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1. Andrioli M, Pecori Giraldi F, Losa M, Terreni M, Invitti C, Cavagnini F: Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report. Endocr J; 2010;57(9):833-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report.
  • Double pituitary adenomas are rare occurrences in autoptical, surgical and neuroradiological series and are mostly due to non-functioning pituitary adenomas, GH-secreting and prolactin-secreting adenomas.
  • ACTH secreting tumours are more rare and, to our knowledge, two distinct ACTH-producing adenomas within the same pituitary have never been reported.
  • We herewith describe a 56 year old woman with Cushing' s disease due to two clearly distinct ACTH-secreting pituitary adenomas.
  • She presented with signs and symptoms of hypercortisolism and hormonal testing was indicative for pituitary-dependent Cushing' s syndrome.
  • Sellar MRI visualized an asymmetric pituitary gland with suspect lesions in both the right and the left pituitary lobes.
  • Pathology confirmed the existence of two distinct adenomas located in different sites in the gland.
  • Both presented ACTH immunoreactivity but displayed distinct morphological features.
  • Our case indicates that double ACTH-secreting pituitary adenomas may occur in patients with Cushing' s disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary ACTH Hypersecretion / etiology
  • [MeSH-minor] Cushing Syndrome / etiology. Female. Humans. Middle Aged. Pituitary Neoplasms / pathology

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  • (PMID = 20595779.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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2. 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

  • [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

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  • (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
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3. Tani Y, Inoshita N, Sugiyama T, Kato M, Yamada S, Shichiri M, Hirata Y: Upregulation of CDKN2A and suppression of cyclin D1 gene expressions in ACTH-secreting pituitary adenomas. Eur J Endocrinol; 2010 Oct;163(4):523-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Upregulation of CDKN2A and suppression of cyclin D1 gene expressions in ACTH-secreting pituitary adenomas.
  • OBJECTIVE: Cushing's disease (CD) is usually caused by ACTH-secreting pituitary microadenomas, while silent corticotroph adenomas (SCA) are macroadenomas without Cushingoid features.
  • However, the molecular mechanism(s) underlying their different tumor growth remains unknown.
  • The aim of the current study was to evaluate and compare the gene expression profile of cell cycle regulators and cell growth-related transcription factors in CD, SCA, and non-functioning adenomas (NFA).
  • DESIGN AND METHODS: Tumor tissue specimens resected from 43 pituitary tumors were studied: CD (n=10), SCA (n=11), and NFA (n=22).
  • The gene expressions of cyclins D1, E1, and B1, but not of A1, in CD were significantly suppressed than those in NFA.
  • The gene expressions of E2F1, RB1, BUB1, BUBR1, ETS1, and ETS2 did not differ between each group.
  • Thus, it is suggested that upregulated CDKN2A with the concomitant downregulated cyclin gene family is partly involved in the small size of ACTH-secreting adenoma.

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  • (PMID = 20616110.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 136601-57-5 / Cyclin D1
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4. Teshima T, Hara Y, Shigihara K, Takekoshi S, Nezu Y, Harada Y, Yogo T, Teramoto A, Osamura RY, Tagawa M: Coexistence of corticotroph adenoma and thyrotroph hyperplasia in a dog. J Vet Med Sci; 2009 Jan;71(1):93-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coexistence of corticotroph adenoma and thyrotroph hyperplasia in a dog.
  • Pituitary thyrotroph hyperplasia results from prolonged primary hypothyroidism in humans, mice and rats.
  • In dogs with Cushing's disease, many cases have low serum thyroid hormones concentrations due to euthyroid sick syndrome.
  • A 6-year-old castrated male Beagle diagnosed with Cushing's disease had a high serum thyroid stimulating hormone (TSH) concentration that was treated by hypophysectomy.
  • On histological examination, the resected pituitary gland contained both a corticotroph adenoma and thyrotroph hyperplasia.
  • The TSH-positive cell ratio in this case was greater than that of healthy Beagles.
  • In the present case, the pituitary thyrotroph hyperplasia was probably caused by primary hypothyroidism.
  • In conclusion, this Beagle is the first histological confirmation of the coexistence of a corticotroph adenoma and thyrotroph hyperplasia.

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  • (PMID = 19194082.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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5. De Menis E, Roncaroli F, Calvari V, Chiarini V, Pauletto P, Camerino G, Cremonini N: Corticotroph adenoma of the pituitary in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene. Eur J Endocrinol; 2005 Aug;153(2):211-5
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corticotroph adenoma of the pituitary in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene.
  • We report the occurrence of an ACTH-secreting adenoma in a patient with X-linked congenital adrenal hypoplasia.
  • DESIGN AND METHODS: Detailed clinical, radiological and pathological investigation of the pituitary adenoma.
  • ACTH was 24 980 pg/ml and nuclear magnetic resonance disclosed a huge pituitary adenoma.
  • Three transsphenoidal operations and radiotherapy were necessary to remove the tumor mass and control ACTH secretion.
  • Histologically, the adenoma was composed of chromophobic and basophilic neoplastic cells with positive immunostaining for ACTH.
  • CONCLUSIONS: This case suggests that in adrenal hypoplasia congenita the development of a pituitary adenoma should be considered when a sudden rise of ACTH occurs despite adequate steroid substitution.
  • [MeSH-major] Adenoma / complications. Adrenal Insufficiency / complications. Adrenal Insufficiency / genetics. DNA-Binding Proteins / genetics. Pituitary Neoplasms / complications. Receptors, Retinoic Acid / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Adult. Chromosomes, Human, X. DAX-1 Orphan Nuclear Receptor. Family Health. Female. Frameshift Mutation. Humans. Magnetic Resonance Imaging. Male. Pituitary ACTH Hypersecretion / complications. Pituitary ACTH Hypersecretion / metabolism. Pituitary ACTH Hypersecretion / pathology

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  • (PMID = 16061826.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] eng
  • [Grant] Italy / Telethon / / B.38
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / NR0B1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Repressor Proteins; 9002-60-2 / Adrenocorticotropic Hormone
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6. 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
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  • [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

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  • (PMID = 19387839.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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7. Guignat L, Assie G, Bertagna X, Bertherat J: [Corticotroph adenoma]. Presse Med; 2009 Jan;38(1):125-32
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  • [Title] [Corticotroph adenoma].
  • [Transliterated title] Adénome corticotrope.
  • Corticotroph adenomas cause ACTH oversecretion responsible for Cushing's disease.
  • This represents the most frequent cause of Cushing's syndrome, or chronic excess of endogenous glucocorticoids.
  • Ninety percent of corticotroph adenomas are microadenomas, sometime not visible on MRI.
  • Corticotroph macroadenomas are rare, but can be responsible for an aggressive tumor.
  • Cushing's disease diagnosis requires careful hormonal and imaging investigations, aiming first at the diagnosis of Cushing's syndrome and in a second step at the diagnosis of its pituitary origin.
  • The treatment of corticotroph adenoma is mainly based on pituitary surgery.
  • In case of failure of pituitary surgery, or in patients in whom surgery is not appropriate as a first line treatment, medical therapy (mainly anticortisolic drugs), pituitary radiotherapy or surgical bilateral adrenalectomy can be discussed.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / complications
  • [MeSH-minor] Adrenalectomy. Adrenocorticotropic Hormone / analysis. Chemotherapy, Adjuvant. Corticotropin-Releasing Hormone / analysis. Cushing Syndrome / diagnosis. Cushing Syndrome / etiology. Cushing Syndrome / therapy. Diagnosis, Differential. Humans. Hydrocortisone / analysis. Hydrocortisone / antagonists & inhibitors. Magnetic Resonance Imaging. Neoadjuvant Therapy. Radiotherapy, Adjuvant

