting in secondary amenorrhea mimicking polycystic ovary syndrome (PCOS).
  • She visited a gynecologic clinic where PCOS was impressed according to the clinical manifestation and ultrasound finding.
  • Endocrine studies revealed: serum prolactin 21 ng/mL (3.0-20 ng/mL), FSH 5.69 mIU/mL (3.4-10.0 mIU/mL), LH 1.01 mIU/mL (1.1-11.6 mIU/mL), E2 < 20 pg/mL (follicular phase 53-258 pg/mL), ACTH 110 pg/mL (0-46.0 pg/mL), cortisol 26.7 microg/dL at 8 a.m. (5.0-25 microg/dL), cortisol 21.3 microg/dL at 11 p.m. (half of normal morning value).
  • Right pituitary macroadenoma was diagnosed through a series of dexamethasone tests and MRI.
  • CONCLUSION: PCOS is a common disease resulting in secondary amenorrhea.
  • However, Cushing's syndrome resulting from pituitary macroadenoma should also be considered.
  • Therefore, a careful history, observation, physical examination, and endocrine studies can differentiate between patients with PCOS and Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / diagnosis. Amenorrhea / etiology. Pituitary Neoplasms / complications. Pituitary Neoplasms / diagnosis. Polycystic Ovary Syndrome / diagnosis
  • [MeSH-minor] Adult. Craniotomy. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • MedlinePlus Health Information. consumer health - Polycystic Ovary Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17197364.001).
  • [ISSN] 1875-6263
  • [Journal-full-title] Taiwanese journal of obstetrics & gynecology
  • [ISO-abbreviation] Taiwan J Obstet Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  •  go-up   go-down


34. Tinnel BA, Henderson MA, Witt TC, Fakiris AJ, Worth RM, Des Rosiers PM, Edmondson JW, Timmerman RD, Lo SS: Endocrine response after gamma knife-based stereotactic radiosurgery for secretory pituitary adenoma. Stereotact Funct Neurosurg; 2008;86(5):292-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endocrine response after gamma knife-based stereotactic radiosurgery for secretory pituitary adenoma.
  • PURPOSE: To examine treatment outcomes of Gamma Knife-based stereotactic radiosurgery (GK-based SRS) for secretory pituitary adenomas.
  • MATERIALS AND METHODS: 25 patients were treated with GK-based SRS for secretory pituitary adenomas with >or=12 months of follow-up.
  • For adrenocorticotrophic hormone-secreting tumors, 6 of 12 patients (50%) showed normalization of their endocrine levels at a median of 10 months.
  • For growth hormone-secreting tumors, 4 of 9 patients (44%) showed normalization of endocrine levels at a median time of 30 months.
  • CONCLUSION: GK-based SRS provides a reasonable rate of endocrine normalization of secretory pituitary adenoma.
  • [MeSH-major] Pituitary Neoplasms / surgery. Prolactin / blood. Prolactin / secretion. Prolactinoma / surgery. Radiosurgery
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / secretion. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / secretion. Adenoma / surgery. Adrenocorticotropic Hormone / secretion. Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / secretion. Growth Hormone-Secreting Pituitary Adenoma / surgery. Human Growth Hormone / secretion. Humans. Hydrocortisone / blood. Insulin-Like Growth Factor I / metabolism. Male. Middle Aged. Retrospective Studies. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18758206.001).
  • [ISSN] 1423-0372
  • [Journal-full-title] Stereotactic and functional neurosurgery
  • [ISO-abbreviation] Stereotact Funct Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


35. Choe JH, Lee KS, Jeun SS, Cho JH, Hong YK: Endocrine outcome of endoscopic endonasal transsphenoidal surgery in functioning pituitary adenomas. J Korean Neurosurg Soc; 2008 Sep;44(3):151-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endocrine outcome of endoscopic endonasal transsphenoidal surgery in functioning pituitary adenomas.
  • OBJECTIVE: Microscopic and endoscopic transsphenoidal approach (TSA) are major surgical techniques in the treatment of pituitary adenoma.
  • Endoscopic endonasal transsphenoidal approach (EETSA) has been increasingly used for pituitary adenomas, however, its surgical outcome particularly in functioning pituitary adenoma has been debated.
  • Here, we investigated the endocrine outcome of the patients with growth hormone (GH) and adrenocorticotropic hormone (ACTH) secreting pituitary adenoma treated by EETSA.
  • METHODS: We treated 80 patients with pituitary adenoma by EETSA since 2004, of which 12 patients were affected by functioning pituitary adenomas (9 GH, 3 ACTH, 0 PRL; 9 macro, 3 micro).
  • Surgical outcome of those patients treated by EETSA was compared with that of the 11 functioning pituitary adenoma patients (8 GH, 3 ACTH; 8 macro, 3 micro) who underwent sublabial microscopic TSA between 1997 and 2003.
  • CONCLUSION: EETSA appears to be an effective and safe method for the treatment of functioning pituitary adenomas.

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Rhinol. 2007 Jul-Aug;21(4):510-4 [17882925.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Apr;86(4):1645-52 [11297598.001]
  • [Cites] Am J Rhinol. 2007 Mar-Apr;21(2):203-6 [17424881.001]
  • [Cites] Neuroendocrinology. 2006;83(3-4):240-8 [17047389.001]
  • [Cites] Neurosurgery. 2005 Jun;56(6):1222-33; discussion 1233 [15918938.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):379-87 [15757854.001]
  • [Cites] Surg Neurol. 1997 Mar;47(3):213-22; discussion 222-3 [9068690.001]
  • [Cites] Neurosurgery. 1996 Jul;39(1):189-92; discussion 192-3 [8805160.001]
  • [Cites] J Laryngol Otol. 1994 Jan;108(1):19-22 [8133158.001]
  • [Cites] Laryngoscope. 1992 Feb;102(2):198-202 [1738293.001]
  • [Cites] J Clin Endocrinol Metab. 1988 May;66(5):1056-64 [3360898.001]
  • [Cites] Neurosurgery. 1987 Aug;21(2):218-22 [2821447.001]
  • [Cites] Clin Neurosurg. 1969;16:185-217 [5811707.001]
  • [Cites] Surg Neurol. 2002 Dec;58(6):371-5; discussion 375-6 [12517610.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):187-95 [11761435.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] Laryngoscope. 2007 Aug;117(8):1329-32 [17597634.001]
  • (PMID = 19096666.001).
  • [ISSN] 2005-3711
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2588303
  • [Keywords] NOTNLM ; ACTH-secreting pituitary adenoma / Endoscopy / GH-secreting pituitary adenoma / Transsphenoidal approach
  •  go-up   go-down


36. Tauchmanovà L, Pivonello R, Di Somma C, Rossi R, De Martino MC, Camera L, Klain M, Salvatore M, Lombardi G, Colao A: Bone demineralization and vertebral fractures in endogenous cortisol excess: role of disease etiology and gonadal status. J Clin Endocrinol Metab; 2006 May;91(5):1779-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone demineralization and vertebral fractures in endogenous cortisol excess: role of disease etiology and gonadal status.
  • INTRODUCTION: The effects of endogenous cortisol (F) excess on bone mass and vertebral fractures have still not been thoroughly investigated.
  • Cushing's disease and adrenal and ectopic Cushing's syndrome.
  • MATERIALS AND METHODS: Eighty consecutive patients and 80 controls were prospectively enrolled: 37 patients (21 females) with pituitary ACTH-secreting adenoma, 18 (14 females) with adrenocortical adenoma, 15 (11 females) with adrenal carcinoma of mixed secretion, and 10 (three females) with ectopic ACTH secretion.
  • At diagnosis, bone mineral density (BMD) was determined by the dual-energy x-ray absorptiometry technique at the lumbar spine (L1-L4) and femoral neck; vertebral fractures were investigated by standard spinal radiographs.
  • RESULTS: When comparing the groups with different etiology of F excess, the patients with ectopic ACTH secretion had higher F and lower BMD values than the other subgroups.
  • Only multiple fractures were more frequent in patients with ectopic ACTH hypersecretion (P < 0.05).
  • The harmful effects of F excess at the spine were partly counterbalanced by the increased androgen production but were not affected by gonadal status in women.
  • [MeSH-minor] Adenoma / blood. Adolescent. Adrenal Gland Neoplasms / blood. Adrenocorticotropic Hormone / blood. Adult. Aged. Biomarkers. Body Mass Index. Carcinoma / blood. Case-Control Studies. Cross-Sectional Studies. Female. Humans. Male. Middle Aged. Prospective Studies. Risk Factors

  • MedlinePlus Health Information. consumer health - Spine Injuries and Disorders.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16522701.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


37. Pawlikowski M: Immunohistochemical detection of dopamine D2 receptors in human pituitary adenomas. Folia Histochem Cytobiol; 2010 Sep 30;48(3):394-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical detection of dopamine D2 receptors in human pituitary adenomas.
  • Thirty one pituitary adenomas and 3 samples of peritumoral anterior pituitary tissue were immunostained with an antibody raised against dopamine D2 receptor protein.
  • The positive reactions were found in cell cytoplasm, a subpopulation of cell nuclei and the intratumoral blood vessels walls.
  • As expected, the positive immunostaining was shown in cytoplasm and/or cell nuclei of all examined prolactinomas (7/7).
  • In acromegaly the positive D2 staining occurred in 5/7 samples, in gonadotropinomas in 6/8 and in plurihormonal adenomas 2/4.
  • The lowest expression was observed in corticotropinomas (1/5).
  • Moreover, the presence of D2 receptors in intratumoral blood vessels walls constitutes the possibility of the anti-angiogenic action of D2 agonists in pituitary adenomas.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21071344.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Receptors, Dopamine D2
  •  go-up   go-down


38. Gondim JA, Schops M, de Almeida JP, de Albuquerque LA, Gomes E, Ferraz T, Barroso FA: Endoscopic endonasal transsphenoidal surgery: surgical results of 228 pituitary adenomas treated in a pituitary center. Pituitary; 2010;13(1):68-77
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic endonasal transsphenoidal surgery: surgical results of 228 pituitary adenomas treated in a pituitary center.
  • Pituitary tumors are challenging tumors in the sellar region.
  • Surgical approaches to the pituitary have undergone numerous refinements over the last 100 years.
  • The introduction of the endoscope have revolutionized pituitary surgery.
  • The aim of this study is to report the results of a consecutive series of patients undergoing pituitary surgery using a pure endoscopic endonasal approach and to evaluate the efficacy and safety of this procedure.
  • We reviewed the data of 228 consecutive patients who underwent endonasal transsphenoidal adenoma removal over an 10-year period.
  • Tumor removal rate, endocrinological outcomes, and complications were retrospectively assessed in 228 patients with pituitary adenomas who underwent 251 procedures between December 1998 and December 2007.
  • There were 93 nonfunctioning adenomas, 58 growth hormone-secreting, 41 prolactin-secreting, 28 adrenocorticotropin hormone secreting, 7 FSH-LH secreting and 1 thyroid-stimulating hormone-secreting adenomas.
  • The remission results for patients with nonfunctioning adenomas was 83% and for functioning adenomas were 76.3% (70.6% for GH hormone-secreting, 85.3% for prolactin hormone-secreting, 71.4% for ACTH hormone-secreting, 85.7% for FSH-LH hormone-secreting and 100% for TSH hormone-secreting), with no recurrence at the time of the last follow-up.
  • The endoscopic endonasal approach for resection of pituitary adenomas, provides acceptable results representing a safe alternative procedure to the microscopic approach.
  • This less invasive method, associated with a small number of complications, provides excellent tumor removal rates and represents an important tool for the achievement of good results in the pituitary surgery, mainly for the complete removal of large adenomas.
  • [MeSH-major] Adenoma / surgery. Endoscopy / methods. Pituitary Neoplasms / surgery
  • [MeSH-minor] Humans. Pituitary Hormones / blood. Postoperative Complications. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Endoscopy.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Endocrinol. 2005 Dec;153(6):737-40 [16322377.001]
  • [Cites] Neurosurgery. 2004 May;54(5):1043-48; discussions 1048-50 [15113457.001]
  • [Cites] Laryngoscope. 2006 Oct;116(10):1882-6 [17003708.001]
  • [Cites] Minim Invasive Neurosurg. 2005 Dec;48(6):348-54 [16432784.001]
  • [Cites] Am J Otolaryngol. 2008 Jan-Feb;29(1):48-50 [18061832.001]
  • [Cites] Zhonghua Yi Xue Za Zhi (Taipei). 2000 Apr;63(4):301-10 [10820909.001]
  • [Cites] Arq Neuropsiquiatr. 2003 Sep;61(3B):836-41 [14595492.001]
  • [Cites] Laryngoscope. 1984 Aug;94(8):1066-74 [6379349.001]
  • [Cites] J Neurosurg. 1993 Jul;79(1):70-5 [8315471.001]
  • [Cites] Neurosurgery. 2004 Oct;55(4):933-40; discussion 940-1 [15458602.001]
  • [Cites] Monatsschr Ohrenheilkd Laryngorhinol. 1970;104(10):451-6 [5478133.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Dec;89(12):6348-57 [15579802.001]
  • [Cites] Neuroendocrinology. 2006;83(3-4):240-8 [17047389.001]
  • [Cites] Acta Neurochir (Wien). 1996;138(12):1416-25 [9030348.001]
  • [Cites] Minim Invasive Neurosurg. 1998 Jun;41(2):66-73 [9651913.001]
  • [Cites] Clin Neurol Neurosurg. 2009 Feb;111(2):119-22 [18986756.001]
  • [Cites] Neurosurgery. 2008 May;62(5):1006-15; discussion 1015-7 [18580798.001]
  • [Cites] J Neurosurg. 1981 Apr;54(4):448-54 [7009800.001]
  • [Cites] Horm Res. 1985;22(3):222-7 [4054842.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):187-95 [11761435.001]
  • [Cites] J Neurosurg. 1998 Sep;89(3):353-8 [9724106.001]
  • [Cites] Neurosurgery. 1997 Feb;40(2):225-36; discussion 236-7 [9007854.001]
  • [Cites] J Neurosurg. 1997 Jul;87(1):44-51 [9202264.001]
  • [Cites] Br Med J (Clin Res Ed). 1985 Nov 30;291(6508):1547-50 [3933746.001]
  • [Cites] Laryngoscope. 1992 Feb;102(2):198-202 [1738293.001]
  • [Cites] J Neurosurg. 2003 Feb;98(2):350-8 [12593622.001]
  • [Cites] Eur J Endocrinol. 2006 May;154(5):675-84 [16645014.001]
  • [Cites] Clin Neurosurg. 1969;16:185-217 [5811707.001]
  • [Cites] J Neurosurg. 2002 Aug;97(2):293-8 [12186456.001]
  • [Cites] Neurosurgery. 1998 Feb;42(2):226-31; discussion 231-2 [9482172.001]
  • [Cites] J Neurosurg. 1999 Aug;91(2):175-9 [10433303.001]
  • [Cites] Surg Neurol. 2002 Dec;58(6):371-5; discussion 375-6 [12517610.001]
  • [Cites] Neurosurgery. 1998 Feb;42(2):219-24; discussion 224-5 [9482171.001]
  • [Cites] J R Soc Med. 1986 May;79(5):262-9 [3014145.001]
  • [Cites] Laryngoscope. 1999 Nov;109(11):1838-40 [10569418.001]
  • [Cites] Surg Neurol. 2009 Jul;72 (1):15-9; discussion 19 [18440607.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Oct;45(4):407-13 [8959078.001]
  • [Cites] Surg Neurol. 1997 Mar;47(3):213-22; discussion 222-3 [9068690.001]
  • [Cites] Mayo Clin Proc. 1999 Jul;74(7):661-70 [10405694.001]
  • [Cites] J Neurosurg. 2001 Dec;95(6):1083-96 [11765830.001]
  • (PMID = 19697135.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones
  •  go-up   go-down


39. Pecori Giraldi F, Bucciarelli LG, Saccani A, Scacchi M, Pesce S, Losa M, Cavagnini F: Ghrelin stimulates adrenocorticotrophic hormone (ACTH) secretion by human ACTH-secreting pituitary adenomas in vitro. J Neuroendocrinol; 2007 Mar;19(3):208-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ghrelin stimulates adrenocorticotrophic hormone (ACTH) secretion by human ACTH-secreting pituitary adenomas in vitro.
  • Ghrelin is a brain-gut peptide with wide-ranging endocrine, metabolic, cardiovascular and neural effects.
  • Ghrelin, like its synthetic counterparts, the growth hormone (GH) secretagogues, has been shown to markedly stimulate adrenocorticotrophic hormone (ACTH) and cortisol secretion in humans and the ACTH-releasing effect of GH secretagogues is even greater in patients with pituitary ACTH-secreting tumours.
  • The aim of the present study was to evaluate the effect of ghrelin on ACTH secretion by human pituitary corticotroph tumours in vitro to test the functionality of this circuit.
  • Nine ACTH-secreting pituitary tumours (four microadenomas, five macroadenomas) were collected during surgery and incubated with 10-100 nM human ghrelin or with 10 nM human corticotrophin-releasing hormone (CRH).
  • Control experiments were performed in rat anterior pituitary primary cultures.
  • ACTH secretion was assessed after 4 h and 24 h incubation by immunometric assay.
  • After 4 h of incubation with ghrelin, medium ACTH concentrations were two- to ten-fold higher compared to ACTH concentrations in unstimulated wells.
  • The ACTH-releasing effect of ghrelin was significantly less than the response elicited by 10 nM CRH (up to 40-fold) Similar results were obtained after 24 h of incubation and a superimposable response pattern was observed in rat anterior pituitary primary cultures.
  • The present study demonstrates that the endogenous GH secretagogue, ghrelin, stimulates ACTH secretion directly from human tumoural corticotrophs, as well as from normal rat pituitary, and indicates that the marked ACTH release elicited by ghrelin in patients with Cushing's disease in vivo is due, at least in part, to its action on the pituitary tumour.
  • Moreover, these data uphold the concept of a functional intratumoural ghrelin paracrine circuit in human corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Corticotrophs / secretion. Peptide Hormones / physiology
  • [MeSH-minor] Adult. Animals. Corticotropin-Releasing Hormone / physiology. Female. Ghrelin. Humans. In Vitro Techniques. Male. Middle Aged. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland, Anterior / metabolism. Rats