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  • (PMID = 19041214.001).
  • [ISSN] 2213-0276
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone
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8. Fujimura M, Ikeda H, Takahashi A, Ezura M, Yoshimoto T, Tominaga T: Diagnostic value of super-selective bilateral cavernous sinus sampling with hypothalamic stimulating hormone loading in patients with ACTH-producing pituitary adenoma. Neurol Res; 2005 Jan;27(1):11-5
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic value of super-selective bilateral cavernous sinus sampling with hypothalamic stimulating hormone loading in patients with ACTH-producing pituitary adenoma.
  • AIMS: Early diagnosis and early treatment by transsphenoidal surgery is desirable for ACTH-producing pituitary microadenoma, but accurate localization of the functional lesion is not always possible before surgery because magnetic resonance (MR) imaging may provide false negative and/or positive findings.
  • The diagnostic value of super-selective bilateral cavernous sinus sampling with the administration of corticotropin-releasing hormone (CRH) was assessed in patients with functioning ACTH-producing pituitary adenoma.
  • METHODS: Fifteen patients with pituitary adenoma (14 with microadenoma) aged from 23 to 74 years (mean 46.7 years) underwent cavernous sinus sampling with or without the CRH loading test and subsequent transsphenoidal surgery in our institute from October 1997 through to November 2002.
  • To eliminate the bias due to uneven blood flow in the cavernous sinuses and the multi-hormonal response to CRH administration, the ACTH/FSH ratios were evaluated.
  • The inter-cavernous gradient (ICG) was calculated as the higher/lower ACTH venous blood levels in the right and left cavernous sinuses with or without CRH loading.
  • The adjusted ICG was calculated using the ACTH/FSH ratios.
  • RESULTS: Transsphenoidal surgery revealed the functioning lesion on the right in five cases, the left in six, the midline in three and the bilateral lateral wings (double adenoma) in one.
  • CONCLUSIONS: Super-selective cavernous sinus sampling with hypothalamic stimulating hormone administration can provide accurate localization of the responsible lesion in patients with ACTH-producing pituitary adenoma.
  • [MeSH-major] Adenoma / diagnosis. Adrenocorticotropic Hormone / blood. Corticotropin-Releasing Hormone. Petrosal Sinus Sampling / methods. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Gadolinium DTPA. Humans. Hypophysectomy / methods. Magnetic Resonance Imaging. Male. Middle Aged. Predictive Value of Tests. Radiography. Regional Blood Flow / drug effects. Regional Blood Flow / physiology

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  • (PMID = 15829152.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; K2I13DR72L / Gadolinium DTPA
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9. Hanson JM, Mol JA, Leegwater PA, Bilodeau S, Drouin J, Meij BP: Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas. Domest Anim Endocrinol; 2008 Apr;34(3):217-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas.
  • Pituitary-dependent hyperadrenocorticism (PDH) in dogs is caused by a pituitary corticotroph adenoma.
  • Although PDH is a common disorder in dogs, little is known about the underlying pathogenesis.
  • In the pituitary glands of humans and mice, the pro-opiomelanocortin (POMC)-expressing cell lineages, the corticotrophs and melanotrophs, have a specific marker in common, the T-box transcription factor Tpit (Tbx19), which is obligate for POMC expression.
  • Tpit also regulates the late differentiation of the corticotrophs and melanotrophs, and therefore may contribute to the pathogenesis of the corticotroph adenomas.
  • The aim of this study was to perform an expression and mutation analysis of Tpit in the normal canine pituitary and in corticotroph adenomas.
  • The distribution of the Tpit protein in the pituitary gland was studied with immunohistochemistry and the expression of the gene with RT-PCR.
  • Tpit was expressed in corticotroph and melanotroph cells of the normal and adenomatous canine pituitary, and remained present in non-adenomatous corticotrophs of pituitaries from PDH dogs.
  • No tumor-specific mutation in the Tpit cDNA from the corticotroph adenomas was found.
  • It is concluded that Tpit can be used as a reliable marker for the corticotroph and melanotroph cells in the canine pituitary tissue and that mutations in the Tpit gene are unlikely to play a major role in the pathogenesis of canine corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adenoma / veterinary. Dog Diseases / genetics. Pituitary Gland / chemistry. Pituitary Neoplasms / veterinary. T-Box Domain Proteins / genetics

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  • (PMID = 17544240.001).
  • [ISSN] 0739-7240
  • [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 / T-Box Domain Proteins; 9007-49-2 / DNA
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10. Aznar Rodríguez S, Moreno Pérez O, Revert Marrahí P, Martínez Fuster S, Boix Carreño E, Picó Alfonso AM: Silent corticotroph adenomas of the pituitary gland: apropos of two cases. Endocrinol Nutr; 2008 Oct;55(8):367-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silent corticotroph adenomas of the pituitary gland: apropos of two cases.
  • Clinically silent corticotroph adenomas are rare.
  • Given the absence of clinical and biochemical features of hypercortisolism, the definitive diagnosis is histological.

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  • [Copyright] Copyright © 2008 Sociedad Española de Endocrinología y Nutrición. Published by Elsevier Espana. All rights reserved.
  • (PMID = 22975601.001).
  • [ISSN] 1575-0922
  • [Journal-full-title] Endocrinología y nutrición : órgano de la Sociedad Española de Endocrinología y Nutrición
  • [ISO-abbreviation] Endocrinol Nutr
  • [Language] eng; spa
  • [Publication-type] Journal Article
  • [Publication-country] Spain
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11. de Bruin C, Pereira AM, Feelders RA, Romijn JA, Roelfsema F, Sprij-Mooij DM, van Aken MO, van der Lelij AJ, de Herder WW, Lamberts SW, Hofland LJ: Coexpression of dopamine and somatostatin receptor subtypes in corticotroph adenomas. J Clin Endocrinol Metab; 2009 Apr;94(4):1118-24

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coexpression of dopamine and somatostatin receptor subtypes in corticotroph adenomas.
  • CONTEXT: Previous studies have demonstrated the expression of somatostatin receptor subtypes (mainly sst(5)) and dopamine (DA) receptor subtypes (mainly D(2)) in smaller series of human corticotroph adenomas.
  • In line with these findings, sst(5) and D(2)-targeting agents have already been used clinically in patients with Cushing's disease (CD) and have shown promising results in subsets of patients.
  • To what extent these receptor subtypes are coexpressed within individual adenomas, is not known however.
  • OBJECTIVE: The aim of the study was to investigate the (co-)expression of both sst and DA receptors in a large series of human corticotroph adenomas.
  • DESIGN: We performed in vitro analysis of corticotroph adenoma tissue obtained via transsphenoidal adenomectomy.
  • PATIENTS: Adenoma tissue from 30 patients with CD was analyzed in this study.
  • RESULTS: Analyzed by quantitative RT-PCR, D(2) and sst(5) were significantly (co-) expressed in the majority (60%) of adenomas, whereas 23% of adenomas only expressed D(2), but not sst(5).
  • The remaining 17% of adenomas did not significantly express either sst(5) or D(2).
  • Corticotroph adenomas with invasive growth invariably showed loss of sst(5) and D(2) expression.
  • CONCLUSIONS: Sst(5) and especially D(2) are highly expressed in the majority of human corticotroph adenomas, with coexpression of sst(5) and D(2) being a common phenomenon.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Receptors, Dopamine / genetics. Receptors, Somatostatin / genetics

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  • (PMID = 19141584.001).
  • [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 / DNA Primers; 0 / Receptors, Dopamine; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin
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12. 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
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  • [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

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  • (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
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13. van Rijn SJ, Grinwis GC, Penning LC, Meij BP: Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas. Domest Anim Endocrinol; 2010 May;38(4):244-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas.
  • Pituitary-dependent hypercortisolism (PDH), which is caused by adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas, is a common endocrinopathy in dogs.
  • The aim of this study was to investigate the expression of the proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA) and the cell-cycle inhibitor p27kip1 in corticotroph adenomas in enlarged and non-enlarged pituitaries.
  • The expression of Ki-67, PCNA, and p27kip1 was analyzed by immunohistochemical staining of 17 pituitary adenoma samples harvested during pituitary surgery in dogs with PDH.
  • However, a trend toward significance was observed when comparing the expression of p27kip1 in enlarged pituitaries versus normal pituitary tissue.
  • It is concluded that Ki-67 and PCNA are not useful as proliferative markers for studying the pathobiology of pituitary corticotroph adenomas in dogs.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Cyclin-Dependent Kinase Inhibitor p27 / analysis. Dog Diseases / metabolism. Ki-67 Antigen / analysis. Pituitary Neoplasms / veterinary. Proliferating Cell Nuclear Antigen / analysis

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  • [Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20022446.001).
  • [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 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone
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14. Alarifi A, Alzahrani AS, Salam SA, Ahmed M, Kanaan I: Repeated remissions of Cushing's disease due to recurrent infarctions of an ACTH-producing pituitary macroadenoma. Pituitary; 2005;8(2):81-7
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  • [Title] Repeated remissions of Cushing's disease due to recurrent infarctions of an ACTH-producing pituitary macroadenoma.
  • Infarction of prolactin-secreting or growth hormone-secreting pituitary adenomas is not unusual.
  • However, Infarction of ACTH-secreting adenomas has rarely been reported.
  • Cyclical course of Cushing's syndrome alternating with adrenal insufficiency due to recurrent infarction of an ACTH-secreting pituitary adenoma has not been reported.
  • We report here a 20-year-old lady who presented with florid signs of Cushing's syndrome but was found to have adrenal insufficiency on biochemical evaluation.
  • Magnetic resonance imaging (MRI) of the pituitary gland showed that she had infarction of an ACTH-secreting macroadenoma.
  • Over the next 6 years, her disease ran a cyclical course characterized by periods of hypercortisolism alternating with adrenal insufficiency due to repeated episodes of infarctions of the ACTH-secreting pituitary macroadenoma with corresponding changes in the pituitary adenoma on serial MRIs.
  • The case alerts clinicians to this possibility when a patient presents with clinical picture of Cushing's syndrome but has adrenal insufficiency on biochemical testing.
  • It also suggests that silent or subclinical infarction of pituitary adenomas is not uncommon and is probably under diagnosed.
  • [MeSH-major] Adenoma / blood supply. Adrenocorticotropic Hormone / secretion. Infarction / physiopathology. Pituitary ACTH Hypersecretion / physiopathology. Pituitary Neoplasms / blood supply

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  • (PMID = 16195779.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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15. Evang JA, Borota OC, Melum E, Holm R, Ramm-Pettersen J, Bollerslev J, Berg JP: HDAC2 expression and variable number of repeats in exon 1 of the HDAC2 gene in corticotroph adenomas. Clin Endocrinol (Oxf); 2010 Aug;73(2):229-35
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  • [Title] HDAC2 expression and variable number of repeats in exon 1 of the HDAC2 gene in corticotroph adenomas.
  • OBJECTIVES: Alterations in protein expression of histone deacetylase 2 (HDAC2) have been demonstrated in various neoplasms, and lack of nuclear expression of HDAC2 has previously been shown in some human and canine corticotroph adenomas.
  • This study aimed to examine HDAC2 expression in a Norwegian cohort of corticotroph adenomas, screen for exonic HDAC2 gene variants in the adenomas and correlate the results with clinical data.
  • PATIENTS AND DESIGN: Forty-four patients with verified Cushing's disease or Nelson's syndrome, positive ACTH staining and tissue available for immunohistochemistry and/or DNA sequencing were included.
  • RESULTS: Histone deacetylase 2 expression examined by immunohistochemistry was strongly reduced in 3/30 adenomas.
  • A previously unidentified insertion of three bases in a region coding for a polyserine cluster in exon 1 of the HDAC2 gene was identified in 6/32 adenomas.
  • The same insertion was also found in 28/94 of the controls (i.e., not significantly different from the patients).
  • CONCLUSIONS: Strongly reduced HDAC2 protein expression was confirmed in a small portion of corticotroph tumours.
  • Mutations in HDAC2 exons are unlikely to play an important role in the development of corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Histone Deacetylase 2 / genetics. Minisatellite Repeats

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  • (PMID = 20346000.001).
  • [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] EC 3.5.1.98 / HDAC2 protein, human; EC 3.5.1.98 / Histone Deacetylase 2
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16. 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
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  • [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

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  • (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
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17. Candrina R, Sleiman I, Zorzi F: ACTH-secreting pituitary adenoma within an ovarian teratoma. Eur J Intern Med; 2005 Sep;16(5):359-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ACTH-secreting pituitary adenoma within an ovarian teratoma.
  • The differential diagnosis of Cushing's syndrome is one of the most difficult tasks in medicine, and it is especially problematic in cases with "occult" ectopic ACTH syndrome.
  • We describe the case of a 26-year-old woman who was found to suffer from ectopic ACTH syndrome due to pituitary microadenoma, localized within a mature ovarian teratoma.
  • Cushing's syndrome caused by ovarian neoplasia is unusual, but when it occurs, it is most often due to excessive cortisol production by the ovary.
  • Only rarely has ectopic ACTH syndrome in association with an ovarian tumor been described.

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  • (PMID = 16137552.001).
  • [ISSN] 0953-6205
  • [Journal-full-title] European journal of internal medicine
  • [ISO-abbreviation] Eur. J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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18. Trapani F, Del Basso De Caro ML, Insabato L, Papparella S, Paciello O: Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog. Folia Histochem Cytobiol; 2010 Sep 30;48(3):403-6
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  • [Title] Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.
  • The Silent Corticotroph Adenoma (SCA) is a pituitary adenoma variant characterized by the immunoreactivity for adrenocorticotropic hormone (ACTH) and related peptides, without the clinical signs of Cushing's disease.
  • SCA has been postulated to either secrete structurally abnormal ACTH that is inactive but detectable by immunohistochemistry or radioimmunoassay, or to secrete ACTH intermittently or at low levels continuously.
  • Excess of ACTH has been associated to type II muscle atrophy.
  • We describe a case of type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.
  • The tumour showed a trabecular growth pattern and immunohistochemical analysis demonstrated the presence of cytoplasmic immunoreactivity for ACTH.
  • The muscle atrophy was considered to be related to an excess of inactive ACTH.