  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17280594.001).
  • [ISSN] 0953-8194
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
  •  go-up   go-down


40. Cho HY, Cho SW, Kim SW, Shin CS, Park KS, Kim SY: Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas. Clin Endocrinol (Oxf); 2010 May;72(5):648-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas.
  • OBJECTIVE: The prevalence of silent corticotroph adenomas (SCAs) is not rare among nonfunctioning pituitary adenomas (NFPAs); however, it is unknown whether the clinical significance of SCAs differs from that of NFPAs without ACTH immunoreactivity (non-SCAs).
  • MEASUREMENTS: We analysed whether clinical manifestations at diagnosis, postoperative recurrence rate and recurrence characteristics differed between SCA and non-SCA patients.
  • The mean age at the time of diagnosis was 44 years (range, 13-67 years) in the SCA group and 50 years (18-79 years) in the non-SCA group (P = 0.026), with respective follow-up periods of 5.2 (range, 1.0-16.0 years) and 4.2 years (0.5-16.1 years) (P = 0.255).
  • [MeSH-major] Adenoma / pathology. Adrenocorticotropic Hormone / analysis. Neoplasm Recurrence, Local. Pituitary Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19650787.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


46. Patil CG, Lad SP, Harsh GR, Laws ER Jr, Boakye M: National trends, complications, and outcomes following transsphenoidal surgery for Cushing's disease from 1993 to 2002. Neurosurg Focus; 2007;23(3):E7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] National trends, complications, and outcomes following transsphenoidal surgery for Cushing's disease from 1993 to 2002.
  • OBJECT: Information about complications, patient outcomes, and mortality rate after transsphenoidal surgery (TSS) for Cushing's disease has been derived largely from single-institution series.
  • In this study the authors report on inpatient death, morbidity, and outcomes following TSS for Cushing's disease on a national level.
  • METHODS: All patients in the Nationwide Inpatient Sample (NIS) database who had undergone transsphenoidal resection of a pituitary tumor for Cushing's disease between 1993 and 2002 were included in the study.
  • RESULTS: According to the NIS, there were an estimated 3525 cases of TSS for Cushing's disease in the US between 1993 and 2002.
  • During this period, there was a trend toward a small increase in the number of TSSs for Cushing's disease.
  • CONCLUSIONS: The authors provided a national perspective on trends, inpatient complications, and outcomes after TSS for Cushing's disease in the US.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Neurosurgical Procedures / adverse effects. Neurosurgical Procedures / utilization. Pituitary ACTH Hypersecretion / surgery. Sphenoid Sinus / surgery

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17961019.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


47. Domino JP, Chionh SB, Lomanto D, Katara AN, Rauff A, Cheah WK: Laparoscopic partial adrenalectomy for bilateral cortisol-secreting adenomas. Asian J Surg; 2007 Apr;30(2):154-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic partial adrenalectomy for bilateral cortisol-secreting adenomas.
  • Bilateral cortisol-secreting adenomas are a rare cause of Cushing's syndrome.
  • We report a case of a 35-year-old woman who presented with ACTH-independent Cushing's syndrome and bilateral adrenal adenomas.
  • Adrenal venous sampling confirmed both adenomas to be hyper-secreting cortisol.

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17475590.001).
  • [ISSN] 1015-9584
  • [Journal-full-title] Asian journal of surgery
  • [ISO-abbreviation] Asian J Surg
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


48. Moore AF, Grinspoon SK: A dural tale. J Clin Endocrinol Metab; 2007 Sep;92(9):3367-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Dura Mater / pathology
  • [MeSH-minor] Adult. Cushing Syndrome / diagnosis. Cushing Syndrome / etiology. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17823272.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


49. Chacko G, Chacko AG, Lombardero M, Mani S, Seshadri MS, Kovacs K, Scheithauer BW: Clinicopathologic correlates of giant pituitary adenomas. J Clin Neurosci; 2009 May;16(5):660-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathologic correlates of giant pituitary adenomas.
  • Giant adenomas comprise a clinical/therapeutic subset of pituitary adenomas that pose a surgical challenge.
  • The study population consisted of 28 patients who had giant pituitary adenomas, which are defined as tumors with a diameter greater than 5cm.
  • Clinically, five tumors (18%) were endocrinologically functional and 23 (82%) were not.
  • During surgery, one tumor was radically excised, four were subtotally excised, 12 were partially excised, and 11 were biopsied.
  • All of the tumors showed typical histological features of pituitary adenoma.
  • Of the 23 clinically non-functional adenomas, 18 were gonadotrophic tumors, four were null cell adenomas and one was a silent corticotroph adenoma.
  • The present study found giant adenomas to be invasive but slow growing, histologically benign and often gonadotrophic in subtype.
  • [MeSH-major] Adenoma / pathology. Adenoma / therapy. Pituitary Neoplasms / pathology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Antigens, CD34 / metabolism. Female. Follow-Up Studies. Humans. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Treatment Outcome. Young Adult

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19285407.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Ki-67 Antigen; 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


50. Colao A, Filippella M, Pivonello R, Di Somma C, Faggiano A, Lombardi G: Combined therapy of somatostatin analogues and dopamine agonists in the treatment of pituitary tumours. Eur J Endocrinol; 2007 Apr;156 Suppl 1:S57-63
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined therapy of somatostatin analogues and dopamine agonists in the treatment of pituitary tumours.
  • Pituitary tumours express both somatostatin and dopamine receptors.
  • Medical treatment with somatostatin analogues is a cornerstone of GH- and TSH-secreting tumours, while treatment with dopamine agonists is a cornerstone of prolactin-secreting tumours.
  • Dopamine agonists have also demonstrated some efficacy in patients with GH- and TSH-secreting adenomas.
  • Neither ACTH-secreting nor clinically non-functioning tumours have a well-established medical treatment.
  • Nevertheless, some recent results have indicated a potential usefulness of the dopamine agonist cabergoline in patients with pituitary-dependent Cushing's disease.
  • Some studies conducted in small series have documented an additive effect of both drugs in patients with GH-secreting adenomas.
  • No data are available in other pituitary tumour histotypes.
  • Preliminary observations in patients with clinically non-functioning adenomas are very promising.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Eur J Endocrinol. 2007 Oct;157(4):543
  • (PMID = 17413190.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Receptors, Dopamine; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 59
  •  go-up   go-down


51. Daly AF, Jaffrain-Rea ML, Ciccarelli A, Valdes-Socin H, Rohmer V, Tamburrano G, Borson-Chazot C, Estour B, Ciccarelli E, Brue T, Ferolla P, Emy P, Colao A, De Menis E, Lecomte P, Penfornis F, Delemer B, Bertherat J, Wémeau JL, De Herder W, Archambeaud F, Stevenaert A, Calender A, Murat A, Cavagnini F, Beckers A: Clinical characterization of familial isolated pituitary adenomas. J Clin Endocrinol Metab; 2006 Sep;91(9):3316-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical characterization of familial isolated pituitary adenomas.
  • CONTEXT: Familial pituitary adenomas occur rarely in the absence of multiple endocrine neoplasia type 1 (MEN1) and Carney complex (CNC).
  • OBJECTIVE: Our objective was to characterize the clinical and genealogical features of non-MEN1/CNC familial isolated pituitary adenomas (FIPA).
  • RESULTS: Sixty-four FIPA families including 138 affected individuals were identified [55 prolactinomas, 47 somatotropinomas, 28 nonsecreting adenomas (NS), and eight ACTH-secreting tumors].
  • A single tumor phenotype occurred in 30 families (homogeneous), and heterogeneous phenotypes occurred in 34 families.
  • FIPA cases were younger at diagnosis than sporadic cases (P = 0.015); tumors were diagnosed earlier in the first vs. the second generation of multigenerational families.
  • Somatotropinomas occurred as isolated familial somatotropinoma cases and within heterogeneous FIPA families; isolated familial somatotropinoma cases represented 18% of FIPA cases and were younger at diagnosis than patients with sporadic somatotropinomas.
  • Familial NS cases were younger at diagnosis (P = 0.03) and had more frequently invasive tumors (P = 0.024) than sporadic cases.
  • CONCLUSIONS: Homogeneous and heterogeneous expression of prolactinomas, somatotropinomas, NS, and Cushing's disease can occur within families in the absence of MEN1/CNC.
  • [MeSH-major] Adenoma / genetics. Adenoma / pathology. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Adult. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit. Cyclic AMP-Dependent Protein Kinases / genetics. Female. Gonadotropins, Pituitary / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Pedigree. Pituitary Hormones, Anterior / metabolism. Prolactinoma / genetics. Prolactinoma / pathology. Retrospective Studies. Sequence Analysis, DNA


52. Wan H, Chihiro O, Yuan S: MASEP gamma knife radiosurgery for secretory pituitary adenomas: experience in 347 consecutive cases. J Exp Clin Cancer Res; 2009;28:36
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MASEP gamma knife radiosurgery for secretory pituitary adenomas: experience in 347 consecutive cases.
  • BACKGROUND: Secretory pituitary adenomas are very common brain tumors.
  • Historically, the treatment armamentarium for secretory pituitary adenomas included neurosurgery, medical management, and fractionated radiotherapy.
  • In recent years, MASEP gamma knife radiosurgery (MASEP GKRS) has emerged as an important treatment modality in the management of secretory pituitary adenomas.
  • The goal of this research is to define accurately the efficacy, safety, complications, and role of MASEP GKRS for treatment of secretory pituitary adenomas.
  • METHODS: Between 1997 and 2007 a total of 347 patients with secretory pituitary adenomas treated with MASEP GKRS and with at least 60 months of follow-up data were identified.
  • Of the 68 patients with adrenocorticotropic hormone-secreting(ACTH) adenomas, 89.7% showed tumor volume decrease or remain unchanged and 27.9% experienced normalization of hormone level.
  • Of the 176 patients with prolactinomas, 23.3% had normalization of hormone level and 90.3% showed tumor volume decrease or remain unchanged.
  • Of the 103 patients with growth hormone-secreting(GH) adenomas, 95.1% experienced tumor volume decrease or remain unchanged and 36.9% showed normalization of hormone level.
  • CONCLUSION: MASEP GKRS is safe and effective in treating secretory pituitary adenomas.
  • However, treatment must be tailored to meet the patient's symptoms, tumor location, tumor morphometry, and overall health.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery. Radiosurgery / methods

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Stereotact Funct Neurosurg. 1999;72 Suppl 1:111-8 [10681698.001]
  • [Cites] J Neurosurg. 2007 May;106(5):833-8 [17542527.001]
  • [Cites] Neurosurgery. 2000 Jul;47(1):33-6; discussion 37-9 [10917344.001]
  • [Cites] J Neurooncol. 2000 Mar;47(1):79-84 [10930104.001]
  • [Cites] J Neurosurg. 2000 Nov;93(5):738-42 [11059652.001]
  • [Cites] J Neurosurg. 2000 Dec;93 Suppl 3:14-8 [11143231.001]
  • [Cites] Neurosurgery. 2001 Aug;49(2):284-91; discussion 291-2 [11504104.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):197-203 [11761436.001]
  • [Cites] Neuropathology. 2002 Mar;22(1):19-25 [12030411.001]
  • [Cites] Strahlenther Onkol. 2002 Apr;178(4):173-86 [12040754.001]
  • [Cites] Neurosurgery. 2002 Jul;51(1):57-61; discussion 61-2 [12182435.001]
  • [Cites] Neurosurg Clin N Am. 2003 Jan;14(1):25-39, vi [12690977.001]
  • [Cites] Neurosurg Clin N Am. 2003 Jan;14(1):147-66 [12690986.001]
  • [Cites] Neurosurgery. 2003 Jul;53(1):51-9; discussion 59-61 [12823873.001]
  • [Cites] Yonsei Med J. 2003 Aug 30;44(4):602-7 [12950114.001]
  • [Cites] Arch Neurol. 1981 Apr;38(4):217-9 [7213145.001]
  • [Cites] Acta Paediatr Scand. 1986 May;75(3):388-95 [3014807.001]
  • [Cites] Can J Neurol Sci. 1990 Feb;17(1):74-7 [2155694.001]
  • [Cites] Am J Clin Oncol. 1992 Dec;15(6):467-73 [1449108.001]
  • [Cites] Ann Neurol. 1995 Jan;37(1):67-73 [7818260.001]
  • [Cites] Radiother Oncol. 1996 Oct;41(1):45-53 [8961367.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Sep 1;39(2):437-44 [9308948.001]
  • [Cites] J Neurosurg. 1998 Jun;88(6):1002-8 [9609294.001]
  • [Cites] Stereotact Funct Neurosurg. 1998 Oct;70 Suppl 1:119-26 [9782243.001]
  • [Cites] Neurosurg Clin N Am. 1999 Apr;10(2):327-36 [10099097.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):119-31 [10207687.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):133-42 [10207688.001]
  • [Cites] Stereotact Funct Neurosurg. 1999;72 Suppl 1:119-24 [10681699.001]
  • (PMID = 19284583.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2660297
  •  go-up   go-down


53. Salgado LR, Machado MC, Cukiert A, Liberman B, Kanamura CT, Alves VA: Cushing's disease arising from a clinically nonfunctioning pituitary adenoma. Endocr Pathol; 2006;17(2):191-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's disease arising from a clinically nonfunctioning pituitary adenoma.
  • A 49-yr-old woman with a large pituitary tumor leading to visual loss and galactorrhea- amenorrhea was submitted to transcranial pituitary surgery, when a clinically nonfunctioning pituitary adenoma was partially removed.
  • Histopathology and immunohistochemistry confirmed the diagnosis of "non-secreting atypical adenoma."
  • Two years later, she presented high free urinary cortisol levels and a positive ACTH response to desmopressin testing on dexametasone 2 mg overnight.
  • A pituitary biopsy confirmed aggressive growth as well as positive immunoreactivity for ACTH, p53, Ki-67, and c-erb-B2.
  • The overall clinical, laboratory, and pathological data suggest a transition from a clinically nonfunctioning to a hypersecreting ACTH-producing tumor.
  • Putative mechanisms of tumor transformation and the possibility of a silent corticotropinoma evolving into clinical Cushing s syndrome are discussed.
  • [MeSH-major] Adenoma / complications. Adenoma / pathology. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / complications. Pituitary Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pituitary. 2000 Oct;3(2):117-22 [11141695.001]
  • [Cites] Neurosurgery. 1996 Apr;38(4):765-70; discussion 770-1 [8692397.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 May;46(5):599-606 [9231056.001]
  • [Cites] Endocr Pathol. 1996 Spring;7(1):21-35 [12114677.001]
  • [Cites] J Neurosurg. 2004 Nov;101(5):874-7 [15540932.001]
  • [Cites] Aust N Z J Med. 1987 Apr;17(2):249-51 [3039955.001]
  • [Cites] Arch Intern Med. 1983 May;143(5):1040-2 [6089681.001]
  • [Cites] J Endocrinol Invest. 1997 Apr;20(4):240-4 [9211134.001]
  • [Cites] Clin Endocrinol (Oxf). 1985 Feb;22(2):147-53 [2985300.001]
  • [Cites] Neurosurgery. 1996 Jan;38(1):99-106; discussion 106-7 [8747957.001]
  • [Cites] Endocr J. 2002 Jun;49(3):285-92 [12201210.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Nov;79(5):1513-6 [7962351.001]
  • [Cites] Front Horm Res. 2004;32:205-16 [15281348.001]
  • [Cites] Br J Neurosurg. 2005 Feb;19(1):38-42 [16147581.001]
  • [Cites] J Clin Endocrinol Metab. 1998 May;83(5):1619-23 [9589666.001]
  • [Cites] Endocrinol Metab Clin North Am. 1989 Jun;18(2):339-58 [2663478.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Nov;41(5):661-6 [7828356.001]
  • [Cites] Pituitary. 2002;5(4):221-3 [14558669.001]
  • [Cites] J Clin Endocrinol Metab. 1993 May;76(5):1089-94 [8496297.001]
  • [Cites] J Clin Endocrinol Metab. 1979 Jul;49(1):23-9 [221528.001]
  • [Cites] Endocr Pathol. 1996 Summer;7(2):145-150 [12114642.001]
  • (PMID = 17159252.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


54. Bademci G: Pitfalls in the management of Cushing's disease. J Clin Neurosci; 2007 May;14(5):401-8; discussion 409
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pitfalls in the management of Cushing's disease.
  • Cushing's disease is caused by functional corticotroph adenomas of the pituitary gland, most commonly noninvasive microadenomas.
  • Transsphenoidal microsurgery is an effective means of control for patients with adrenocorticotrophic hormone-producing microadenomas.
  • The major causes of surgical failure in the treatment of Cushing's disease lies in inadequate preoperative evaluation, unsuccessful identification of the adenoma and inexperience of the surgeon.
  • For optimal results in this rare disease, endocrinological, radiological and surgical procedures should be co-ordinated in a specialized center.
  • [MeSH-major] Pituitary ACTH Hypersecretion / therapy. Treatment Failure