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  • (PMID = 21071346.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.3.99.1 / Succinate Dehydrogenase; EC 1.6.- / NADH Tetrazolium Reductase
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19. 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
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  • [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

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  • (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
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20. Kim K, Yamada S, Usui M, Sano T: Co-localization of honeycomb golgi and ACTH granules in a giant ACTH-producing pituitary adenoma. Endocr Pathol; 2005;16(3):239-44
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  • [Title] Co-localization of honeycomb golgi and ACTH granules in a giant ACTH-producing pituitary adenoma.
  • We document the co-localization of honeycomb golgi and ACTH-immunopositive granules in giant ACTH-producing pituitary adenoma cells.
  • A 42-yr-old woman presented with Cushing's disease and a giant adenoma that invaded the sphenoid and cavernous sinus.
  • Some of the adenoma cells were ACTH-positive and upon electron-microscopic (EM) study most were found to contain sparse granules and no type-I filaments.
  • Immunohistochemical study of mirror sections of portions containing cells with honeycomb golgi revealed that the cells with honeycomb golgi showed ACTH-immunopositivity.
  • Honeycomb golgi, which was formerly considered a morphological marker of gonadotroph adenomas in females, has previously been identified in large ACTH-producing pituitary adenomas but there has been no direct evidence that individual cells with honeycomb golgi are cells that produce ACTH.
  • Our immunohistochemical documentation of ACTH-immunoreactivity in individual adenoma cells containing honeycomb golgi clearly confirms that honeycomb golgi is not confined only to gonadotroph adenomas in females.
  • Rather, the existence of honeycomb golgi in cells of other adenoma types may be due to their low hormone production and/or to disturbances in the regulation of the exocytotic pathway.
  • [MeSH-major] Adenoma / ultrastructure. Adrenocorticotropic Hormone / secretion. Golgi Apparatus / ultrastructure. Pituitary Neoplasms / ultrastructure. Secretory Vesicles / ultrastructure

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  • (PMID = 16299407.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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21. 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
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  • [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

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  • (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
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22. de Bruin C, Hanson JM, Meij BP, Kooistra HS, Waaijers AM, Uitterlinden P, Lamberts SW, Hofland LJ: Expression and functional analysis of dopamine receptor subtype 2 and somatostatin receptor subtypes in canine cushing's disease. Endocrinology; 2008 Sep;149(9):4357-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and functional analysis of dopamine receptor subtype 2 and somatostatin receptor subtypes in canine cushing's disease.
  • Cushing's disease (CD) is a severe disorder characterized by chronic hypercortisolism due to an ACTH-secreting pituitary adenoma.
  • Finding an effective and safe medical treatment for CD may improve long-term clinical outcome.
  • The recent demonstration of expression of somatostatin receptor subtypes (mainly sst5) and dopamine receptor subtype 2 (D2) in human corticotroph adenomas offers the possibility for medical treatment of CD with novel somatostatin analogs and dopamine agonists.
  • Interestingly, CD is a frequent disorder in dogs with striking clinical similarities with CD in humans.
  • Therefore, we investigated the expression and functional role of D2 and somatostatin receptors in corticotroph adenoma cells from 13 dogs with active CD that underwent therapeutic hypophysectomy and normal anterior pituitary cells from five dogs.
  • Quantitative RT-PCR and immunohistochemistry revealed that both in CD and normal anterior pituitary, sst2 was the predominant receptor subtype expressed, whereas D2 was modestly expressed and sst5 was expressed only at very low levels.
  • In primary cultures of canine adenomas (n = 7), the sst2-preferring agonist octreotide also showed the strongest ACTH-suppressive effects.
  • In conclusion, canine corticotroph adenomas provide an interesting model to study CD, but differences in somatostatin and dopamine receptor expression between humans and dogs should be taken into account when using dogs with CD as a model to evaluate efficacy of novel somatostatin analogs and dopamine agonists for human CD.
  • [MeSH-major] Dog Diseases / genetics. Pituitary ACTH Hypersecretion / genetics. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / physiology. Receptors, Somatostatin / genetics. Receptors, Somatostatin / physiology
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Animals. Cells, Cultured. Dexamethasone / pharmacology. Dogs. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic / drug effects. Male. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism

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  • (PMID = 18483151.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC2553383
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23. 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

  • [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

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  • (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
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24. Iino K, Oki Y, Matsushita F, Yamashita M, Hayashi C, Miura K, Nishizawa S, Nakamura H: Immunohistochemical properties of silent corticotroph adenoma and Cushing's disease. Pituitary; 2007;10(1):35-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical properties of silent corticotroph adenoma and Cushing's disease.
  • Proopiomelanocortin processing in corticotroph cells is known to be operated by prohormone convertase (PC) 1/3 which is activating several pro-proteins and prohormones by intracellular limited proteolysis processing.
  • In this study, we hypothesized that PC1/3 expression differs between Cushing's disease (CD) and silent corticotroph adenoma (SCA), and investigated whether PC1/3 expression is involved in the adrenocorticotropin (ACTH) silence of SCA.
  • We performed immunohistochemical analysis of pituitary adenoma specimens for six adenohypophysial hormones, PC1/3 and chromogranin A (CgA).
  • Subjects for this study consisted of 12 anterior pituitary adenomas of CD (1 male, 11 female; 14-70 years old) and 31 non-functioning adenomas (23 male, 8 female; 32-71 years old).ACTH immunoreactivity was observed in all of CD and three of 31 non-functioning adenomas.
  • Cushing's adenomas and SCAs were all positive for PC1/3.
  • PC1/3-positive cells did not always colocalize with ACTH but some of them colocalized with CgA in SCAs.
  • Even if PC1/3 is not present in corticotroph cells, PC1/3 immunoreactivity in SCA may originate from CgA-positive cells.
  • We conclude that immunohistochemistry for PC1/3 is not helpful for differential diagnosis between CD and SCA in clinical practice, though the regulation of PC1/3 expression is likely to be an important etiological factor in ACTH silence of SCA.
  • The diversity of immunohistochemical properties of SCA leads us to speculate that it is not a single entity and may be a general diagnostic term for adenomas of varying etiology.
  • [MeSH-major] Adenoma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Aged. Chromogranin A / blood. Corticotropin-Releasing Hormone. Female. Follicle Stimulating Hormone / metabolism. Gonadotropin-Releasing Hormone. Growth Hormone-Releasing Hormone. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Proprotein Convertases / blood. Thyrotropin