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17386367.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Number-of-references] 82
  •  go-up   go-down


55. Mounier C, Pasquet F, Trouillas J, Perrin G, Jouanneau E, Borson-Chazot F, Colle B: [Nelson's syndrome: course of aggressive pituitary corticotroph adenoma]. Ann Endocrinol (Paris); 2007 Feb;68(1):28-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Nelson's syndrome: course of aggressive pituitary corticotroph adenoma].
  • [Transliterated title] Syndrome de Nelson: évolution d'un adénome hypophysaire corticotrope agressif.
  • Nelson's syndrome was defined in 1958 as the association of an expanding pituitary tumor with high ACTH secretion after bilateral adrenalectomy for Cushing's disease.
  • Pituitary MRI and ACTH measurements led to the definition of Nelson's syndrome as the proliferation of a corticotrophic microadenoma or an aggressive and highly proliferative tumor residue induced by the decreased glucocorticoid inhibition after bilateral adrenalectomy.
  • Now, the problem is not the definition of Nelson's syndrome but rather the identification of markers predictive of tumor growth.
  • Based on a typical case and a review of the literature, we point out some predictive markers of tumor growth after bilateral adrenalectomy: young age at diagnosis, presence of tumor residue on pituitary MRI before adrenalectomy, markers of tumor aggressiveness (Ki-67>3%, mitoses, nuclear PTTG) and increase of ACTH levels during the first months following adrenalectomy.
  • [MeSH-major] Adenoma / physiopathology. Nelson Syndrome / physiopathology. Pituitary Neoplasms / physiopathology
  • [MeSH-minor] Adrenocorticotropic Hormone / analysis. Adrenocorticotropic Hormone / secretion. Adult. Female. Humans. Magnetic Resonance Imaging. Pituitary Gland / pathology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17306208.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


56. Korbonits M, Carlsen E: Recent clinical and pathophysiological advances in non-functioning pituitary adenomas. Horm Res; 2009 Apr;71 Suppl 2:123-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent clinical and pathophysiological advances in non-functioning pituitary adenomas.
  • Pituitary adenomas are being recognized and diagnosed with increasing frequency.
  • One of the most common forms of pituitary lesion is the clinically non-functioning pituitary adenoma (NFPA), which is often diagnosed incidentally.
  • The vast majority of pituitary adenomas are sporadic, but familial adenomas can occur in the multiple pituitary adenoma type 1 syndrome, in Carney complex or in familial isolated pituitary adenoma.
  • Most often these are silent gonadotroph adenomas, with silent corticotroph or somatotroph adenomas occurring less frequently.
  • It is unclear why these silent adenomas do not release hormones at a clinically recognizable level, although it is probable that there is a continuum between fully functional and completely silent adenomas.
  • Temozolomide has been successfully used for the treatment of a few aggressive pituitary adenomas, and the response to this drug could be influenced by the expression of the DNA repair enzyme O-6-methylguanine DNA methyltransferase.
  • The early diagnosis, prediction of long-term outcome and treatment of NFPAs remain a challenge for endocrinologists.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma. Prolactinoma
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / therapy. Female. Humans. Male

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407508.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 58
  •  go-up   go-down


57. Horiguchi K, Yamada M, Umezawa R, Satoh T, Hashimoto K, Tosaka M, Yamada S, Mori M: Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment. Endocr J; 2007 Jun;54(3):371-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment.
  • TSH-secreting adenoma is a rare pituitary adenoma, and the expression levels of the specific subtypes of somatostatin receptors (sstr) mRNAs have remained obscure.
  • To determine the quantitative expression of the sstr1-5 mRNAs in TSH-secreting adenomas that may be related to the efficacy of treatment with a somatostatin analogue, expression of the sstr1-5 mRNAs was examined and compared in TSH-secreting adenomas and other pituitary adenomas.
  • The pituitary adenomas were obtained at transsphenoidal surgery from 4 cases of TSH-secreting adenoma, including 1 patient showing a significant shrinkage of the tumor size after only 10 days of octreotide treatment, 2 patients without tumor size reduction and 1 patient without treatment, and 5 GH-secreting adenomas, 6 prolactinomas, 5 nonfunctioning adenomas, 4 ACTH-secreting adenomas and normal pituitaries at autopsy from 4 normal subjects.
  • In comparison to the normal pituitary, sstr2A>sstr1>sstr5>sstr3 mRNAs were expressed in the TSH-secreting adenomas examined.
  • The expression level of sstr2 mRNA was significantly higher than those in normal pituitary, prolactinomas, ACTH-secreting and nonfunctioning pituitary adenomas.
  • The patient with marked shrinkage of the tumor showed the highest expression of both sstr2 and sstr5 mRNAs among all the cases of pituitary adenoma.
  • A TSH-secreting tumor without shrinkage showed a similar expression level of sstr2 mRNA.
  • These findings demonstrated that TSH-secreting adenomas express sstr1, 2A, 3 and 5 mRNAs, predominantly sstr2A, and in addition to the expression of sstr2 mRNA, the expression level of sstr5 mRNA may be a factor affecting the tumor shrinkage by somatostatin analogues against TSH-secreting adenomas.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / genetics. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / genetics. Receptors, Somatostatin / genetics. Thyrotrophs / pathology. Tumor Burden / drug effects

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17420609.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


58. Schaefer S, Meyer S, Brueck CC, Weber M, Luedecke D, Wagner HJ, Kann PH: Sarcoidosis following Cushing's syndrome: A report of two cases and review of the literature. Exp Clin Endocrinol Diabetes; 2010 Mar;118(3):147-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sarcoidosis following Cushing's syndrome: A report of two cases and review of the literature.
  • Cushing's syndrome is characterized by excessive elevation of glucocorticoid concentrations.
  • In rare cases, the treatment of Cushing's syndrome may result in unmasking or aggravation of diseases responsive to glucocorticoid medication.
  • We report two cases of sarcoidosis following Cushing's syndrome.
  • A 43 year-old male developed cutaneous sarcoidosis and mediastinal lymphadenopathy after resection of an ACTH-secreting pituitary microadenoma.
  • A 32 year-old female showed cutaneous sarcoidosis, arthralgia, mediastinal lymphadenopathy and elevation of angiotensin-converting enzyme and interleukin 2-receptor concentrations after traumatic adrenal bleeding, which ceased formerly undiagnosed hypercortisolism caused by an adrenal adenoma.
  • Skin affections were present and suggestive for the diagnosis in all reported cases.
  • As some cases are probably missed when skin affections are lacking, a more frequent evaluation of patients after Cushing's syndrome for the possible diagnosis of sarcoidosis might be necessary.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Cushing Syndrome / surgery. Sarcoidosis / etiology. Skin Diseases / etiology
  • [MeSH-minor] Adult. Arthralgia / diagnosis. Arthralgia / etiology. Female. Humans. Lymphatic Diseases / diagnosis. Lymphatic Diseases / etiology. Male. Mediastinal Diseases / diagnosis. Mediastinal Diseases / etiology. Peptidyl-Dipeptidase A / analysis. Receptors, Interleukin-2 / analysis

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • Genetic Alliance. consumer health - Sarcoidosis.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Sarcoidosis.
  • MedlinePlus Health Information. consumer health - Skin Conditions.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart * New York.
  • (PMID = 20162506.001).
  • [ISSN] 1439-3646
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Receptors, Interleukin-2; EC 3.4.15.1 / Peptidyl-Dipeptidase A
  • [Number-of-references] 13
  •  go-up   go-down


59. Thodou E, Argyrakos T, Kontogeorgos G: Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas. Hormones (Athens); 2007 Jul-Sep;6(3):227-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas.
  • OBJECTIVE: Galectin-3 (Gal-3) belongs to the family of carbohydrate-binding proteins with high affinity for galactoside and is involved in many biological processes including cell growth and differentiation, cell adhesion, tumor progression, apoptosis and metastasis.
  • The aim of this study was to disclose differences in the expression of Gal-3 in silent and functioning corticotroph pituitary adenomas.
  • DESIGN: We examined 30 pituitary adenomas (19 functioning corticotroph, 11 silent corticotroph adenomas).
  • Two prolactinomas and 2 functioning somatotroph adenomas served as positive controls.
  • The independent variables t-test was used for comparison of the mean expression of Gal-3 in the two different corticotroph adenoma subgroups.
  • RESULTS: Eighteen of the functioning corticotroph adenomas (94.73%) were positive for Gal-3 with a cytoplasmic and focally membranous distribution; two cases also exhibited nuclear expression, whereas 9 of the silent corticotroph adenomas (81.81%) had zero or<1% expression of Gal-3 (p=0.001).
  • CONCLUSIONS: Gal-3 is highly expressed in functioning corticotroph adenomas of the pituitary gland, while silent adenomas exhibit very focal to null expression of Gal-3.
  • This observation can be used in the pathological diagnosis to separate functioning from silent corticotroph adenomas of the pituitary.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / metabolism. Galectin 3 / metabolism
  • [MeSH-minor] Humans. Immunohistochemistry. Pituitary Gland / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17724007.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3
  •  go-up   go-down


60. Kiehna EN, Keil M, Lodish M, Stratakis C, Oldfield EH: Pseudotumor cerebri after surgical remission of Cushing's disease. J Clin Endocrinol Metab; 2010 Apr;95(4):1528-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pseudotumor cerebri after surgical remission of Cushing's disease.
  • CONTEXT: Pseudotumor cerebri has only been described after successful surgery for Cushing's disease (CD) in case reports.
  • All underwent resection of an ACTH-secreting adenoma, and postoperative serum cortisol reached a nadir of less than 2 microg/dl.
  • Three patients did not receive treatment, and their symptoms resolved over several months.
  • A patient exhibiting signs of intracranial hypertension after surgery for CD should undergo an evaluation for pseudotumor cerebri.

  • Genetic Alliance. consumer health - Pseudotumor cerebri.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. ACETAZOLAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Lancet. 1973 Aug 25;2(7826):418-21 [4124896.001]
  • [Cites] J Neurosurg. 1973 Oct;39(4):480-4 [4730337.001]
  • [Cites] J Neurosurg. 1975 Jun;42(6):690-5 [1141965.001]
  • [Cites] Neurosurgery. 1981 Jun;8(6):699-702 [6269017.001]
  • [Cites] Neurosurgery. 1982 Feb;10(2):297 [6280099.001]
  • [Cites] Endocr Pract. 2004 Nov-Dec;10(6):492-6 [16033722.001]
  • [Cites] Neurol Clin. 1991 Feb;9(1):73-95 [2011112.001]
  • [Cites] Postgrad Med J. 1994 Feb;70(820):115-7 [8170882.001]
  • [Cites] J Child Neurol. 1994 Apr;9(2):144-9 [8006364.001]
  • [Cites] Can J Neurol Sci. 1997 Aug;24(3):219-21 [9276106.001]
  • [Cites] Am J Ophthalmol. 1999 Feb;127(2):178-82 [10030560.001]
  • [Cites] Neurosurgery. 1983 Aug;13(2):195-8 [6310437.001]
  • (PMID = 20164289.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / NICHD NIH HHS / HD / Z01-HD-000642-04; United States / Intramural NIH HHS / /
  • [Publication-type] Case Reports; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Carbonic Anhydrase Inhibitors; 0 / Steroids; O3FX965V0I / Acetazolamide; WI4X0X7BPJ / Hydrocortisone
  • [Other-IDs] NLM/ PMC2853987
  •  go-up   go-down


61. Hofmann BM, Hlavac M, Martinez R, Buchfelder M, Müller OA, Fahlbusch R: Long-term results after microsurgery for Cushing disease: experience with 426 primary operations over 35 years. J Neurosurg; 2008 Jan;108(1):9-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results after microsurgery for Cushing disease: experience with 426 primary operations over 35 years.
  • OBJECTIVES: The aim of this paper was to demonstrate the long-term results following microsurgery in a single surgeon's continuous series of patients with Cushing disease (CD), to assess the influence of changes in surgical procedures, and to compare the results with those of other treatment modalities.
  • In particular, preoperative diagnosis, tumor size, results of histological examination, and complications were considered.
  • Pre-operative measures included clinical examination, endocrinological workup (testing of the hypothalamic-pituitary-adrenal axis, and 2- and 8-mg dexamethasone overnight suppression tests), sellar imaging (polytomography, computed tomography, and magnetic resonance [MR] imaging), and in patients with negative results on imaging studies, inferior petrosal sinus sampling.
  • RESULTS: During microsurgery as first treatment, the adenoma finding rate was 86.6%.
  • If no adenoma was found, exploration of the sella turcica was performed in 45.6%, hypophysectomy in 3.5%, and hemihypophysectomy in 50.9% of these patients, leading to an early remission in 37.9%.
  • In case of persistence or recurrence, further treatment (repeated operation, adrenalectomy, radio-therapy, or medical treatment) was used to control the disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Microsurgery. Pituitary ACTH Hypersecretion / surgery

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18173305.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


62. Oki K, Yamane K, Oda Y, Kamei N, Watanabe H, Tominaga A, Amatya VJ, Oki Y, Kohno N: Combined acromegaly and subclinical Cushing disease related to high-molecular-weight adrenocorticotropic hormone. J Neurosurg; 2009 Feb;110(2):369-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined acromegaly and subclinical Cushing disease related to high-molecular-weight adrenocorticotropic hormone.
  • The clinical diagnosis of growth hormone (GH)-producing pituitary adenoma was confirmed by MR imaging findings, nonsuppression of serum GH levels during a 75-g oral glucose tolerance test (trough GH 6.33 ng/ml), and elevated serum insulin-like growth factor-I levels (1361.3 ng/ml).
  • Moreover, autonomic adrenocorticotropic hormone (ACTH) secretion was suspected, based on inadequate suppression of ACTH or cortisol levels by an 0.5-mg overnight dexamethasone suppression test.
  • Analysis of the patient's plasma by using the gel filtration method revealed the presence of a high-molecular-weight (HMW) form of ACTH known to exhibit low biological activity.
  • Transsphenoidal adenomectomy was performed for the pituitary tumor.
  • Immunohistochemical investigation of the resected specimen showed strong and diffuse immunoreactivity to GH and focal immunoreactivity to ACTH.
  • Although there have been a few cases of pituitary adenoma that produced GH and ACTH concomitantly, this is the first report of the detection of HMW ACTH in patients with GH- and ACTH-producing adenomas.
  • Furthermore, the previous cases also did not exhibit typical cushingoid features.
  • It is suggested that the secretion of ACTH in patients with concurrent GH- and ACTH-secreting adenomas might consist of the HMW form and that the HMW ACTH is consequently associated with a subclinical Cushing state.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adrenocorticotropic Hormone / blood. Growth Hormone-Secreting Pituitary Adenoma / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pituitary ACTH Hypersecretion / diagnosis. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] Adult. Craniotomy. Humans. Male. Molecular Weight. Pituitary Function Tests. Radioimmunoassay. Sphenoid Bone / surgery

  • Genetic Alliance. consumer health - Acromegaly.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18991502.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


63. Lodish MB, Sinaii N, Patronas N, Batista DL, Keil M, Samuel J, Moran J, Verma S, Popovic J, Stratakis CA: Blood pressure in pediatric patients with Cushing syndrome. J Clin Endocrinol Metab; 2009 Jun;94(6):2002-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONTEXT: Hypertension (HTN) has been reported in up to 60% of children with Cushing syndrome (CS), but its course, side effects, and potential differences among various causes of CS have not been adequately studied.
  • DESIGN: Data from 86 children with corticotropinomas [Cushing disease (CD)] and 27 children with ACTH-independent CS (AICS) were analyzed.

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Endocrinol (Oxf). 2004 Dec;61(6):768-77 [15579193.001]
  • [Cites] Curr Hypertens Rep. 2004 Dec;6(6):493-9 [15527696.001]
  • [Cites] Pituitary. 2004;7(4):253-6 [16416038.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2006 Sep;20(3):467-82 [16980206.001]
  • [Cites] Pediatrics. 2007 Sep;120(3):e575-86 [17698579.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2007 Nov;3(11):748-57 [17955016.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):1-2 [19126630.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):117-23 [11231987.001]
  • [Cites] Hypertension. 2000 Nov;36(5):912-6 [11082166.001]
  • [Cites] Semin Nephrol. 2002 Jan;22(1):44-53 [11785068.001]
  • [Cites] J Clin Endocrinol Metab. 2002 May;87(5):2018-23 [11994335.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jun;88(6):2527-33 [12788849.001]
  • [Cites] Hypertension. 2003 Dec;42(6):1206-52 [14656957.001]
  • [Cites] Metabolism. 1980 Feb;29(2):115-9 [7354720.001]
  • [Cites] J Clin Endocrinol Metab. 1986 Feb;62(2):275-9 [3510223.001]
  • [Cites] Lancet. 1990 Mar 31;335(8692):765-74 [1969518.001]
  • [Cites] Arch Intern Med. 1993 Mar 8;153(5):598-615 [8439223.001]
  • [Cites] Cardiology. 1993;82(2-3):191-222 [8324780.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Jan;78(1):131-7 [7507118.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Apr;40(4):479-84 [8187313.001]
  • [Cites] N Engl J Med. 1994 Sep 8;331(10):629-36 [8052272.001]
  • [Cites] Am J Hypertens. 1996 Jan;9(1):77-80 [8834710.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jun;82(6):1734-8 [9177372.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3196-202 [9329338.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Aug;84(8):2664-72 [10443657.001]
  • [Cites] Curr Hypertens Rep. 2005 Jun;7(3):212-8 [15913497.001]
  • (PMID = 19293264.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Other-IDs] NLM/ PMC2690429
  •  go-up   go-down


64. Dehdashti AR, Gentili F: Current state of the art in the diagnosis and surgical treatment of Cushing disease: early experience with a purely endoscopic endonasal technique. Neurosurg Focus; 2007;23(3):E9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current state of the art in the diagnosis and surgical treatment of Cushing disease: early experience with a purely endoscopic endonasal technique.
  • OBJECT: Transsphenoidal pituitary surgery is the primary therapy for Cushing disease because of its potential to produce lasting remission without the need for long-term drug or hormone replacement therapy.
  • The authors evaluated the current role of pure endoscopic endonasal pituitary surgery in the treatment of Cushing disease.
  • METHODS: Twenty-five patients underwent pure endoscopic surgery for confirmed Cushing disease.
  • Final histological results were consistent with adrenocorticotropin hormone (ACTH)-secreting adenoma in 20 patients.
  • Three patients presented with new anterior pituitary deficiency, but no one had permanent diabetes insipidus.
  • Treatment failure was attributable to involvement of the cavernous sinus in two patients, incomplete tumor removal in one, negative exploration in one, and nodular corticotroph hyperplasia of the pituitary gland in one.
  • CONCLUSIONS: Early results indicated that endoscopic endonasal surgery is a safe and effective treatment for ACTH-producing adenomas.
  • Further studies with a larger number of patients and longer follow-ups are required to determine whether this more minimally invasive pure endoscopic approach should become the standard of care for the surgical treatment of Cushing disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Endoscopy. Paranasal Sinuses / surgery. Pituitary ACTH Hypersecretion / diagnosis. Pituitary ACTH Hypersecretion / surgery

  • MedlinePlus Health Information. consumer health - Endoscopy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17961027.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


65. Bronstein MD, Melmed S: [Pituitary tumorigenesis]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):615-25
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pituitary tumorigenesis].
  • Pituitary adenomas, almost invariably adenomas, account for 10% to 15% of all intracranial neoplasms and are incidentally detected in up to 27% of non selected autopsies.
  • Functionally, they are classified as secreting adenomas (PRL, GH, ACTH, TSH, LH, and FSH, and those co-secreting two or more hormones), and clinically non secreting or "non functioning" tumors.
  • Diagnosis is based on the hypersecretion phenotype (acromegaly, Cushing, etc), and on mass effect of macroadenomas leading to neurological disturbances, mainly visual complaints and headache.
  • Pituitary tumorigenesis mechanisms include those of primary hypothalamic versus pituitary origin, the latter is supported by evidence of pituitary adenoma monoclonality, as well as the absence of hyperplastic tissue surrounding the surgically removed tumor, and the relative independence of tumor hypothalamic control.
  • Nevertheless, a permissive role of the hypothalamus on tumor progression is also postulated.
  • Several molecular mechanisms involved in pituitary tumorigenesis have been unraveled including oncogenes, tumor suppressor genes and growth factors involved in neoplastic development, and will be described in this review.
  • [MeSH-major] Adenoma. Pituitary Neoplasms

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16444345.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 68
  •  go-up   go-down


66. Giacomini D, Páez-Pereda M, Theodoropoulou M, Gerez J, Nagashima AC, Chervin A, Berner S, Labeur M, Refojo D, Renner U, Stalla GK, Arzt E: Bone morphogenetic protein-4 control of pituitary pathophysiology. Front Horm Res; 2006;35:22-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone morphogenetic protein-4 control of pituitary pathophysiology.
  • Bone morphogenetic protein-4 (BMP-4), a member of the transforming growth factor-Beta(TGF-Beta) family, is overexpressed in different prolactinoma models and induces the development of these lineage adenomas.
  • SMAD proteins activated by growth factors of the TGF-Beta and BMP family interact with estrogen receptors to stimulate the proliferation of prolactin and growth hormone-secreting cells.
  • Furthermore, BMP-4 presents differential expression in normal and adenomatous corticotropes and inhibitory action on corticotropinoma cell proliferation.
  • The present review highlights not only the crucial and opposite role of BMP-4 in the progression of pituitary adenomas but also that BMP-4 and retinoic acid interaction might serve as a potential new mechanism target for therapeutic approaches for Cushing disease.
  • [MeSH-major] Bone Morphogenetic Proteins / physiology. Pituitary Diseases / etiology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Bone Morphogenetic Protein 4. Gene Expression. Humans. Models, Biological. Neurons / secretion. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Pituitary Gland / secretion. Receptors, Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / physiology. Tretinoin / pharmacology

  • MedlinePlus Health Information. consumer health - Pituitary Disorders.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16809920.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 5688UTC01R / Tretinoin; 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 42
  •  go-up   go-down


67. Barber TM, Adams E, Ansorge O, Byrne JV, Karavitaki N, Wass JA: Nelson's syndrome. Eur J Endocrinol; 2010 Oct;163(4):495-507
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nelson's syndrome is a potentially life-threatening condition that does not infrequently develop following total bilateral adrenalectomy (TBA) for the treatment of Cushing's disease.
  • In this review article, we discuss some controversial aspects of Nelson's syndrome including diagnosis, predictive factors, aetiology, pathology and management based on data from the existing literature and the experience of our own tertiary centre.
  • We propose that Nelson's syndrome should be diagnosed in any patient with prior TBA for the treatment of Cushing's disease and with at least one of the following criteria: i) an expanding pituitary mass lesion compared with pre-TBA images;.
  • ii) an elevated 0800 h plasma level of ACTH (>500 ng/l) in addition to progressive elevations of ACTH (a rise of >30%) on at least three consecutive occasions.
  • Regarding predictive factors for the development of Nelson's syndrome post TBA, current evidence favours the presence of residual pituitary tumour on magnetic resonance imaging (MRI) post transsphenoidal surgery (TSS); an aggressive subtype of corticotrophinoma (based on MRI growth rapidity and histology of TSS samples); lack of prophylactic neoadjuvant pituitary radiotherapy at the time of TBA and a rapid rise of ACTH levels in year 1 post TBA.
  • Finally, more studies are needed to assess the efficacy of therapeutic strategies in Nelson's syndrome, including the alkylating agent, temozolomide, which holds promise as a novel and effective therapeutic agent in the treatment of associated aggressive corticotroph tumours.

  • Hazardous Substances Data Bank. DACARBAZINE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20668020.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 101
  •  go-up   go-down


68. Suzuki K, Hattori Y, Aoki C, Nakano A, Tomizawa A, Kase H, Kasai K: An ACTH-secreting pituitary adenoma within the sphenoid sinus. Intern Med; 2010;49(8):763-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An ACTH-secreting pituitary adenoma within the sphenoid sinus.
  • She was found to have a markedly elevated plasma ACTH-cortisol level.
  • Magnetic resonance imaging (MRI) revealed a mass in the left sphenoidal sinus, which had become enlarged to a point where it could not be removed by transsphenoidal surgery.
  • We decided to proceed with radiation therapy to shrink the tumor.
  • We describe a rare case of an ACTH-secreting pituitary adenoma within the sphenoid sinus.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Paranasal Sinus Neoplasms / diagnosis. Sphenoid Sinus / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20424367.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


69. Saeger W: [Effects of irradiation therapy and inhibiting drugs on the pituitary and its adenomas]. Pathologe; 2006 Feb;27(1):57-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of irradiation therapy and inhibiting drugs on the pituitary and its adenomas].
  • Radiation therapies of pituitary adenomas induce an increase in fibroses and nuclear pleomorphism.
  • Most growth hormone (GH) secreting pituitary adenomas react to somatostatin analogues by a distinct decrease of GH secretion.
  • Some cases show a shrinkage of adenomas that correlates with fibrosis of the tumor.
  • With these drugs, thyroid stimulating hormone secreting adenomas can also be treated.
  • Prolactin secreting adenomas are mostly treated primarily with dopamine agonists.
  • Up to 90% of cases show a strong decrease in hormone secretion and a distinct shrinkage of the adenomas based on strong decrease in adenoma cell volume.
  • Long-term medication with high doses of glucocorticoids induces Crooke's cells in the anterior pituitary.
  • These are suppressed ACTH cells and characterized by increased numbers of large lysosomes and dense bundles of cytofilaments.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Pituitary Gland / pathology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / radiotherapy. Radiotherapy / adverse effects

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • MedlinePlus Health Information. consumer health - Radiation Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocrine. 2004 Nov;25(2):141-5 [15711028.001]
  • [Cites] Endocr Pathol. 2000 Winter;11(4):341-352 [12114758.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Pathol Res Pract. 1986 Jun;181(3):280-90 [3748874.001]
  • [Cites] Histol Histopathol. 1987 Apr;2(2):135-42 [2980713.001]
  • [Cites] Ultrastruct Pathol. 2005 May-Aug;29(3-4):163-7 [16036872.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] Pathol Res Pract. 1993 Nov;189(9):1044-51 [8302723.001]
  • [Cites] Exp Clin Endocrinol. 1992;100(3):106-11 [1305059.001]
  • [Cites] Acta Endocrinol (Copenh). 1991 Apr;124(4):487-91 [2031445.001]
  • [Cites] Mayo Clin Proc. 1997 Oct;72(10):893-900 [9379690.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):151-66 [11761432.001]
  • [Cites] Microsc Res Tech. 1992 Jan 15;20(2):162-76 [1547357.001]
  • [Cites] Exp Clin Endocrinol. 1988 Sep;92(1):59-68 [2906615.001]
  • (PMID = 16362259.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dopamine Agonists; 0 / Glucocorticoids
  •  go-up   go-down


70. Banasiak MJ, Malek AR: Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management. Neurosurg Focus; 2007;23(3):E13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management.
  • Nelson syndrome (NS) is a rare clinical manifestation of an enlarging pituitary adenoma that can occur following bilateral adrenal gland removal performed for the treatment of Cushing disease.
  • It is characterized by excess adreno-corticotropin secretion and hyperpigmentation of the skin and mucus membranes.
  • The authors present a comprehensive review of the pathophysiology, diagnosis, and management of NS.
  • Corticotroph adenomas in NS remain challenging tumors that can lead to significant rates of morbidity and mortality.
  • Although the primary treatment for each tumor type may vary, it is important to consider all of the available options and select the one that is most appropriate for the individual case, particularly in cases of lesions resistant to intervention.


71. Erickson D, Erickson B, Watson R, Patton A, Atkinson J, Meyer F, Nippoldt T, Carpenter P, Natt N, Vella A, Thapa P: 3 Tesla magnetic resonance imaging with and without corticotropin releasing hormone stimulation for the detection of microadenomas in Cushing's syndrome. Clin Endocrinol (Oxf); 2010 Jun;72(6):793-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 3 Tesla magnetic resonance imaging with and without corticotropin releasing hormone stimulation for the detection of microadenomas in Cushing's syndrome.
  • OBJECTIVE: We sought to determine if higher resolution 3 Tesla (T) magnetic resonance imaging (MRI) with or without ovine corticotropin releasing hormone (o-CRH) stimulation would increase the sensitivity for detection of pituitary microadenomas in ACTH-dependent Cushing's syndrome (CS).
  • DESIGN AND PATIENTS: We prospectively identified 23 patients over a 2-year period with clinical and biochemical evidence of ACTH-dependent CS with no lesion (n = 11) or equivocal lesion (n = 10) on 1.5T MRI.
  • MEASUREMENTS AND RESULTS: Both 3T MRI without (P < 0.016) and with o-CRH stimulation (P < 0.013) was significantly more sensitive for detection of pituitary microadenomas than 1.5T MRI for Group 1 (definitive proof of Cushing's disease, n = 10).
  • Group 2 (those in group 1, plus three patients where dynamic/invasive testing suggested pituitary source) also showed a significant (P < 0.012) advantage for 3T.
  • We did not observe a statistically significant difference in other patient groups [patients with recurrent CD (n = 6) and patients with ectopic CS (n = 2)].
  • CONCLUSIONS: The results of our prospective blinded studies suggest that 3T MRI of pituitary gland should be considered in evaluation of patients with ACTH-dependent CD when 1.5T imaging is negative or equivocal.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / radiography. Adenoma / radiography. Corticotropin-Releasing Hormone / therapeutic use. Cushing Syndrome / radiography. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adult. Aged. Diagnostic Techniques, Endocrine. Female. Humans. Male. Middle Aged. Sensitivity and Specificity. Single-Blind Method. Stimulation, Chemical. Tumor Burden / drug effects. Tumor Burden / physiology. Young Adult

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19811509.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 9015-71-8 / Corticotropin-Releasing Hormone
  •  go-up   go-down


72. Salehi F, Scheithauer BW, Moyes VJ, Drake WM, Syro LV, Manoranjan B, Sharma S, Horvath E, Kovacs K: Low immunohistochemical expression of MGMT in ACTH secreting pituitary tumors of patients with Nelson syndrome. Endocr Pathol; 2010 Dec;21(4):227-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low immunohistochemical expression of MGMT in ACTH secreting pituitary tumors of patients with Nelson syndrome.
  • The aim of the present study was to assess immunohistochemical expression of MGMT in ACTH-secreting pituitary adenomas of patients with Nelson syndrome.
  • Our material consisted of eight specimens from ACTH-secreting pituitary adenomas of patients with Nelson syndrome.
  • Absent or low MGMT staining in brain and other neoplasms has been shown to correlate with successful treatment with temozolomide, and recent reports of aggressive pituitary adenomas suggest similar outcomes.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. DNA Modification Methylases / biosynthesis. DNA Repair Enzymes / biosynthesis. Nelson Syndrome / metabolism. Tumor Suppressor Proteins / biosynthesis

  • Genetic Alliance. consumer health - Nelson syndrome.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12 ):1470-5 [17442989.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Oct;65(4):552-3 [16984254.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 Aug;71(2):226-33 [19067722.001]
  • [Cites] Hormones (Athens). 2009 Oct-Dec;8(4):303-6 [20045804.001]
  • [Cites] Anticancer Agents Med Chem. 2008 May;8(4):368-80 [18473722.001]
  • [Cites] Virchows Arch. 2001 Jun;438(6):595-602 [11469692.001]
  • [Cites] J Clin Oncol. 2006 Jul 20;24(21):3431-7 [16849758.001]
  • [Cites] Hum Pathol. 2007 Jan;38(1):185-9 [17056093.001]
  • [Cites] Acta Neuropathol. 2008 Feb;115(2):261-2 [17926052.001]
  • [Cites] Eur J Endocrinol. 2009 Jan;160(1):115-9 [18984772.001]
  • [Cites] Neurosurgery. 2009 Apr;64(4):E773-4; discussion E774 [19349807.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10 ):997-1003 [15758010.001]
  • [Cites] Neurosurg Focus. 2007;23(3):E13 [17961028.001]
  • [Cites] Jpn J Clin Oncol. 2007 Dec;37(12 ):897-906 [18156172.001]
  • (PMID = 21061089.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; YF1K15M17Y / temozolomide
  •  go-up   go-down


73. Sheehan JM, Douds GL, Hill K, Farace E: Transsphenoidal surgery for pituitary adenoma in elderly patients. Acta Neurochir (Wien); 2008 Jun;150(6):571-4; discussion 574
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transsphenoidal surgery for pituitary adenoma in elderly patients.
  • BACKGROUND: As the population continues to age, the number of elderly patients with symptomatic pituitary tumours will continue to increase.
  • Little information exists as to the safety of pituitary surgery in this patient population.
  • Eight patients had new hormonal deficits post-operatively (1 ACTH, 3 TSH, 2 ACTH/TSH, 2 vasopressin).
  • Surgical removal of pituitary adenomas should be considered the mainstay of treatment in elderly patients in whom treatment is necessary.
  • [MeSH-major] Adenoma / surgery. Endoscopy / methods. Microsurgery / methods. Pituitary Neoplasms / surgery. Postoperative Complications / etiology. Sphenoid Sinus / surgery
  • [MeSH-minor] Age Factors. Aged. Aged, 80 and over. Female. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / diagnosis. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Male. Risk Factors


74. Dovio A, Allasino B, Palmas E, Ventura M, Pia A, Saba L, Aroasio E, Terzolo M, Angeli A: Increased osteoprotegerin levels in Cushing's syndrome are associated with an adverse cardiovascular risk profile. J Clin Endocrinol Metab; 2007 May;92(5):1803-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased osteoprotegerin levels in Cushing's syndrome are associated with an adverse cardiovascular risk profile.
  • CONTEXT: Patients with Cushing's syndrome (CS) have a mortality rate four times higher than age- and sex-matched subjects, mainly due to cardiovascular events.
  • Serum osteoprotegerin (OPG) levels are increased in patients with cardiovascular disease and/or excess bone resorption.
  • Twenty-six patients had pituitary-dependent CS; five patients had CS caused by ectopic ACTH secretion; and 17 patients had adrenal-dependent CS, accounted for by cortisol-secreting adenoma (n = 9), ACTH-independent macronodular bilateral adrenal hyperplasia (n = 4), or World Health Organization stage II cortisol-secreting carcinoma (n = 4).
  • RESULTS: Serum OPG (but not sRANKL) levels were significantly higher in CS patients than in controls (P < 0.01).
  • Serum OPG levels were higher in patients with pituitary-dependent CS in comparison with adrenal-dependent CS.
  • [MeSH-minor] Absorptiometry, Photon. Adrenal Glands / physiopathology. Adrenocorticotropic Hormone / blood. Adult. Aged. Cross-Sectional Studies. Female. Humans. Hydrocortisone / blood. Male. Metabolic Syndrome X / metabolism. Middle Aged. Pituitary Function Tests. Pituitary Gland / physiopathology. Receptor Activator of Nuclear Factor-kappa B / blood. Risk