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  • (PMID = 17410413.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 12629-01-5 / Human Growth Hormone; 33515-09-2 / Gonadotropin-Releasing Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 3.4.- / Proprotein Convertases
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25. Castillo VA, Gallelli MF: Corticotroph adenoma in the dog: pathogenesis and new therapeutic possibilities. Res Vet Sci; 2010 Feb;88(1):26-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corticotroph adenoma in the dog: pathogenesis and new therapeutic possibilities.
  • The corticotrophinoma, causing pituitary dependent hypercortisolism, represents the highest percentage of pituitary tumours in the dog.
  • It is not clear either what factors are involved in the tumour genesis; nevertheless, firm candidates are the Rb1 gene, proteins p27, p21 and p16, as are also defects in the glucocorticoid receptor and Nur77/Nurr1.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adenoma / veterinary. Dog Diseases / etiology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19733374.001).
  • [ISSN] 1532-2661
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 95
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26. Giorgi RR, Correa-Giannella ML, Casarini AP, Machado MC, Bronstein MD, Cescato VA, Giannella-Neto D: Metallothionein isoform 3 gene is differentially expressed in corticotropin-producing pituitary adenomas. Neuroendocrinology; 2005;82(3-4):208-14
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metallothionein isoform 3 gene is differentially expressed in corticotropin-producing pituitary adenomas.
  • In order to search for candidate genes related to pituitary adenoma aggressiveness, the present investigation was intended to compare the mRNA expression profile from a pool of four nonfunctional pituitary adenomas (NFPA) with a spinal cord metastasis of a nonfunctional pituitary carcinoma (MNFPC).
  • The metallothionein isoform 3 (MT3) gene was differentially expressed in nonfunctional adenomas in comparison to the metastasis of nonfunctional carcinoma.
  • A microarray dataset comprising 19,881 probes was employed for comparing expression profiles of a spinal cord metastasis of a nonfunctional pituitary carcinoma with a pool of four nonfunctional pituitary adenomas.
  • RT-qPCR confirmed the microarray findings and was used to investigate MT3 mRNA gene expression in tumor samples of a series of 52 different pituitary adenoma subtypes comprising 10 corticotropin (ACTH)-producing, 18 growth hormone (GH)-producing, 8 prolactin (PRL)-producing, and 16 nonfunctional adenomas.
  • MT3 mRNA expression was statistically significantly higher in ACTH-producing pituitary adenomas and in nonfunctional pituitary adenomas in comparison to the other pituitary adenoma subtypes.
  • The more abundant expression of this gene in ACTH-producing pituitary adenomas suggests that MT3 could be related to distinct pituitary cell lineage regulating the activity of some transcription factor of importance in hormone production and/or secretion.
  • [MeSH-major] Adenoma / metabolism. Adrenocorticotropic Hormone / metabolism. Nerve Tissue Proteins / biosynthesis. Pituitary Neoplasms / metabolism

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  • (PMID = 16601360.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / growth inhibitory factor; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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27. Raverot G, Wierinckx A, Jouanneau E, Auger C, Borson-Chazot F, Lachuer J, Pugeat M, Trouillas J: Clinical, hormonal and molecular characterization of pituitary ACTH adenomas without (silent corticotroph adenomas) and with Cushing's disease. Eur J Endocrinol; 2010 Jul;163(1):35-43
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical, hormonal and molecular characterization of pituitary ACTH adenomas without (silent corticotroph adenomas) and with Cushing's disease.
  • OBJECTIVE: Silent corticotroph adenomas (SCAs) are rare pituitary tumours immunoreactive for ACTH, but without clinical evidence of Cushing's disease.
  • We characterized SCAs based on clinical, hormonal and molecular data, and compared the characteristics of these tumours with those of macro (MCA)- and micro (mCA)-ACTH adenomas with Cushing's disease.
  • METHODS: Fifty ACTH adenomas (14 SCAs, 15 MCAs and 21 mCAs) with complete corresponding clinical, radiological and biochemical data were selected.
  • Histological corticotroph differentiation; immunostaining for ACTH, beta-endorphin and beta-LPH; and mRNA expression levels of TPIT, POMC, GRalpha, prohormone convertase 1/3 (PC1/3) and galectin-3 were compared in 21 representative tumours.
  • RESULTS: Despite the absence of clinical hypercortisolism in patients with SCA, elevated plasma ACTH levels that were similar to those associated with mCA were observed.
  • The cortisol/ACTH ratio was similar between SCA and MCA groups and lower than that found with mCA (P<0.05).
  • After an i.v. dexamethasone suppression test, ACTH levels were significantly higher in patients with MCA than in those with mCA (P<0.05).
  • Cytological and immunocytochemical analyses as well as mRNA expression levels of TPIT, POMC and GRalpha confirmed corticotroph differentiation in both mCAs and MCAs and in half of the SCAs, with a strong correlation between TPIT and POMC mRNA expression levels in SCAs (R(2)=0.72; P<0.01) and in MCAs (R(2)=0.65; P<0.05).
  • CONCLUSIONS: Despite the absence of hypercortisolism, SCAs exhibit histological, biochemical and molecular corticotroph differentiation.

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  • (PMID = 20385723.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Galectin 3; 0 / Homeodomain Proteins; 0 / Receptors, Glucocorticoid; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / glucocorticoid receptor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.21.93 / Proprotein Convertase 1; WI4X0X7BPJ / Hydrocortisone
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28. Timmers HJ, van Ginneken EM, Wesseling P, Sweep CG, Hermus AR: A patient with recurrent hypercortisolism after removal of an ACTH-secreting pituitary adenoma due to an adrenal macronodule. J Endocrinol Invest; 2006 Nov;29(10):934-9
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A patient with recurrent hypercortisolism after removal of an ACTH-secreting pituitary adenoma due to an adrenal macronodule.
  • A 41-yr-old female was referred for signs and symptoms of Cushing's syndrome.
  • Cortisol was not suppressed by 1 mg dexamethasone (0.41 micromol/l).
  • Midnight cortisol and ACTH were 0.44 micromol/l and 18 pmol/l, respectively.
  • A magnetic resonance imaging (MRI) revealed a pituitary lesion of 7 mm.
  • ACTH and cortisol levels were unaltered by administration of human CRH and high-dose dexamethasone.
  • Inferior sinus petrosus sampling showed CRH-stimulated ACTH levels of 128.4 (left sinus) vs a peripheral level of 19.2 pmol/l, indicating Cushing's disease.
  • After 4 months of pre-treatment with metyrapone and dexamethasone, endoscopic transsphenoidal resection of an ACTH-positive pituitary adenoma was performed.
  • ACTH levels decreased to 2.6 pmol/l and fasting cortisol was 0.35 micromol/l.
  • Despite clinical regression of Cushing's syndrome and normalization of urinary cortisol, cortisol was not suppressed by 1 mg dexamethasone (0.30 micromol/l).
  • Ten months post-operatively, signs and symptoms of Cushing's syndrome reoccurred.
  • A high dose dexamethasone test according to Liddle resulted in undetectable ACTH, but no suppression of cortisol levels, pointing towards adrenal-dependent Cushing's syndrome.
  • This case illustrates, that longstanding ACTH stimulation by a pituitary adenoma can induce unilateral macronodular adrenal hyperplasia with autonomous cortisol production.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Adrenal Glands / metabolism. Adrenal Glands / pathology. Cushing Syndrome / etiology
  • [MeSH-minor] Adrenocorticotropic Hormone / blood. Adult. Female. Humans. Hydrocortisone / blood. Hyperplasia / complications. Hyperplasia / diagnosis. Hyperplasia / metabolism. Hyperplasia / pathology. Pituitary ACTH Hypersecretion / complications. Pituitary ACTH Hypersecretion / metabolism. Pituitary ACTH Hypersecretion / pathology. Recurrence

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  • (PMID = 17185905.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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29. Hashiba T, Saitoh Y, Asanuma N, Kouhara H, Maruo T, Fujinaka T, Kasayama S, Yoshimine T: Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome. Endocr J; 2006 Apr;53(2):203-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome.
  • Endocrinologic tests sometimes fail to distinguish adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma from ectopic ACTH-secreting tumor.
  • The authors experienced a case of Cushing's disease associated with a pancreatic tumor.
  • Venous sampling contributed to the final diagnosis of Cushing's disease in this complex case, while endocrinologic tests showed paradoxical results.
  • A 54-year-old woman presented with Cushing's syndrome and pancreatic tumor.
  • Magnetic resonance imaging (MRI) failed to reveal a pituitary tumor, but a gadolinium-enhanced tumor with cystic components was seen in the pancreatic tail.
  • Results of conventional endocrinologic tests suggested ectopic ACTH syndrome, but venous sampling including cavernous sinus sampling indicated an ACTH-secreting pituitary adenoma.
  • Transsphenoidal surgery revealed a pituitary microadenoma, and total removal of the tumor was achieved.
  • Postoperative abdominal MRI revealed that the pancreatic tumor diminished gradually without treatment.
  • Selective cavernous sinus sampling was useful for distinguishing ACTH-secreting pituitary adenoma from ectopic ACTH syndrome in this complex case.
  • This was a rare case in which the pancreatic tumor diminished after total removal of the ACTH-secreting pituitary adenoma.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Cushing Syndrome / diagnosis. Pancreatic Neoplasms / complications. Pituitary Neoplasms / secretion
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. Adenoma / secretion. Adenoma / surgery. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Middle Aged. Pituitary ACTH Hypersecretion / diagnosis. Positron-Emission Tomography


30. Hofland LJ: Somatostatin and somatostatin receptors in Cushing's disease. Mol Cell Endocrinol; 2008 May 14;286(1-2):199-205
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin and somatostatin receptors in Cushing's disease.
  • Cushing's disease is caused by an ACTH secreting pituitary adenoma.
  • Somatostatin (SS) receptors (sst) are expressed on normal and tumoral corticotroph cells.
  • However, the role of somatostatin and in particular the current clinically available sst(2)-preferring SS analogs in the regulation of normal ACTH secretion, as well as in lowering ACTH and cortisol hypersecretion in patients with Cushing's disease, has been shown to be limited.
  • Recent studies have provided renewed insights into the expression of sst subtypes, as well as into the functional role of SS-analogs in the regulation of ACTH secretion by corticotroph tumors.
  • Sst(2) and sst(5) seem the predominantly expressed sst in corticotroph adenoma cells and targeting both these receptors with a new generation of multiligand SS analogs showed promising effects in terms of lowering ACTH release and urinary free cortisol (UFC) levels in patients with Cushing's disease.
  • In this review an overview of the current insights into the role of SS and sst in the regulation of normal and pathological ACTH secretion is provided.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Pituitary ACTH Hypersecretion / drug therapy. Pituitary Neoplasms / drug therapy. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / metabolism

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  • (PMID = 18221833.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Hormone Antagonists; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 69
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31. Sahli R, Christ ER, Seiler R, Kappeler A, Vajtai I: Clinicopathologic correlations of silent corticotroph adenomas of the pituitary: report of four cases and literature review. Pathol Res Pract; 2006;202(6):457-64
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  • [Title] Clinicopathologic correlations of silent corticotroph adenomas of the pituitary: report of four cases and literature review.
  • Silent corticotroph adenomas (SCA) are rare pituitary tumors with histologic hallmarks of corticotroph differentiation, including ACTH immunoreactivity, but lacking clinical evidence of Cushing's syndrome.
  • We report on four female patients, aged 19-66 years, each presenting with a nonfunctional macroadenoma.
  • Three patients had marked obesity; none of them presented constitutional signs of Cushing's syndrome.
  • MRI scans revealed intratumoral hemorrhage and/or cystic change in three cases, as well as tumor-related occlusive hydrocephalus in one.
  • Histologically, all four lesions were diagnosed as SCA subtype I displaying intense immunoreactivity for ACTH.
  • In addition, Crooke's hyaline change was noted in a significant number of tumor cells and in residual non-neoplastic corticotrophs in one case each.
  • With MIB-1 labeling indices of 1-3%, none of the tumors qualified as atypical adenoma.
  • Subtle morphologic evidence of corticotroph suppression in residual pituitary adjacent to tumor lends further support to literature data indicating minimal or intermittent functional activity in this tumor type.
  • [MeSH-major] Adenoma / pathology. Adrenocorticotropic Hormone / metabolism. Pituitary Gland, Anterior / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Female. Humans. Hydrocortisone / blood. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging. Middle Aged. Prognosis. Treatment Outcome

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  • (PMID = 16497445.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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32. Hofland LJ, van der Hoek J, Feelders R, van Aken MO, van Koetsveld PM, Waaijers M, Sprij-Mooij D, Bruns C, Weckbecker G, de Herder WW, Beckers A, Lamberts SW: The multi-ligand somatostatin analogue SOM230 inhibits ACTH secretion by cultured human corticotroph adenomas via somatostatin receptor type 5. Eur J Endocrinol; 2005 Apr;152(4):645-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The multi-ligand somatostatin analogue SOM230 inhibits ACTH secretion by cultured human corticotroph adenomas via somatostatin receptor type 5.
  • OBJECTIVE: Currently, there is no effective medical treatment for patients with pituitary-dependent Cushing's disease.
  • We compared the in vitro effects of the sst(2)-preferring SS analogue octreotide (OCT) and the multi-ligand SOM230 on ACTH release by human and mouse corticotroph tumour cells.
  • METHODS: By quantitative RT-PCR the sst subtype expression level was determined in human corticotroph adenomas.
  • In vitro, the inhibitory effect of OCT and SOM230 on ACTH release by dispersed human corticotroph adenoma cells and mouse AtT20 corticotroph adenoma cells was determined.
  • RESULTS: Corticotroph adenomas expressed predominantly sst(5) mRNA (six out of six adenomas), whereas sst(2) mRNA expression was detected at significantly lower levels.
  • In a 72 h incubation with 10 nmol/l SOM230, ACTH release was inhibited in three out of five cultures (range -30 to -40%).
  • Ten nmol/l OCT slightly inhibited ACTH release in only one of five cultures (- 28%).
  • In AtT20 cells, expressing sst(2), sst(3) and sst(5), SOM230 inhibited ACTH secretion with high potency (IC(50) 0.2 nmol/l).
  • Dexamethasone (10 nmol/l) pre-treatment did not influence the sensitivity of the cells to the inhibitory effect of SOM230, suggesting that sst(5) is relatively resistant to negative control by glucocorticoids.
  • CONCLUSIONS: The selective expression of sst(5) receptors in corticotroph adenomas and the preferential inhibition of ACTH release by human corticotroph adenoma cells by SOM230 in vitro, suggest that SOM230 may have potential in the treatment of patients with pituitary-dependent Cushing's disease.