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17327380.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Osteoprotegerin; 0 / Receptor Activator of Nuclear Factor-kappa B; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


75. Saveanu A, Gunz G, Guillen S, Dufour H, Culler MD, Jaquet P: Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas. Neuroendocrinology; 2006;83(3-4):258-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas.
  • AIM: We report the comparative efficacy of octreotide, cabergoline and multiple ligands directed towards the different somatostatin subtypes (ssts), such as BIM-23A779 and SOM-230, and of chimeric analogs which bind both somatostatin and the dopamine D2 receptors (D2R), such as BIM-23A760 and BIM-23A781, in cell cultures from human growth hormone (GH)-secreting pituitary adenomas.
  • PROCEDURES: RT-PCR analysis of the quantitative expression of the different ssts and D2R mRNAs was performed on tumor fragments of 22 GH-secreting adenomas collected after surgery.
  • Pharmacological studies, using the different ligands, were performed on cell cultures of such tumors.
  • In each tumor tested, 3 patterns of response, in terms of GH suppression, were observed.
  • Among the compounds tested, the most potent inhibitors of GH secretion were the sst2, sst5, D2R chimeric compound BIM-23A760, followed by the sst universal ligand SOM-230.
  • The effect of multiple receptor activation on the functions of other pituitary tumor types, such as prolactinomas and corticotropinomas, is not presently analyzed, and the efficacy of multireceptor ligands remains to be elucidated.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Dopamine / analogs & derivatives. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adult. Drug Screening Assays, Antitumor. Ergolines / therapeutic use. Female. Human Growth Hormone / drug effects. Human Growth Hormone / metabolism. Humans. Ligands. Male. Octreotide / therapeutic use. RNA, Messenger / analysis. Receptors, Dopamine D2 / drug effects. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Receptors, Somatostatin / classification. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Recombinant Fusion Proteins / therapeutic use. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. DOPAMINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17047391.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / BIM 23268; 0 / Ergolines; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
  •  go-up   go-down


76. Roelfsema F, Kok S, Kok P, Pereira AM, Biermasz NR, Smit JW, Frolich M, Keenan DM, Veldhuis JD, Romijn JA: Pituitary-hormone secretion by thyrotropinomas. Pituitary; 2009;12(3):200-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary-hormone secretion by thyrotropinomas.
  • Hormone secretion by somatotropinomas, corticotropinomas and prolactinomas exhibits increased pulse frequency, basal and pulsatile secretion, accompanied by greater disorderliness.
  • Regulation of non-TSH pituitary hormones in this context is not well understood.
  • Cross-ApEn synchrony between TSH and GH did not differ between patients and controls, but TSH and PRL synchrony was reduced in patients.
  • We conclude that TSH secretion by thyrotropinomas shares many characteristics of other pituitary hormone-secreting adenomas.
  • In addition, abnormalities in GH and PRL secretion exist ranging from decreased (joint) regularity to overt hypersecretion, although not always clinically obvious, suggesting tumoral transformation of thyrotrope lineage cells.
  • [MeSH-major] Adenoma / physiopathology. Pituitary Hormones / blood. Pituitary Hormones / secretion. Pituitary Neoplasms / blood

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Endocrinol. 1994 Oct;131(4):331-40 [7921220.001]
  • [Cites] J Clin Invest. 1994 Sep;94(3):1277-88 [8083369.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Dec;79(6):1706-15 [7989479.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Aug;80(8):2518-22 [7543115.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14100-5 [8943067.001]
  • [Cites] Endocr Rev. 1996 Dec;17(6):610-38 [8969971.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Nov;47(5):599-612 [9425400.001]
  • [Cites] Thyroid. 1998 Jan;8(1):9-14 [9492147.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):476-86 [10022404.001]
  • [Cites] Eur J Endocrinol. 1999 Mar;140(3):192-200 [10216513.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2005 Feb;288(2):R440-6 [15486096.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Feb;62(2):176-81 [15670193.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1570-7 [15598691.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Jul;289(1):E160-5 [15727954.001]
  • [Cites] Tissue Cell. 2005 Aug;37(4):269-80 [15921714.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Nov;90(11):6185-91 [16091498.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 15;102(46):16880-5 [16272219.001]
  • [Cites] Eur J Endocrinol. 2007 Jul;157(1):39-46 [17609400.001]
  • [Cites] J Neuroendocrinol. 2008 Jan;20(1):1-70 [18081553.001]
  • [Cites] J Neurosurg. 2008 Jul;109(1):17-22 [18590428.001]
  • [Cites] J Neuroendocrinol. 2008 Jun;20(6):687-91 [18601690.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2003 Sep;285(3):R664-73 [12738612.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2290-300 [15126555.001]
  • [Cites] Am J Physiol. 1999 Nov;277(5 Pt 1):E948-57 [10567024.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Apr;85(4):1487-91 [10770186.001]
  • [Cites] Methods Enzymol. 2000;321:149-82 [10909056.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):700-12 [11158034.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Mar;280(3):R721-9 [11171650.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Jun;280(6):R1755-71 [11353681.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2849-53 [11397898.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):3304-10 [11443205.001]
  • [Cites] Mol Endocrinol. 2001 Sep;15(9):1529-38 [11518802.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5572-6 [11701737.001]
  • [Cites] Rev Endocr Metab Disord. 2000 Jan;1(1-2):97-108 [11704998.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):179-86 [11761434.001]
  • [Cites] Ultrastruct Pathol. 2002 Jul-Aug;26(4):219-28 [12227947.001]
  • [Cites] Eur J Endocrinol. 2003 Apr;148(4):433-42 [12656664.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Jun;60(6):765-72 [15163342.001]
  • [Cites] Acta Neuropathol. 2004 Aug;108(2):147-53 [15185102.001]
  • [Cites] J Clin Endocrinol Metab. 1987 Aug;65(2):315-20 [3597710.001]
  • [Cites] Acta Neuropathol. 1988;76(5):458-64 [2847475.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Jun;68(6):1211-5 [2723029.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Jun;70(6):1631-6 [2347898.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1616-23 [2172282.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Feb;72(2):415-21 [1704010.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Feb;72(2):477-83 [1704011.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Dec;73(6):1281-8 [1955510.001]
  • [Cites] Clin Endocrinol (Oxf). 1992 Dec;37(6):504-10 [1286520.001]
  • [Cites] Ann Intern Med. 1993 Aug 1;119(3):236-40 [8323093.001]
  • [Cites] Eur J Endocrinol. 1994 Feb;130(2):113-20 [8130883.001]
  • [Cites] Eur J Endocrinol. 1994 Oct;131(4):355-8 [7921223.001]
  • (PMID = 19051037.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000585
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ PMC2712623
  •  go-up   go-down


77. Castillo VA, Gómez NV, Lalia JC, Cabrera Blatter MF, García JD: Cushing's disease in dogs: cabergoline treatment. Res Vet Sci; 2008 Aug;85(1):26-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's disease in dogs: cabergoline treatment.
  • The treatment of pituitary-dependent hyperadrenocorticism (PDH) in dogs has for a long time been focused on inhibiting the adrenal gland using drugs such as o-p'-DDD, Ketoconazole and Trilostane, without attacking the primary cause: the corticotrophinoma.
  • Corticotroph cells can express the D2 dopaminergic receptor; therefore cabergoline (Cbg) could be effective as a treatment.
  • A year after the treatment, there was a significant decrease in ACTH (p<0.0001), alpha-MSH (p<0.01), urinary cortisol/creatinine ratio (p<0.001), and of the tumor size (p<0.0001) evaluated by nuclear magnetic resonance.
  • [MeSH-major] Dog Diseases / drug therapy. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Pituitary ACTH Hypersecretion / veterinary

  • Hazardous Substances Data Bank. KETOCONAZOLE .
  • Hazardous Substances Data Bank. Corticotropin .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17910968.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone; LL60K9J05T / cabergoline; R9400W927I / Ketoconazole
  •  go-up   go-down


78. Yano S, Kawano T, Kudo M, Makino K, Nakamura H, Kai Y, Morioka M, Kuratsu J: Endoscopic endonasal transsphenoidal approach through the bilateral nostrils for pituitary adenomas. Neurol Med Chir (Tokyo); 2009 Jan;49(1):1-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic endonasal transsphenoidal approach through the bilateral nostrils for pituitary adenomas.
  • The endoscopic endonasal transsphenoidal approach through the bilateral nostrils was evaluated for the treatment of pituitary adenoma.
  • The surgical approach is through the bilateral nostrils via minimal or wide dissection of the septal mucosa, depending on the degree of tumor extension.
  • Tumor removal rate, endocrinological outcomes, and complications were retrospectively assessed in 194 patients with pituitary adenomas who underwent 213 procedures between December 2001 and March 2008.
  • Greater than 95% resection was achieved in 74 of 131 nonfunctioning adenomas, and the removal rate was significantly higher during 2005-2008 compared to 2002-2004 (p < 0.05).
  • Endocrinological remission was achieved in 20 of 26 growth hormone-secreting tumors of Knosp grades 0-2, 16 of 17 microprolactinomas, and 6 of 9 cases of pure Cushing's disease.
  • Postoperative complications were cerebrospinal fluid leakage in 9 cases, visual worsening in 5, anterior pituitary insufficiency in 5, and permanent diabetes insipidus in 2.
  • [MeSH-major] Adenoma / surgery. Endoscopy / methods. Pituitary Neoplasms / surgery
  • [MeSH-minor] Acromegaly / etiology. Adolescent. Adult. Aged. Aged, 80 and over. Diabetes Insipidus / etiology. Female. Humans. Hypopituitarism / etiology. Male. Middle Aged. Nasal Cavity / surgery. Neuronavigation. Pituitary ACTH Hypersecretion / etiology. Pituitary ACTH Hypersecretion / surgery. Postoperative Complications / etiology. Prolactinoma / surgery. Remission Induction. Retrospective Studies. Sphenoid Bone / surgery. Subdural Effusion / etiology. Vision Disorders / etiology. Young Adult

  • MedlinePlus Health Information. consumer health - Endoscopy.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19168995.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


79. Bondioni S, Mantovani G, Polentarutti N, Ambrosi B, Loli P, Peverelli E, Lania AG, Beck-Peccoz P, Spada A: Evaluation of proopiomelanocortin mRNA in the peripheral blood from patients with Cushing's syndrome of different origin. J Endocrinol Invest; 2007 Nov;30(10):828-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of proopiomelanocortin mRNA in the peripheral blood from patients with Cushing's syndrome of different origin.
  • ACTH-dependent Cushing's syndrome is due to ACTH overproduction originating from a pituitary corticotroph adenoma (Cushing's disease) or from ectopic tumors (ectopic ACTH syndrome).
  • Due to difficulties in the differential diagnosis between these two forms of hypercortisolism it would be important to have molecular tools able to discriminate the two conditions.
  • In order to analyse the presence of different POMC transcripts, we extracted total RNA from peripheral lymphocytes of 10 patients with Cushing's disease, 10 with ectopic Cushing syndrome, and 20 controls as well as from pituitary tissues (2 ACTH-omas and a normal pituitary polyA+ sample).
  • Northern blot analysis correctly revealed a 1072 nt mRNA molecule in pituitary ACTH-oma and in the normal pituitary polyA+ RNA samples, whereas neither this molecule nor other alternative transcripts were detected in blood samples from patients and controls.
  • This study further underlines the need for alternative approaches in the diagnosis of ACTH-dependent Cushing's syndrome.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / genetics. Cushing Syndrome / diagnosis. Pro-Opiomelanocortin / genetics
  • [MeSH-minor] Blotting, Northern. Diagnosis, Differential. Humans. RNA, Messenger / blood. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 1998 Dec;83(12):4435-42 [9851791.001]
  • [Cites] J Mol Endocrinol. 1989 May;2(3):175-81 [2568843.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7261-5 [3478693.001]
  • [Cites] Cancer. 1996 Jul 1;78(1):10-6 [8646704.001]
  • [Cites] J Invest Dermatol. 1996 Apr;106(4):673-8 [8618003.001]
  • [Cites] Horm Metab Res. 1988 Apr;20(4):225-9 [2456259.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Jan;50(1):85-94 [10341860.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3201-8 [12107225.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Apr;80(8):2211-5 [6572972.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Aug;77(8):4890-4 [6254047.001]
  • [Cites] Surgery. 1996 Dec;120(6):959-64; discussion 964-5 [8957481.001]
  • [Cites] Eur J Endocrinol. 2000 May;142(5):533-6 [10802534.001]
  • [Cites] Mol Endocrinol. 1987 Oct;1(10):749-57 [2856401.001]
  • [Cites] Endocrinology. 1982 Apr;110(4):1442-4 [7060531.001]
  • [Cites] J Mol Endocrinol. 1989 Jan;2(1):3-9 [2765113.001]
  • [Cites] Nature. 1980 Dec 11;288(5791):610-3 [6255341.001]
  • [Cites] Mol Endocrinol. 1989 Jan;3(1):215-23 [2536890.001]
  • [Cites] Br J Cancer. 2000 May;82(10):1650-5 [10817499.001]
  • [Cites] Endocr Rev. 1980 Winter;1(1):1-27 [6262069.001]
  • [Cites] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3283-6 [198779.001]
  • [Cites] J Clin Endocrinol Metab. 1984 May;58(5):904-8 [6546764.001]
  • [Cites] J Clin Invest. 1990 Sep;86(3):871-7 [2394836.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Nov;80(22):6982-6 [6316340.001]
  • [Cites] J Biol Chem. 1982 Jun 25;257(12):6783-7 [6177687.001]
  • [Cites] J Clin Invest. 1994 May;93(5):2258-62 [8182158.001]
  • [Cites] J Clin Invest. 1985 Nov;76(5):1892-8 [2997296.001]
  • [Cites] J Clin Invest. 1993 Dec;92(6):2790-5 [8254033.001]
  • (PMID = 18075284.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 66796-54-1 / Pro-Opiomelanocortin
  •  go-up   go-down


80. Gao C, Fu X, Pan Y, Li Q: Surgical treatment of pancreatic neuroendocrine tumors: report of 112 cases. Dig Surg; 2010 Aug;27(3):197-204
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: To review the clinical data of a group of patients with pancreatic neuroendocrine tumors (pNETs) and to investigate the role of surgery in the treatment for pNETs by analyzing clinical manifestations and postoperative course of this rare disease.
  • Patients' data related to demographics and characteristics, diagnostic studies, surgical and tumor characteristics and survival were retrospectively reviewed.
  • RESULTS: Forty-six patients (41.1%) had a well-differentiated neuroendocrine tumor (WDT), 44 (48.2%) a well-differentiated neuroendocrine carcinoma (WD-Ca) and 12 (10.7%) a poorly differentiated neuroendocrine carcinoma (PD-Ca).
  • Nonfunctional tumors were seen in 65 (58.0%) patients, whereas functional tumors were found in 47 (42.0%) patients, including 26 insulinomas, 17 gastrinomas, 2 VIPomas, 1 glucagonoma, and 1 ACTHoma.
  • Survival was significantly related to the type of neuroendocrine tumor (p = 0.001).
  • The 5-year survival rate differed significantly between patients with tumor node metastasis (TNM) stage I and II disease and those with stage III and IV tumors (p = 0.011).
  • Malignant cases should be treated with aggressive radical surgery to achieve complete tumor resection and potential for long-term survival.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20571266.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  •  go-up   go-down


81. Rudnik A, Zawadzki T, Wojtacha M, Bazowski P, Zubgałuszka-Ignasiak B, Duda I: [Endoscopic transsphenoidal treatment of pituitary adenomas]. Neurol Neurochir Pol; 2005 Jan-Feb;39(1):17-23; discussion 24-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Endoscopic transsphenoidal treatment of pituitary adenomas].
  • [Transliterated title] Endoskopowe leczenie gruczolaków przysadki.
  • BACKGROUND AND PURPOSE: The aim of this study is to present a new endoscopic transnasal transsphenoidal method of surgical treatment of pituitary adenomas and to evaluate the results and complications of the method.
  • MATERIAL AND SURGICAL TECHNIQUE: From October 2001 to June 2003 in the Department of Neurosurgery of the Medical University of Silesia in Katowice 88 operations of pituitary adenomas were performed using the transnasal transsphenoidal endoscopic method.
  • RESULTS: In the group of 51 nonfunctioning adenomas, in 32 cases we obtained the total removal of the tumor, which amounts to 63%.
  • Among 37 of hyperfunctioning adenomas there were 11 prolactinomas, 19 GH secreting adenomas and 7 ACTH secreting adenomas.
  • In all cases of prolactinomas the tumor was removed totally and in the cases of GH secreting adenomas and ACTH secreting adenomas the total removal of the tumor was performed in 58% and 86% of the cases, respectively.
  • It was the patient with a huge nonfunctioning macroadenoma, with hydrocephalus and preoperative disturbances of consciousness.
  • In this group we noticed the intraoperative CSF leakage in 20 cases but we did not observe the postoperative CSF leakage or any rhinological complications.
  • CONCLUSIONS: The endoscopic transnasal transsphenoidal approach is an efficient method of surgical treatment of pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Hypophysectomy / methods. Neuroendoscopy. Pituitary Neoplasms / surgery. Sphenoid Sinus / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Cavernous Sinus / surgery. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Poland. Retrospective Studies. Time Factors. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15735985.001).
  • [ISSN] 0028-3843
  • [Journal-full-title] Neurologia i neurochirurgia polska
  • [ISO-abbreviation] Neurol. Neurochir. Pol.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