33. 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
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  • [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

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  • (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
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34. 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
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  • [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

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  • (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
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35. Raitila A, Georgitsi M, Karhu A, Tuppurainen K, Mäkinen MJ, Birkenkamp-Demtröder K, Salmenkivi K, Orntoft TF, Arola J, Launonen V, Vahteristo P, Aaltonen LA: No evidence of somatic aryl hydrocarbon receptor interacting protein mutations in sporadic endocrine neoplasia. Endocr Relat Cancer; 2007 Sep;14(3):901-6
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  • Germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene were recently observed in patients with pituitary adenoma predisposition (PAP).
  • Though AIP mutation-positive individuals with prolactin-, mixed growth hormone/prolactin-, and ACTH-producing pituitary adenomas as well as non-secreting pituitary adenomas have been reported, most mutation-positive patients have had growth hormone-producing adenomas diagnosed at relatively young age.
  • Pituitary adenomas are also component tumors of some familial endocrine neoplasia syndromes such as multiple endocrine neoplasia type 1 (MEN1) and Carney complex (CNC).
  • Genes underlying MEN1 and CNC are rarely mutated in sporadic pituitary adenomas, but more often in other lesions contributing to these two syndromes.
  • Thus far, the occurrence of somatic AIP mutations has not been studied in endocrine tumors other than pituitary adenomas.
  • Here, we have analyzed 32 pituitary adenomas and 79 other tumors of the endocrine system for somatic AIP mutations by direct sequencing.
  • However, two out of nine patients with prolactin-producing adenoma were shown to harbor a Finnish founder mutation (Q14X) with a complete loss of the wild-type allele in the tumors.
  • These results are in agreement with previous studies in that prolactin-producing adenomas are component tumors in PAP.
  • The data also support the previous finding that somatic AIP mutations are not common in pituitary adenomas and suggest that such mutations are rare in other endocrine tumors as well.
  • [MeSH-major] Adenoma / genetics. Carcinoma / genetics. Endocrine Gland Neoplasms / genetics. Mutation. Proteins / genetics

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  • (PMID = 17914118.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Proteins; 0 / aryl hydrocarbon receptor-interacting protein
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36. Jiang ZQ, Gui SB, Zhang YZ: Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-secreting pituitary adenomas. Chin Med J (Engl); 2010 Dec;123(23):3455-61

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-secreting pituitary adenomas.
  • BACKGROUND: Adrenocorticotrophin (ACTH)-secreting pituitary adenomas account for approximately 7% - 14% of all pituitary adenomas, but its pathogenesis is still enigmatic.
  • This study aimed to explore mechanisms underlying the pathogenesis of ACTH-secreting pituitary adenomas.
  • METHODS: We used fiber-optic beadarray to examine gene expression in three ACTH-secreting adenomas compared with three normal pituitaries.
  • Four differentially expressed genes from the three ACTH-secreting adenomas and three normal pituitaries were chosen randomly for validation by reverse transcriptase-real time quantitative polymerase chain reaction (RT-qPCR).
  • Bioinformatic and pathway analysis showed that the genes HIGD1B, EPS8, HPGD, DAPK2, and IGFBP3 and the transforming growth factor (TGF)-β signaling pathway and extracellular matrix (ECM)-receptor interaction pathway may play important roles in tumorigenesis and progression of ACTH-secreting pituitary adenomas.
  • CONCLUSIONS: Our data suggest that numerous aberrantly expressed genes and several pathways are involved in the pathogenesis of ACTH-secreting pituitary adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / etiology. Adenoma / etiology. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis / methods. Signal Transduction / physiology
  • [MeSH-minor] Adult. Disease Progression. Expressed Sequence Tags. Extracellular Matrix Proteins / physiology. Female. Fiber Optic Technology. Humans. Male. Middle Aged. Real-Time Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor alpha / physiology

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  • (PMID = 22166531.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Extracellular Matrix Proteins; 0 / Transforming Growth Factor alpha
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37. 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
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  • [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.

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  • (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
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38. Tagliati F, Gentilin E, Buratto M, Molè D, degli Uberti EC, Zatelli MC: Magmas, a gene newly identified as overexpressed in human and mouse ACTH-secreting pituitary adenomas, protects pituitary cells from apoptotic stimuli. Endocrinology; 2010 Oct;151(10):4635-42
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  • [Title] Magmas, a gene newly identified as overexpressed in human and mouse ACTH-secreting pituitary adenomas, protects pituitary cells from apoptotic stimuli.
  • Pituitary tumors are mostly benign, being locally invasive in 5-35% of cases.
  • Deregulation of several genes has been suggested as a possible alteration underlying the development and progression of pituitary tumors.
  • We here report the identification of a cDNA, corresponding to Magmas gene (mitochondria-associated protein involved in granulocyte-macrophage colony-stimulating factor signal transduction), which is highly expressed in two different ACTH-secreting mouse pituitary adenoma cell lines as compared with normal pituitary as well as in two thirds of 64 examined pituitary adenomas as compared with human normal pituitary.
  • Tim 16, the mitochondrial protein encoded by Magmas, was indeed expressed in a mouse ACTH-secreting pituitary adenoma cell line, AtT-20 D16v-F2 cells, in a subcellular compartment likely corresponding to mitochondria.
  • Our data demonstrate that Magmas is overexpressed in mouse and human ACTH-secreting pituitary adenomas.
  • Moreover, our results show that Magmas protects pituitary cells from apoptosis, suggesting its possible involvement in neoplastic transformation.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Apoptosis / genetics. Mitochondrial Proteins / physiology
  • [MeSH-minor] Animals. Cell Proliferation. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Cells, Cultured. Cytoprotection / drug effects. Cytoprotection / genetics. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Pituitary Gland / metabolism. RNA, Small Interfering / pharmacology. Up-Regulation / drug effects

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  • (PMID = 20719856.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mitochondrial Proteins; 0 / RNA, Small Interfering; 0 / magmas protein, human
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39. 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
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  • [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