82. Batista D, Courkoutsakis NA, Oldfield EH, Griffin KJ, Keil M, Patronas NJ, Stratakis CA: Detection of adrenocorticotropin-secreting pituitary adenomas by magnetic resonance imaging in children and adolescents with cushing disease. J Clin Endocrinol Metab; 2005 Sep;90(9):5134-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of adrenocorticotropin-secreting pituitary adenomas by magnetic resonance imaging in children and adolescents with cushing disease.
  • CONTEXT: We recently showed that pre- and postcontrast spoiled gradient-recalled acquisition in the steady-state (SPGR) was superior to conventional pre- and postcontrast T-1 weighted spin echo (SE) acquisition magnetic resonance imaging (MRI) for the diagnostic evaluation of pituitary tumors in adult patients.
  • OBJECTIVE: The present investigation assessed the use of SPGR vs. SE-MRI in the diagnostic evaluation of ACTH-secreting tumors in children and adolescents with Cushing disease.
  • PATIENTS: Thirty children with Cushing disease (13 females and 17 males with a mean age of 12 +/- 3 yr) were studied.
  • Postcontrast SPGR-MRI identified the location of the tumor in 18 of 28 patients, whereas postcontrast SE-MRI identified the location and accurately estimated the size of the tumor in only five patients (P < 0.001).
  • CONCLUSIONS: We conclude that conventional MRI, even with contrast enhancement, mostly failed to identify ACTH-secreting microadenomas in children and adolescents with Cushing disease.
  • Postcontrast SPGR-MRI was superior to SE-MRI and should be used in addition to conventional SE-MRI in the pituitary evaluation of children and adolescents with suspected Cushing disease.
  • [MeSH-major] Adenoma / diagnosis. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Cushing Syndrome / diagnosis. Magnetic Resonance Imaging. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secretion

  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15941871.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


83. Revill K, Dudley KJ, Clayton RN, McNicol AM, Farrell WE: Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma. Endocr Relat Cancer; 2009 Jun;16(2):537-48
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma.
  • The imprinted gene, neuronatin (NNAT), is one of the most abundant transcripts in the pituitary and is thought to be involved in the development and maturation of this gland.
  • In a recent whole-genome approach, exploiting a pituitary tumour cell line, we identified hypermethylation associated loss of NNAT.
  • In this report, we determined the expression pattern of NNAT in individual cell types of the normal gland and within each of the different pituitary adenoma subtypes.
  • Immunohistochemical (IHC) co-localization studies of normal pituitaries showed that each of the hormone secreting cells (GH, PRL, ACTH, FSH and TSH) expressed NNAT.
  • However, 33 out of 47 adenomas comprising, 11 somatotrophinomas, 10 prolactinomas, 12 corticotrophinomas and 14 non-functioning tumours, irrespective of subtype failed to express either NNAT transcript or protein as determined by quantitative real-time RT-PCR and IHC respectively.
  • In normal pituitaries and adenomas that expressed NNAT the promoter-associated CpG island showed characteristics of an imprinted gene where approximately 50% of molecules were densely methylated.
  • However, in the majority of adenomas that showed loss or significantly reduced expression of NNAT, relative to normal pituitaries, the gene-associated CpG island showed significantly increased methylation.
  • Collectively, these findings point to an important role for NNAT in the pituitary and perhaps tumour development in this gland.
  • [MeSH-major] DNA Methylation. Membrane Proteins / genetics. Nerve Tissue Proteins / genetics. Pituitary Gland / pathology. Pituitary Neoplasms / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Animals. CpG Islands. Gene Silencing. Humans. Immunoenzyme Techniques. Loss of Heterozygosity. Mice. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19218280.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / NNAT protein, human; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger
  •  go-up   go-down


84. Salgado LR, Fragoso MC, Knoepfelmacher M, Machado MC, Domenice S, Pereira MA, de Mendonça BB: Ectopic ACTH syndrome: our experience with 25 cases. Eur J Endocrinol; 2006 Nov;155(5):725-33
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic ACTH syndrome: our experience with 25 cases.
  • OBJECTIVE: Ectopic ACTH syndrome (EAS) occurs in about 5-10% of all patients with ACTH-dependent hypercortisolism with most of them caused by intrathoracic neoplasms.
  • We assessed the accuracy of dynamic tests, inferior petrosal sinus sampling (IPSS) using desmopressin, and imaging in the work-up diagnosis of EAS.
  • DESIGN AND SUBJECTS: Tumor markers, imaging, and outcome data from 25 patients (13F/12M) aged 18-72 years.
  • High dexamethasone suppression test (HDDST), desmopressin test, GHRP-6 test, corticotropin-releasing hormone (CRH) test, IPSS, computed tomography (CT), magnetic resonance imaging (MRI), and (111)In-pentetreotide scintigraphy were revised.
  • In 13 patients who underwent desmopressin test, ACTH- and cortisol-positive responses were seen in six and five patients respectively.
  • In the seven patients submitted to IPSS using desmopressin in six of them, none had ACTH gradients.
  • Fourteen patients had intrathoracic tumors, five had pheochromocytomas, three had pancreatic tumors, one had a glomic tumor, and had three occult tumors.
  • CONCLUSIONS: IPSS with desmopressin was helpful for differential diagnosis.

  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17062889.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oligopeptides; 7S5I7G3JQL / Dexamethasone; 87616-84-0 / growth hormone releasing hexapeptide; 9015-71-8 / Corticotropin-Releasing Hormone; ENR1LLB0FP / Deamino Arginine Vasopressin
  •  go-up   go-down


85. Pinchot SN, Sippel R, Chen H: ACTH-producing carcinoma of the pituitary with refractory Cushing's Disease and hepatic metastases: a case report and review of the literature. World J Surg Oncol; 2009;7:39
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ACTH-producing carcinoma of the pituitary with refractory Cushing's Disease and hepatic metastases: a case report and review of the literature.
  • BACKGROUND: Pituitary carcinomas are rare neuroendocrine tumors affecting the adenohypophysis.
  • CASE PRESENTATION: Here, we report the case of a fatal pituitary carcinoma evolving within two years from an adrenocorticotrophic hormone (ACTH)-secreting macroadenoma and review the global literature regarding this rare neuroendocrine tumor.
  • CONCLUSION: Pituitary carcinomas are extremely rare neoplasms, representing only 0.1% to 0.2% of all pituitary tumors.
  • The latency period between initial presentation of a pituitary adenoma and the development of distal metastases marking carcinoma is extremely variable, and some patients may live well over 10 years with pituitary carcinoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Liver Neoplasms / secondary. Pituitary ACTH Hypersecretion / complications

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Minerva Endocrinol. 2007 Sep;32(3):231-6 [17912159.001]
  • [Cites] Endocr Pract. 2007 Sep;13(5):463-71 [17872347.001]
  • [Cites] Carcinogenesis. 2008 Mar;29(3):620-8 [17893233.001]
  • [Cites] Pituitary. 2011 Mar;14(1):92-7 [18949563.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Oct;55(4):549-56 [11678840.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):352-60 [11838811.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3084-9 [12107205.001]
  • [Cites] J Neurooncol. 2003 Sep;64(3):255-8 [14558601.001]
  • [Cites] Neurosurg Focus. 2004 Apr 15;16(4):E7 [15191336.001]
  • [Cites] Henry Ford Hosp Med J. 1984;32(1):61-6 [6746304.001]
  • [Cites] J Neurosurg. 1986 Dec;65(6):733-44 [3095506.001]
  • [Cites] EMBO J. 1994 Sep 15;13(18):4251-9 [7925270.001]
  • [Cites] Ann N Y Acad Sci. 1994 Sep 15;733:393-406 [7978888.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Jan;80(1):165-71 [7829606.001]
  • [Cites] Cancer Res. 1995 Mar 1;55(5):1146-51 [7867001.001]
  • [Cites] Neurosurgery. 1996 Apr;38(4):765-70; discussion 770-1 [8692397.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jul;81(7):2647-52 [8675592.001]
  • [Cites] Cancer. 1997 Feb 15;79(4):804-12 [9024719.001]
  • [Cites] Eur J Endocrinol. 1997 Aug;137(2):176-80 [9272107.001]
  • [Cites] Cancer Lett. 1998 Apr 24;126(2):209-14 [9585068.001]
  • [Cites] Ann Endocrinol (Paris). 1997;58(6):503-9 [9686010.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):798-827 [9861546.001]
  • [Cites] J Endocrinol Invest. 1999 Jan;22(1):70-5 [10090141.001]
  • [Cites] Acta Neurochir (Wien). 1999;141(2):187-92 [10189502.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Sep;90(9):5478-82 [15956075.001]
  • [Cites] Childs Nerv Syst. 2006 Mar;22(3):290-4 [16047217.001]
  • [Cites] Eur J Endocrinol. 2006 May;154(5):639-43 [16645009.001]
  • [Cites] J Neurooncol. 2006 Oct;80(1):19-20 [16944315.001]
  • [Cites] Can J Neurol Sci. 2006 Aug;33(3):329-32 [17001826.001]
  • [Cites] J Neurosurg. 2006 Oct;105(4):621-6 [17044568.001]
  • [Cites] Surg Neurol. 2006 Nov;66(5):527-33; discussion 533 [17084204.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):172-9 [17062771.001]
  • [Cites] Endocr Pract. 2007 Jan-Feb;13(1):72-6 [17360306.001]
  • [Cites] Ann Surg. 2007 May;245(5):790-4 [17457173.001]
  • [Cites] Neurol Med Chir (Tokyo). 2007 Oct;47(10):475-8 [17965566.001]
  • (PMID = 19356251.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Parathyroid Hormone
  • [Other-IDs] NLM/ PMC2678126
  •  go-up   go-down


86. Ewing I, Pedder-Smith S, Franchi G, Ruscica M, Emery M, Vax V, Garcia E, Czirják S, Hanzély Z, Kola B, Korbonits M, Grossman AB: A mutation and expression analysis of the oncogene BRAF in pituitary adenomas. Clin Endocrinol (Oxf); 2007 Mar;66(3):348-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A mutation and expression analysis of the oncogene BRAF in pituitary adenomas.
  • We speculated that this same gene may be either mutated at this site, or overexpressed, in pituitary adenomas.
  • DESIGN AND MEASUREMENTS: We sequenced 37 pituitary adenomas for a mutation at the V600E position.
  • In addition, we investigated B-Raf mRNA expression in normal pituitary (n = 5) and nonfunctioning pituitary adenomas (NFPA) (n = 6) by semiquantitative PCR, and in a further 27 pituitary adenomas of various types and 10 normal pituitaries using real-time quantitative PCR.
  • B-Raf mRNA was overexpressed in pituitary adenomas compared to normal pituitary, and this was entirely due to overexpression in NFPAs.
  • CONCLUSIONS: Mutations previously seen in the majority of melanomas and a substantial minority of papillary thyroid carcinomas are not a frequent finding in pituitary adenomas.
  • [MeSH-major] Adenoma / chemistry. DNA Mutational Analysis. Gene Expression Regulation, Neoplastic. Pituitary Neoplasms / chemistry. Proto-Oncogene Proteins B-raf / genetics. RNA, Messenger / analysis
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / chemistry. Case-Control Studies. Growth Hormone-Secreting Pituitary Adenoma / chemistry. Humans. Polymerase Chain Reaction / methods. Prolactinoma / chemistry. Statistics, Nonparametric

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17302867.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  •  go-up   go-down


87. Goh KP, Lee HY, Rajasoorya RC: Triple jeopardy in the pituitary. Pituitary; 2008;11(3):331-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Triple jeopardy in the pituitary.
  • Aggressive pituitary tumors are rare the pathogenesis is not well established.
  • The development of pituitary tumor after apoplexy has also been rarely reported.
  • We describe the sequential development of Cushing's disease, apoplexy and aggressive pituitary tumor in the same patient.
  • A 31-year old male presented with eutopic ACTH dependent Cushing's syndrome which failed initial pituitary surgery.
  • An episode of pituitary apoplexy then occurred which was followed by the development of a null-cell pituitary tumor.
  • This second tumor exhibited an aggressive behavior with invasion into the surrounding structures and systemic spread clinically.
  • This case provides important evidence for the hypotheses of the pathogenesis of aggressive pituitary tumors which could have arisen from surviving adenoma cells following apoplexy or as a de novo development of pituitary carcinoma from cells which were not part of the original adenoma.
  • This is the first report of a transformation of Cushing's disease to an aggressive and invasive null cell tumor after pituitary irradiation, apoplexy and surgery.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Carcinoma / etiology. Neoplasms, Second Primary. Pituitary ACTH Hypersecretion / complications. Pituitary Apoplexy / complications. Pituitary Gland / pathology. Pituitary Neoplasms / etiology
  • [MeSH-minor] Adrenalectomy. Adult. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Radiotherapy, Adjuvant

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pituitary. 2000 Oct;3(2):117-22 [11141695.001]
  • [Cites] Neurosurgery. 1996 Apr;38(4):765-70; discussion 770-1 [8692397.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):172-9 [17062771.001]
  • [Cites] BMJ. 1992 May 23;304(6838):1343-6 [1611331.001]
  • [Cites] Endocr J. 2000 Dec;47(6):793-7 [11228056.001]
  • [Cites] Neurosurg Focus. 2004 Apr 15;16(4):E7 [15191336.001]
  • [Cites] Endocr Rev. 1998 Oct;19(5):647-72 [9793762.001]
  • [Cites] Ann Intern Med. 1976 Dec;85(6):731-4 [999109.001]
  • [Cites] Neurosurg Focus. 2004 Apr 15;16(4):E6 [15191335.001]
  • [Cites] Acta Neuropathol. 2001 Aug;102(2):117-20 [11563625.001]
  • [Cites] Cancer. 1997 Feb 15;79(4):804-12 [9024719.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Feb;76(2):529-33 [8432799.001]
  • [Cites] J Clin Endocrinol Metab. 1981 Jan;52(1):95-7 [6256408.001]
  • [Cites] J Clin Endocrinol Metab. 2005 May;90(5):3089-99 [15741248.001]
  • [Cites] Ann Intern Med. 1994 May 15;120(10):817-20 [8154641.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Oct;49(4):533-9 [9876353.001]
  • [Cites] Trends Endocrinol Metab. 2005 Nov;16(9):407-13 [16213744.001]
  • [Cites] JAMA. 1982 May 28;247(20):2816-8 [7077788.001]
  • [Cites] J Endocrinol Invest. 1999 Jan;22(1):70-5 [10090141.001]
  • [Cites] Pituitary. 1998 Apr;1(1):69-81 [11081185.001]
  • [Cites] Can J Neurol Sci. 2001 May;28(2):174-8 [11383946.001]
  • [Cites] Neurosurgery. 2005 May;56(5):1066-74; discussion 1066-74 [15854256.001]
  • [Cites] Acta Neuropathol. 1992;84(2):178-83 [1381860.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Aug;51(2):181-8 [10468988.001]
  • (PMID = 18058238.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


88. Fomekong E, Maiter D, Grandin C, Raftopoulos C: Outcome of transsphenoidal surgery for Cushing's disease: a high remission rate in ACTH-secreting macroadenomas. Clin Neurol Neurosurg; 2009 Jun;111(5):442-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of transsphenoidal surgery for Cushing's disease: a high remission rate in ACTH-secreting macroadenomas.
  • OBJECTIVE: Although numerous studies have shown that transsphenoidal surgery is the best initial treatment for Cushing disease offering 59-95% of success, fewer information is available on the long-term outcome in the subgroup of patients harboring ACTH-secreting macroadenomas.
  • The aims of this study were to analyze our 10-year experience with transsphenoidal surgery in Cushing's disease and to examine whether remission rates were different between micro- and macroadenomas.
  • PATIENTS AND METHODS: Forty consecutive patients with proven Cushing's disease (28 microadenomas, 12 macroadenomas [diameter: 10-25 mm], 3 patients with no visible adenoma at MRI) underwent transsphenoidal surgery (TSS) assisted by neuronavigation in our center between 1996 and 2007.
  • The diagnosis was made using standard endocrinological criteria including bilateral inferior petrosal sinus sampling (BIPSS) with CRH stimulation in all patients with discordant or equivocal biochemical and radiological testing.
  • Interestingly, a very good remission rate (92%) was observed in the subset of macroadenomas, similar to that found in the group of microadenomas (84%, NS), while no post-surgical remission was observed in the 3 patients with no visible adenoma at MRI (p<0.01).
  • Of the 8 patients not in remission after repeated TSS surgery, 3 underwent radiation therapy and three had bilateral adrenalectomy, allowing remission of their hypercortisolism.
  • CONCLUSION: While our overall results are in accordance with other published series, we show here that ACTH-secreting pituitary macroadenomas are usually not associated with a bad outcome, in contrast with patients with no visible adenoma at preoperative MRI.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Cushing Syndrome / surgery. Neurosurgical Procedures. Sphenoid Bone / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Magnetic Resonance Imaging. Male. Middle Aged. Pituitary Hormones / blood. Treatment Outcome. Young Adult

  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19200645.001).
  • [ISSN] 1872-6968
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Pituitary Hormones; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


89. Aghi MK: Management of recurrent and refractory Cushing disease. Nat Clin Pract Endocrinol Metab; 2008 Oct;4(10):560-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of recurrent and refractory Cushing disease.
  • Cushing disease is most frequently caused by pituitary adenomas that secrete adrenocorticotrophic hormone.
  • More challenging for neurosurgeons and endocrinologists, however, is management of the remaining patients whose Cushing disease is refractory to initial transsphenoidal surgery or recurs after initial remission.
  • Here, we review the treatment options and latest surgical, medical, and radiosurgical advances for patients who have persistent or recurrent Cushing disease after transsphenoidal surgery.
  • [MeSH-major] Pituitary ACTH Hypersecretion / therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / surgery. Adrenalectomy. Humans. Hypophysectomy / methods. Ketoconazole / therapeutic use. Models, Biological. Neoplasm Recurrence, Local / surgery. Pituitary Neoplasms / complications. Pituitary Neoplasms / surgery. Radiosurgery / methods. Recurrence. Sphenoid Bone / surgery. Treatment Failure

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. KETOCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18711406.001).
  • [ISSN] 1745-8374
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] R9400W927I / Ketoconazole
  • [Number-of-references] 54
  •  go-up   go-down


90. De Martin M, Pecori Giraldi F, Cavagnini F: Cushing's disease. Pituitary; 2006;9(4):279-87
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's disease.
  • Cushing's disease, i.e., pituitary ACTH-secreting adenoma causing excess glucocorticoid secretion, is a rare disease with significant mortality and morbidity.
  • Timely diagnosis and appropriate treatment can alter the course of the disease and are therefore mandatory.
  • In patients with equivocal results, second line tests, such as the dexamethasone-suppressed CRH test and desmopressin stimulation, usually enable the diagnosis to be confirmed.
  • Measurement of plasma ACTH then allows the distinction between ACTH-dependent (e.g., pituitary or extrapituitary neuroendocrine tumors) and ACTH-independent causes (e.g., adrenal tumors).
  • The last step in the diagnostic algorithm is often the most fraught with problems as the distinction between Cushing's disease and ectopic ACTH secretion relies on judicious interpretation of several diagnostic procedures.
  • Positive responses to stimulation with CRH and inhibition by high doses of dexamethasone, if concurrent, enable a pituitary origin to be established whereas conflicting results call for inferior petrosal sinus sampling, the latter to be performed in experienced centres only.
  • Visualisation of the tumor at pituitary imaging is helpful but not required for the diagnosis, as microadenomas often remain undectected by MRI and/or CT scan and, on the other hand, visualisation of a non-secreting incidentaloma may be misleading.
  • Surgical removal of the pituitary tumor is the optimal treatment choice and should be attempted in every patient.
  • Finally, patients cured of Cushing's disease require long-term monitoring given the risk of relapse and clinical burden of associated ailments.
  • [MeSH-major] Pituitary ACTH Hypersecretion / diagnosis. Pituitary ACTH Hypersecretion / therapy
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. Adrenalectomy. Adrenocorticotropic Hormone / blood. Biomarkers / blood. Biomarkers / urine. Cardiovascular Diseases / etiology. Cardiovascular Diseases / therapy. Combined Modality Therapy. Diagnosis, Differential. Diagnostic Imaging. Endocrine System Diseases / etiology. Endocrine System Diseases / therapy. Eye Diseases / etiology. Eye Diseases / therapy. Humans. Hydrocortisone / blood. Hydrocortisone / urine. Hypophysectomy. Mental Disorders / etiology. Mental Disorders / therapy. Osteoporosis / etiology. Osteoporosis / therapy. Radiotherapy, Adjuvant. Recurrence. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1997 Jan 16;336(3):172-7 [8988897.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Oct 1;42(3):573-80 [9806517.001]
  • [Cites] Neurosurgery. 2001 Aug;49(2):284-91; discussion 291-2 [11504104.001]
  • [Cites] Horm Res. 2004;62(6):300-5 [15557761.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Sep;43(3):359-63 [7586607.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Feb;90(2):800-4 [15562021.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):717-97 [9861545.001]
  • [Cites] Ann Intern Med. 1990 Mar 15;112(6):434-44 [2178536.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Oct;51(4):473-7 [10583315.001]
  • [Cites] J Clin Endocrinol Metab. 1990 May;70(5):1426-30 [2159485.001]
  • [Cites] Strahlenther Onkol. 2002 Apr;178(4):173-86 [12040754.001]
  • [Cites] Lancet. 1999 Sep 11;354(9182):951 [10489980.001]
  • [Cites] Ann Intern Med. 1980 May;92(5):613-9 [6247946.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Nov;43(5):545-50 [8548938.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Aug;87(8):3662-6 [12161492.001]
  • [Cites] J Endocrinol Invest. 2002 Feb;25(2):181-94 [11929092.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Jan;54(1):45-52 [11167925.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jun;58(6):718-24 [12780748.001]
  • [Cites] J Clin Endocrinol Metab. 1987 Sep;65(3):441-7 [3114299.001]
  • [Cites] CNS Drugs. 2001;15(5):361-73 [11475942.001]
  • [Cites] J Neurosurg. 1994 Jan;80(1):37-45 [8271020.001]
  • [Cites] J Endocrinol Invest. 2000 Mar;23(3):145-50 [10803470.001]
  • [Cites] Panminerva Med. 1995 Mar;37(1):1-7 [7478714.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Dec;89(12):6348-57 [15579802.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Mar;89(3):1222-6 [15001614.001]
  • [Cites] Surgery. 1985 Jan;97(1):16-20 [3966225.001]
  • [Cites] Endocr J. 1996 Dec;43(6):645-55 [9075604.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3569-74 [11061503.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):3795-800 [15292307.001]
  • [Cites] J Endocrinol Invest. 1999 Dec;22(11):860-5 [10710275.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jun;88(6):2527-33 [12788849.001]
  • [Cites] Cardiol Rev. 2001 Jul-Aug;9(4):202-7 [11405900.001]
  • [Cites] N Engl J Med. 1977 Nov 3;297(18):957-62 [909542.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Apr;40(4):479-84 [8187313.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 Jan;38(1):73-8 [8435888.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Sep;88(9):4153-7 [12970280.001]
  • [Cites] Eur J Endocrinol. 2000 Dec;143(6):761-8 [11124859.001]
  • [Cites] J Neurosurg. 2000 Nov;93(5):738-42 [11059652.001]
  • [Cites] J Endocrinol Invest. 2000 May;23(5):325-7 [10882152.001]
  • [Cites] J Clin Endocrinol Metab. 1996 May;81(5):1905-11 [8626856.001]
  • [Cites] Nat Med. 2002 Nov;8(11):1281-7 [12379847.001]
  • [Cites] Ann N Y Acad Sci. 2002 Sep;970:119-33 [12381547.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):418-22 [8106630.001]
  • [Cites] Pituitary. 2001 Aug;4(3):153-61 [12138988.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Dec;61(6):768-77 [15579193.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Apr;83(4):1163-7 [9543134.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Aug;84(8):2664-72 [10443657.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):487-92 [10022405.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Apr;62(4):466-72 [15807878.001]
  • [Cites] J Endocrinol Invest. 1994 Feb;17(2):135-9 [8006335.001]
  • [Cites] World J Surg. 1996 Sep;20(7):781-6; discussion 786-7 [8678951.001]
  • [Cites] J Pediatr. 1991 Feb;118(2):256-8 [1993957.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5299-306 [14602765.001]
  • [Cites] Pediatrics. 1975 Nov;56(5):797-803 [1196738.001]
  • [Cites] Ann Clin Biochem. 1997 Jul;34 ( Pt 4):345-59 [9247665.001]
  • [Cites] Clin Endocrinol (Oxf). 1992 Mar;36(3):229-34 [1563076.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Jan;44(1):1-6 [8706280.001]
  • [Cites] Pediatr Clin North Am. 1990 Dec;37(6):1313-32 [2259542.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):3752-63 [15292301.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jun;82(6):1780-5 [9177382.001]
  • [Cites] Clin Endocrinol (Oxf). 1983 Oct;19(4):503-11 [6627701.001]
  • [Cites] Trends Endocrinol Metab. 1996 Aug;7(6):213-6 [18406750.001]
  • [Cites] Lancet. 2003 Nov 29;362(9398):1828-38 [14654323.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Oct;61(4):478-86 [15473881.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):440-8 [10022398.001]
  • [Cites] Eur J Endocrinol. 2000 Aug;143(2):227-34 [10913942.001]
  • [Cites] Am Heart J. 2005 Jan;149(1):54-60 [15660034.001]
  • [Cites] Am J Med. 1952 Nov;13(5):597-614 [12996538.001]
  • [Cites] Ann Clin Biochem. 1997 May;34 ( Pt 3):222-9 [9158818.001]
  • [Cites] Endocr Rev. 1987 Nov;8(4):391-405 [2891500.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):151-66 [11761432.001]
  • [Cites] J Clin Endocrinol Metab. 2003 May;88(5):2076-80 [12727957.001]
  • [Cites] Q J Med. 1973 Jan;42(165):175-204 [4688791.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Nov;77(5):1308-12 [8077325.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 Apr;88(4-5):337-49 [15145443.001]
  • [Cites] Pituitary. 2002;5(2):77-82 [12675504.001]
  • [Cites] JAMA. 1993 May 5;269(17):2232-8 [8386285.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3114-20 [7593411.001]
  • [Cites] Pituitary. 2002;5(3):175-80 [12812309.001]
  • [Cites] J Endocrinol Invest. 1999 Apr;22(4):241-9 [10342356.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Dec;87(12):5465-9 [12466338.001]
  • [Cites] Clin Endocrinol (Oxf). 1985 Feb;22(2):169-77 [3921294.001]
  • [Cites] J Clin Endocrinol Metab. 1983 May;56(5):985-91 [6300181.001]
  • [Cites] Eur J Endocrinol. 2001 May;144(5):499-507 [11331216.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):211-22 [10207692.001]
  • [Cites] Endocrinol Metab Clin North Am. 1991 Jun;20(2):363-9 [1652435.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3568-73 [11502780.001]
  • (PMID = 17077950.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 90
  •  go-up   go-down


91. van der Hoek J, Waaijers M, van Koetsveld PM, Sprij-Mooij D, Feelders RA, Schmid HA, Schoeffter P, Hoyer D, Cervia D, Taylor JE, Culler MD, Lamberts SW, Hofland LJ: Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells. Am J Physiol Endocrinol Metab; 2005 Aug;289(2):E278-87
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells.
  • In a series of human corticotroph adenomas, we recently found predominant mRNA expression of somatostatin (SS) receptor subtype 5 (sst5).
  • After 72 h, the multiligand SS analog SOM230, which has a very high sst5 binding affinity, but not Octreotide (OCT), significantly inhibited basal ACTH release.
  • To further explore the role of sst5 in the regulation of ACTH release, we conducted additional studies with mouse AtT-20 cells.
  • SOM230 showed a 7-fold higher ligand binding affinity and a 19-fold higher potency in stimulating guanosine 5'-O-(3-thiotriphosphate) binding in AtT-20 cell membranes compared with OCT.
  • SOM230 potently suppressed CRH-induced ACTH release, which was not affected by 48-h dexamethasone (DEX) pretreatment.
  • However, DEX attenuated the inhibitory effects of OCT on ACTH release, whereas it increased the inhibitory potency of BIM-23268, an sst5-specific analog, on ACTH release.
  • Quantitative PCR analysis showed that DEX lowered sst(2A+2B) mRNA expression significantly after 24 and 48 h, whereas sst5 mRNA levels were not significantly affected by DEX treatment.
  • Finally, after SS analog preincubation, compared with OCT both SOM230 and BIM-23268 showed a significantly higher inhibitory effect on CRH-induced ACTH release.
  • In conclusion, our data support the concept that the sst5 receptor might be a target for new therapeutic agents to treat Cushing's disease.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Corticotropin-Releasing Hormone / physiology. Pituitary Gland / secretion. Receptors, Somatostatin / physiology
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Down-Regulation. Glucocorticoids / physiology. Mice. Octreotide / pharmacology. Pituitary Neoplasms. RNA, Messenger / analysis. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Stimulation, Chemical. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15769796.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIM 23268; 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
  •  go-up   go-down


92. Tateno T, Kato M, Tani Y, Oyama K, Yamada S, Hirata Y: Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas. Endocr J; 2009;56(4):579-84
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas.
  • Somatostatin analogs and dopamine agonists are clinically used for medical therapy of functioning pituitary tumors, such as growth hormone- and prolactin-secreting tumors, however, their effects on ACTH-secreting tumors are controversial.
  • This study was aimed to determine whether somatostatin receptor (SSTR) subtype (1-5) and dopamine receptor type 2 (D2R) are differentially expressed in pituitary tumors causing Cushing's disease (CD), silent corticotroph adenoma (SCA), and non-functioning pituitary tumor (NFT).
  • Tissue specimens were obtained from 35 pituitary tumors during transsphenoidal surgery.
  • Both SSTR1 and 2 mRNA levels in SCA were greater than CD, while SSTR1 mRNA levels, but not SSTR2, in SCA were also greater than NFT.
  • SSTR5 mRNA levels in CD were greater than SCA, but did not differ between NFT and SCA.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Pituitary ACTH Hypersecretion / metabolism. Pituitary Neoplasms / genetics. Receptors, Dopamine D2 / genetics. Receptors, Somatostatin / physiology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19318729.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 0 / somatostatin receptor type 1; 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


93. Gejman R, Batista DL, Zhong Y, Zhou Y, Zhang X, Swearingen B, Stratakis CA, Hedley-Whyte ET, Klibanski A: Selective loss of MEG3 expression and intergenic differentially methylated region hypermethylation in the MEG3/DLK1 locus in human clinically nonfunctioning pituitary adenomas. J Clin Endocrinol Metab; 2008 Oct;93(10):4119-25
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective loss of MEG3 expression and intergenic differentially methylated region hypermethylation in the MEG3/DLK1 locus in human clinically nonfunctioning pituitary adenomas.
  • CONTEXT: MEG3 is an imprinted gene encoding a novel noncoding RNA that suppresses tumor cell growth.
  • Although highly expressed in the normal human pituitary, it is unknown which of the normal pituitary cell types and pituitary tumors express MEG3.
  • OBJECTIVES: Our objectives were 1) to investigate cell-type- and tumor-type-specific expression of MEG3 in the human pituitary and 2) to investigate whether methylation in the intergenic differentially methylated region (IG-DMR) at the DLK1/MEG3 locus is involved in the loss of MEG3 expression in tumors.
  • DESIGN AND METHODS: RT-PCR, quantitative RT-PCR, Northern blot, and a combination of in situ hybridization and immunofluorescence were used to determine the cell-type- and tumor-type-specific MEG3 expression.
  • Bisulfite treatment and PCR sequencing of genomic DNA were used to measure the CpG methylation status in the normal and tumor tissues.
  • Five normal human pituitaries and 17 clinically nonfunctioning, 11 GH-secreting, seven prolactin-secreting, and six ACTH-secreting pituitary adenomas were used.
  • RESULTS: All normal human pituitary cell types express MEG3.
  • However, loss of MEG3 expression occurs only in nonfunctioning pituitary adenomas of a gonadotroph origin.
  • All other pituitary tumor phenotypes examined express MEG3.
  • Hypermethylation of the IG-DMR at the DLK1/MEG3 locus is present in nonfunctioning pituitary adenomas.
  • CONCLUSIONS: MEG3 is the first human gene identified expressed in multiple normal human pituitary cell types with loss of expression specifically restricted to clinically nonfunctioning pituitary adenomas.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genome Res. 2004 Sep;14(9):1741-8 [15310658.001]
  • [Cites] Genes Cells. 2000 Mar;5(3):211-20 [10759892.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1427-33 [1977759.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Sep;77(3):644-6 [7690360.001]
  • [Cites] Cancer. 1994 Jul 15;74(2):693-6 [8033049.001]
  • [Cites] Cancer Res. 1996 Jun 1;56(11):2493-6 [8653683.001]
  • [Cites] Mol Carcinog. 1997 Aug;19(4):221-4 [9290697.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 2000;64:343-69 [10697414.001]
  • [Cites] Mol Cell Endocrinol. 2008 Feb 13;283(1-2):127-32 [18201819.001]
  • [Cites] Mol Endocrinol. 2001 Feb;15(2):209-18 [11158328.001]
  • [Cites] Genome Res. 2001 Dec;11(12):2085-94 [11731499.001]
  • [Cites] Hum Mol Genet. 2002 Jan 1;11(1):77-86 [11773001.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Mar;87(3):1170-6 [11889182.001]
  • [Cites] Mamm Genome. 2003 Apr;14(4):231-41 [12682775.001]
  • [Cites] Endocr Relat Cancer. 2003 Jun;10(2):323-30 [12790793.001]
  • [Cites] Nat Genet. 2003 Sep;35(1):97-102 [12937418.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5119-26 [14602737.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Oncogene. 2004 Jan 29;23(4):936-44 [14647444.001]
  • [Cites] Nat Neurosci. 2004 Aug;7(8):847-54 [15220929.001]
  • [Cites] Dev Dyn. 1998 Jun;212(2):214-28 [9626496.001]
  • [Cites] Endocrinology. 1998 Jul;139(7):3342-51 [9645710.001]
  • [Cites] Genes Chromosomes Cancer. 1999 Apr;24(4):328-36 [10092131.001]
  • [Cites] Horm Res. 2004;62 Suppl 3:117-23 [15539812.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Apr;90(4):2179-86 [15644399.001]
  • [Cites] Br J Cancer. 2005 Apr 25;92(8):1574-80 [15798773.001]
  • [Cites] J Neurosci. 2005 Nov 23;25(47):11045-54 [16306417.001]
  • [Cites] Acta Neuropathol. 2006 Jan;111(1):1-7 [16328527.001]
  • [Cites] Int J Biochem Cell Biol. 2006;38(10):1808-20 [16793321.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Apr;2(4):220-30 [16932287.001]
  • [Cites] Endocr Relat Cancer. 2006 Sep;13(3):707-16 [16954426.001]
  • [Cites] J Biol Chem. 2007 Aug 24;282(34):24731-42 [17569660.001]
  • [Cites] J Clin Invest. 1990 Jul;86(1):336-40 [1973174.001]
  • (PMID = 18628527.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK040947; United States / NIDDK NIH HHS / DK / R01 DK-40947
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DLK1 protein, human; 0 / DNA, Intergenic; 0 / Intercellular Signaling Peptides and Proteins; 0 / MEG3 non-coding RNA, human; 0 / Membrane Proteins; 0 / Proteins; 0 / RNA, Long Noncoding
  • [Other-IDs] NLM/ PMC2579639
  •  go-up   go-down


94. Gruszka A, Kunert-Radek J, Pawlikowski M, Stepien H: Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas. Pituitary; 2005;8(2):163-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas.
  • The purpose of our study was to evaluate serum concentrations of endostatin in patients harbouring various pituitary adenoma types and to examine the relationship of serum endostatin levels to circulating vascular endothelial growth factor (VEGF) levels.
  • Preoperative serum endostatin and VEGF concentrations were measured using competitive enzyme immunoassays in 71 patients with pituitary adenomas (20 somatotropinomas, 3 corticotropinomas, 6 prolactinomas and 42 clinically nonfunctioning pituitary adenomas - CNFPAs) and compared with levels from age-matched controls.
  • Serum endostatin concentrations were significantly higher in all pituitary adenoma types, except for prolactinomas (somatotropinomas: 124 +/- 16; p < 0.02, corticotropinomas: 157 +/- 42; p < 0.02, prolactinomas: 141 +/- 37; p > 0.05, CNFPAs: 169 +/- 11 ng/ml; p < 0.000005 vs 73 +/- 10 ng/ml in controls).
  • There was a significant positive correlation between endostatin and VEGF serum levels in patients with pituitary adenomas (r = +0.322; p = 0.006).
  • The simultaneous elevation of endostatin and VEGF may attenuate the pro-angiogenic action of VEGF and be responsible for rather weak neovascularization of pituitary adenomas.
  • Prospective studies are required to assess the usefulness of circulating endostatin and VEGF as markers of progression or recurrence of pituitary tumors.
  • [MeSH-major] Adenoma / blood. Endostatins / blood. Pituitary Neoplasms / blood. Vascular Endothelial Growth Factor A / blood

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Endocrinol. 2002 Feb;146(2):143-51 [11834422.001]
  • [Cites] J Biol Chem. 1999 Apr 23;274(17):11721-6 [10206987.001]
  • [Cites] Endocr Pathol. 1997 Autumn;8(3):189-193 [12114722.001]
  • [Cites] Nat Med. 1995 Jan;1(1):27-31 [7584949.001]
  • [Cites] J Biol Chem. 2002 Aug 2;277(31):27872-9 [12029087.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1159-62 [10720055.001]
  • [Cites] Mediators Inflamm. 2003 Aug;12(4):229-35 [14514474.001]
  • [Cites] Cancer. 2001 Apr 15;91(8):1525-9 [11301401.001]
  • [Cites] Int J Cancer. 1998 Mar 2;75(5):780-6 [9495249.001]
  • [Cites] Neuroendocrinology. 1986;43(2):159-65 [3523276.001]
  • [Cites] EMBO J. 1999 Aug 16;18(16):4414-23 [10449407.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5361-6 [15328173.001]
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4628-34 [11156212.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):263-9 [10634397.001]
  • [Cites] Cancer Lett. 2004 Feb 10;204(1):87-95 [14744538.001]
  • [Cites] FEBS Lett. 2000 Dec 15;486(3):247-51 [11119712.001]
  • [Cites] EMBO J. 2000 Mar 15;19(6):1187-94 [10716919.001]
  • [Cites] Urology. 2003 Apr;61(4):719-23 [12670552.001]
  • [Cites] Cell. 1997 Jan 24;88(2):277-85 [9008168.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):203-12 [10667560.001]
  • [Cites] J Endocrinol. 1996 Jul;150(1):99-106 [8708569.001]
  • [Cites] Cancer. 2003 Jun 1;97(11):2767-75 [12767089.001]
  • [Cites] J Gastroenterol Hepatol. 2005 Apr;20(4):583-8 [15836707.001]
  • [Cites] Cytobios. 2000;101(398):151-9 [10755214.001]
  • [Cites] Ann Surg Oncol. 2001 Oct;8(9):741-5 [11597016.001]
  • [Cites] Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2004 Apr;26(2):164-7 [15171554.001]
  • [Cites] Clin Cancer Res. 2002 Sep;8(9):2933-8 [12231538.001]
  • [Cites] J Cell Physiol. 1992 Dec;153(3):557-62 [1447317.001]
  • [Cites] Folia Histochem Cytobiol. 2001;39(2):105-6 [11374779.001]
  • [Cites] Endocr Rev. 2003 Oct;24(5):600-32 [14570746.001]
  • [Cites] Cancer Res. 1999 Dec 15;59(24):6052-6 [10626789.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8345-50 [14678995.001]
  • [Cites] Br J Surg. 2004 Oct;91(10):1354-60 [15376182.001]
  • (PMID = 16379029.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endostatins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  •  go-up   go-down


95. Bernreuther C, Flitsch J, Lüdecke DK, Hagel C: A 61-year-old man with hyponatremia. Brain Pathol; 2008 Apr;18(2):283-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Endocrinologically, low levels for ADH, cortisol and testosterone as well as low-normal values for ACTH, LH and FSH were detected.
  • Cranial computed tomography and MRI scans revealed an intra- and suprasellar tumor of adenoma-like appearance with elevation of the optic chiasm.
  • After transsphenoidal resection of the tumor, no additional anterior lobe insufficiencies or diabetes insipidus occurred.
  • Histological examination revealed a tumor consisting of spindle-shaped cells of uniformly high cellularity with no evidence of hypocellular areas.
  • An intrasellar cellular schwannoma clinically and radiologically mimicking a non-secreting pituitary adenoma is uncommon.
  • However, rare entities like schwannomas, melanocytomas or pituicytomas have to be considered in addition to the more common tumors like pituitary adenomas and meningiomas.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18363939.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Switzerland
  •  go-up   go-down


96. Teshima T, Hara Y, Takekoshi S, Teramoto A, Osamura RY, Tagawa M: Expression of genes related to corticotropin production and glucocorticoid feedback in corticotroph adenomas of dogs with Cushing's disease. Domest Anim Endocrinol; 2009 Jan;36(1):3-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of genes related to corticotropin production and glucocorticoid feedback in corticotroph adenomas of dogs with Cushing's disease.
  • Cushing's disease caused by pituitary corticotroph adenoma is a common endocrine disease in dogs.
  • A characteristic biochemical feature of corticotroph adenomas is their relative resistance to negative feedback by glucocorticoids.
  • In this study, we examined gene expression related to adrenocorticotropic hormone (ACTH) production and secretion, and the negative feedback by glucocorticoids in canine corticotroph adenoma.
  • We used resected corticotroph adenomas from 10 dogs with Cushing's disease.
  • In order to investigate the alteration of gene expression between corticotroph adenoma and normal corticotrophic cells, ACTH-positive cells in the anterior lobe were microdissected using a laser-capture microdissection system, and mRNA levels of proopiomelanocortin (POMC), corticotropin releasing hormone receptor 1 (CRHR1), glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and 11 beta hydroxysteroid dehydrogenase (11HSD) type 1 and type 2 were determined using real-time RT-PCR.
  • POMC, CRHR1, and 11HSD2 mRNA levels in corticotroph adenoma were greater than those in normal corticotrophic cells (POMC, 5.5-fold; CRHR1, 4.9-fold; 11HSD2, 4.2-fold, P<0.01, respectively).
  • MR and 11HSD1 mRNA levels in corticotroph adenoma were lower than those in normal corticotrophic cells (MR, 2.2-fold; 11HSD1, 2.9-fold, P<0.01, respectively).
  • GR mRNA levels did not differ between corticotroph adenoma and normal corticotrophic cells.
  • Our results may help to understand the increased ACTH production and the resistance to negative feedback suppression by glucocorticoids in canine corticotroph adenomas.
  • These changes in gene expression may have a role in the growth of canine corticotroph adenoma, and help elucidate the pathophysiology of dogs with Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adrenocorticotropic Hormone / biosynthesis. Dog Diseases / genetics. Glucocorticoids / physiology. Pituitary ACTH Hypersecretion / veterinary. Pituitary Neoplasms / veterinary
  • [MeSH-minor] 11-beta-Hydroxysteroid Dehydrogenases / genetics. Animals. Dogs. Feedback, Physiological. Female. Gene Expression / genetics. Male. Pro-Opiomelanocortin / genetics. RNA, Messenger / analysis. Receptors, Corticotropin-Releasing Hormone / genetics. Receptors, Glucocorticoid / genetics. Receptors, Mineralocorticoid / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • MedlinePlus Health Information. consumer health - Steroids.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18818046.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Glucocorticoid; 0 / Receptors, Mineralocorticoid; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases
  •  go-up   go-down


97. Rosales C, Fierrard H, Bertagna X, Raffin-Sanson ML: [Management of hypercortisolism]. Rev Med Interne; 2008 Apr;29(4):337-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Cushing's syndrome is a rare but frequently considered disease.
  • Its diagnosis can lead to some difficulties, including confirming the effective endogenous hypercortisolism and determining its cause.
  • The severity of this disease, the diversity of its complications and the multiple therapeutic options make its management challenging.
  • The aim of this review is to present the most recent data about management of Cushing's syndrome, especially diagnostic approaches and therapeutic options.
  • MAIN POINTS: We retained the following points: midnight salivary cortisol is a useful tool in the diagnosis of Cushing's syndrome; the desmopressin test can help to distinguish between Cushing's syndrome and "pseudoCushing's" due to alcohol consumption or psychiatric disorders; cavernous sinus and inferior petrosal sinus sampling is indicated in the evaluation of ACTH-dependent Cushing's syndromes when pituitary imaging is normal or equivocal or when dynamic tests are contradictory; multislice computed-tomography of the chest and the abdomen and somatostatin analogue scintigraphy, eventually combined, are the best imaging procedures in occult ectopic ACTH syndromes; patients with Cushing's disease should be referred to a neurosurgeon experienced in corticotroph adenomas surgery; metabolic consequences of Cushing's syndrome, such as cardiovascular risk factors and osteoporosis need an aggressive treatment.
  • PERSPECTIVES: The incidence of Cushing's syndrome is only 1/100000 per year.
  • Endocrinological management of the disease improves metabolic disorders in these patients.
  • If these results are confirmed, screening for Cushing's syndrome should be systematically performed in these populations.

  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • Hazardous Substances Data Bank. MITOTANE .
  • Hazardous Substances Data Bank. KETOCONAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18226430.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Enzyme Inhibitors; 78E4J5IB5J / Mitotane; R9400W927I / Ketoconazole
  • [Number-of-references] 42
  •  go-up   go-down


98. Chowdhury IN, Sinaii N, Oldfield EH, Patronas N, Nieman LK: A change in pituitary magnetic resonance imaging protocol detects ACTH-secreting tumours in patients with previously negative results. Clin Endocrinol (Oxf); 2010 Apr;72(4):502-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A change in pituitary magnetic resonance imaging protocol detects ACTH-secreting tumours in patients with previously negative results.
  • OBJECTIVE: While detection of pituitary tumours with magnetic resonance imaging (MRI) may reduce diagnostic costs and improve surgical outcomes for patients with Cushing's disease, the optimal T1-weighted spin-echo (SE) MRI protocol remains unknown.
  • We hypothesized that specific MR scanning parameters influence detection of corticotropinomas.
  • DESIGN AND PATIENTS: Between December 1997 and November 2004, 21 of 84 consecutive patients with Cushing's disease had a falsely negative initial pituitary MRI study and a lesion identified subsequently at the National Institutes of Health Clinical Center.
  • This study retrospectively reviewed and compared technical parameters used for the two pituitary T1-weighted SE MRIs in 18 patients with available scans.
  • Immunohistochemistry of tumours resected at transsphenoidal surgery confirmed all to be corticotropinomas.
  • CONCLUSIONS: Not all 'T1-weighted SE' scans are equally accurate.
  • We recommend that endocrinologists consider pituitary MRI parameters when interpreting the results.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Magnetic Resonance Imaging / methods. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] Adult. False Negative Reactions. Female. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / pathology. Pituitary Gland / pathology. Retrospective Studies

  • MedlinePlus Health Information. consumer health - MRI Scans.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] AJR Am J Roentgenol. 1989 Jan;152(1):145-51 [2783269.001]
  • [Cites] J Comput Assist Tomogr. 1988 Sep-Oct;12(5):728-35 [3170830.001]
  • [Cites] Neurosurgery. 1988 Feb;22(2):380-5 [2832783.001]
  • [Cites] AJNR Am J Neuroradiol. 1988 Jan-Feb;9(1):5-11 [3124586.001]
  • [Cites] Radiology. 1987 May;163(2):421-6 [3562821.001]
  • [Cites] Radiology. 1986 Dec;161(3):761-5 [3786729.001]
  • [Cites] Radiol Clin North Am. 1989 Mar;27(2):265-81 [2645603.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jul;89(7):3371-6 [15240617.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Apr;88(4):1565-9 [12679440.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Sep;49(3):293-300 [9861318.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3114-20 [7593411.001]
  • [Cites] Radiology. 1990 Aug;176(2):419-28 [2164234.001]
  • [Cites] Radiographics. 1989 Jul;9(4):587-98 [2756189.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):3795-800 [15292307.001]
  • (PMID = 19500112.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD008833-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS139974; NLM/ PMC2866063
  •  go-up   go-down


99. Pandey P, Ojha BK, Mahapatra AK: Pediatric pituitary adenoma: a series of 42 patients. J Clin Neurosci; 2005 Feb;12(2):124-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric pituitary adenoma: a series of 42 patients.
  • Pituitary adenomas are uncommon in childhood.
  • This report describes the presentation, endocrinological profile, management and outcome of 42 children with pituitary adenomas.
  • The majority of the tumors were functioning adenomas (40/42, 95.2%).
  • Amongst the functioning tumors, there were 20 patients (47.6%) with prolactinomas, 11 patients (26.2%) with Cushing's disease and nine patients (21.4%) with growth hormone (GH)-secreting adenomas.
  • The majority of tumors were macroadenomas, with only eight patients (all with Cushing's disease) having a microadenoma.
  • Transsphenoidal tumor decompression was performed in most cases (71.4%).
  • Of these, 89% of the children with GH-secreting tumors and 100% of the children with Cushing's disease achieved remission.
  • We conclude that the transsphenoidal approach is effective and safe in surgery for pituitary adenomas in children and is the procedure of choice if there is no contraindication.
  • [MeSH-major] Adenoma. Pituitary Neoplasms
  • [MeSH-minor] Adolescent. Child. Female. Humans. Male. Pituitary ACTH Hypersecretion / etiology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15749410.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  •  go-up   go-down


100. Pawlikowski M, Kunert-Radek J, Radek M: "Silent"corticotropinoma. Neuro Endocrinol Lett; 2008 Jun;29(3):347-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] "Silent"corticotropinoma.
  • OBJECTIVES: The aim of the study was to evaluate the ACTH-immunopositive pituitary adenomas, especially those without manifestation of Cushing's disease MATERIAL AND METHODS: 148 pituitary adenomas removed surgically in years 1994--2007 were studied.
  • The paraffin sections were immunostained with antibodies against the pituitary hormones.
  • In 79 adenomas the immunostaining with anti-ACTH antibody was performed Additionally, 23 tumors were also immunostained with anti-Ki-67 (MIB-1) antibody.
  • RESULTS: ACTH immunopositivity was found in 34 cases (23%).
  • Fourteen ACTH-immunopositive tumors manifested themselves as Cushing's disease (including 1 case of Nelson's syndrome).
  • In the remaining 20 cases in spite of the positive immunostaining for ACTH of the tumor cells, no features of hypercortisolism were observed (in several cases even hypocortisolism was found).
  • Thus, those tumors represented so-called "silent" corticotropinomas.
  • Over one third (37%) of "clinically" nonfunctioning pituitary adenomas, when immunostained with anti-ACTH antibody, showed ACTH immunopositivity.
  • Three adenomas in patients with Cushing's disease (21.4%) and 7 "silent" corticotropinomas (35%) were recurrent tumors.
  • In contrast, the recurrence rate in the group of ACTH-immunonegative clinically nonfunctioning pituitary adenomas was 14.7%.
  • The "silent" corticotropinomas exhibited a tendency towards the higher expression of a proliferation marker, Ki-67 antigen as compared to the "active" corticotropinomas.
  • CONCLUSIONS: (i) "Silent" corticotropinomas are rather frequent. (ii) This adenoma type should be considered as aggressive. (iii) It is hypothetized that--like in Nelson's syndrome--the lack of hypercortisolism or even presence of hypocortisolism favorizes the exaggerated growth of tumoral corticotrophs.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Adrenocorticotropic Hormone / metabolism
  • [MeSH-minor] Adult. Cushing Syndrome / blood. Cushing Syndrome / pathology. Female. Humans. Immunohistochemistry. Ki-67 Antigen / blood. Male. Nelson Syndrome / blood. Paraffin Embedding. Pituitary Hormones / metabolism

  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18580839.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Pituitary Hormones; 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down






Advertisement