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  • (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
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40. Mittelbronn M, Psaras T, Capper D, Meyermann R, Honegger J: ACTH- and prolactin-producing pituitary gland microadenoma with biphasic features of atypia and intermediate filament expression. Neuro Endocrinol Lett; 2006 Feb-Apr;27(1-2):89-92
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  • [Title] ACTH- and prolactin-producing pituitary gland microadenoma with biphasic features of atypia and intermediate filament expression.
  • Endocrinological examinations led to the diagnosis of Cushing's disease.
  • Neuroradiological examination revealed an intrasellar tumor mass of 7 mm in diameter.
  • Subsequently, transsphenoidal tumor resection was performed.
  • Histological and immunohistochemical investigations revealed a pituitary gland adenoma showing a biphasic tumor growth pattern with two morphologically different tumor areas producing ACTH and prolactin respectively.
  • Co-expression of ACTH and prolactin is exceedingly rare in pituitary adenoma.
  • To our surprise, both tumor areas exhibited features of atypia consisting in elevated MIB-1 proliferation index in the ACTH-producing portion as well as p53 expression selectively in the prolactin-producing tumor parts.
  • To our knowledge, this is the first case of an ACTH- and prolactin-producing pituitary gland adenoma exhibiting biphasic features of atypia.
  • [MeSH-major] Adenoma / metabolism. Adrenocorticotropic Hormone / biosynthesis. Intermediate Filament Proteins / biosynthesis. Pituitary Neoplasms / metabolism. Prolactin / biosynthesis
  • [MeSH-minor] Adult. Cell Proliferation. Female. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Pituitary Hormones / chemistry. Pituitary Hormones / metabolism. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 16648816.001).
  • [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 / Intermediate Filament Proteins; 0 / Ki-67 Antigen; 0 / Pituitary Hormones; 0 / Tumor Suppressor Protein p53; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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41. Kreutzer J, Jeske I, Hofmann B, Blumcke I, Fahlbusch R, Buchfelder M, Buslei R: No effect of the PPAR-gamma agonist rosiglitazone on ACTH or cortisol secretion in Nelson's syndrome and Cushing's disease in vitro and in vivo. Clin Neuropathol; 2009 Nov-Dec;28(6):430-9
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  • [Title] No effect of the PPAR-gamma agonist rosiglitazone on ACTH or cortisol secretion in Nelson's syndrome and Cushing's disease in vitro and in vivo.
  • OBJECTIVE: Surgical tumor resection remains the primary treatment strategy in ACTH-secreting pituitary adenomas, i.e.
  • Cushing's disease (CD) and Nelson's syndrome (NS).
  • However, an effective long-term pharmacological regime is not available in patients with persistent ACTH-hypersecretion.
  • The nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-gamma) is abundantly expressed in most pituitary adenomas.
  • First encouraging data reported that the PPAR-gamma ligand rosiglitazone antagonizes ACTH hypersecretion and exerts also antiproliferative effects in pituitary cell lines.
  • Herein, we studied the potential therapeutical effects of rosiglitazone in patients with ACTH-secreting pituitary adenomas in vitro and in vivo.
  • MATERIALS AND METHODS: Seven patients with persistent ACTH-hypersecretion (3 with NS, 4 with persistent CD) were treated 5 months with rosiglitazone (4 - 16 mg/day).
  • In vitro assays were performed in primary cell cultures obtained from eight additional patients with ACTH-secreting pituitary adenomas applying 80 microM rosiglitazone repeatedly over a time period of 14 days.
  • RESULTS: Our long-term clinical trial with the PPAR-gamma activator rosiglitazone showed no amelioration of clinical symptoms nor an inhibiting effect on ACTH-secretion in vivo.
  • In vitro, rosiglitazone treatment led to a statistically significant decrease of ACTH levels in 2 out of 8 primary cell cultures after 14 days compared to untreated controls.
  • CONCLUSION: In contrast to the initially promising laboratory data gathered in pituitary cell line experiments and nude mice models, our experimental data obtained in primary human ACTH-expressing pituitary adenoma cell cultures as well as our clinical experience with a long-term rosiglitazone trial in approved antidiabetic doses support the recently reported disappointing reports on acute or short-term medical treatment of ACTH-hypersecretion with PPAR-gamma activators.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Hydrocortisone / secretion. Nelson Syndrome / blood. PPAR gamma / agonists. Pituitary ACTH Hypersecretion / blood. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adenoma / pathology. Adenoma / secretion. Adult. Female. Humans. In Vitro Techniques. Magnetic Resonance Imaging. Male. Middle Aged. Pituitary Neoplasms / pathology. Pituitary Neoplasms / secretion. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 19919817.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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42. Siddiqui AA, Bashir SH: Giant pituitary macroadenoma at the age of 4 months: case report and review of the literature. Childs Nerv Syst; 2006 Mar;22(3):290-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Giant pituitary macroadenoma at the age of 4 months: case report and review of the literature.
  • CASE REPORT: Adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma is extremely rare.
  • We report the youngest patient of Cushing's disease due to ACTH-secreting pituitary macroadenoma at the age of 4 months.
  • Serum cortisol level was 97 microg/dl, with increased secretion of urinary free cortisol; plasma ACTH level was 353 pg/ml.
  • Magnetic resonance imaging of the brain showed a large contrast-enhancing solid mass sitting in the sellar region, with suprasellar and lateral extension.
  • Surgical resection was done, and immunohistochemistry confirmed the diagnosis of ACTH-secreting pituitary adenoma.
  • CONCLUSION: Cushing's disease due to ACTH-secreting pituitary macroadenoma is a possible diagnosis in early infancy.
  • This surgical morbidity is possibly attributed to difficult peroperative hemostasis due to vasculopathy in Cushing's disease, which leads to excessive blood loss, adverse hemodynamic changes, myocardial dysfunction and disseminated intravascular coagulopathy.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Cushing Syndrome / surgery. Disseminated Intravascular Coagulation / etiology. Postoperative Complications / etiology

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  • (PMID = 16047217.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 15
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43. Stilling G, Sun Z, Zhang S, Jin L, Righi A, Kovācs G, Korbonits M, Scheithauer BW, Kovacs K, Lloyd RV: MicroRNA expression in ACTH-producing pituitary tumors: up-regulation of microRNA-122 and -493 in pituitary carcinomas. Endocrine; 2010 Aug;38(1):67-75
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  • [Title] MicroRNA expression in ACTH-producing pituitary tumors: up-regulation of microRNA-122 and -493 in pituitary carcinomas.
  • MicroRNAs (miRNAs) are involved in cell proliferation, differentiation, and apoptosis, and can function as tumor suppressor genes or oncogenes.
  • The expression of miRNAs in pituitary carcinomas has not been previously examined.
  • We used miRNA profiling with 1,145 probes to study miRNA expression in normal anterior pituitary (6 cases), adrenocorticotropin (ACTH)-producing adenomas (8 cases), and ACTH-producing pituitary carcinomas (two cases).
  • Real-time RT-PCR and in situ hybridization were used to confirm and independently validate miRNAs that were significantly up-regulated or down-regulated between the pituitary tissues.
  • There were more miRNAs up- (188) or down-regulated (160) between adenomas and normal pituitaries compared to carcinomas and normal pituitaries (92 up- and 91 down-regulated) or between carcinomas and adenomas (46 up- and 52 down-regulated).
  • Both real-time RT-PCR and in situ hybridization showed significant up-regulation of miRNA-122 between pituitary carcinomas and adenomas.
  • MiRNA-493 was also up-regulated in carcinomas compared to ACTH adenomas.
  • Analysis of genes that miRNA-493 interacts with included LGALS3 and RUNX2 ( http://microrna.sanger.ac.uk ) both of which have been shown to have roles in pituitary tumor cell growth.
  • These results provide information about marker miRNAs that may lead to further insights into the regulation of pituitary tumor growth and development.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. MicroRNAs / genetics
  • [MeSH-minor] Adult. Aged. Female. Humans. In Situ Hybridization. Oligonucleotide Array Sequence Analysis. Pituitary Gland, Anterior / pathology. Pituitary Gland, Anterior / physiology. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation / genetics

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  • (PMID = 20960104.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MIRN122 microRNA, human; 0 / MIRN493 microRNA, human; 0 / MicroRNAs
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44. Bucciarelli LG, Pecori Giraldi F, Cavagnini F: No mutations in TPIT, a corticotroph-specific gene, in human tumoral pituitary ACTH-secreting cells. J Endocrinol Invest; 2005 Dec;28(11):1015-8
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] No mutations in TPIT, a corticotroph-specific gene, in human tumoral pituitary ACTH-secreting cells.
  • BACKGROUND: TPIT is a recently identified transcription factor specific to proopiomelanocortin (POMC)-expressing cells within the pituitary and plays a pivotal role in the embryonal development of POMC lineage.
  • As with other transcription factors, TPIT could theoretically also be involved in corticotroph adenomatous transformation and ACTH hypersecretion and published data indicate that TPIT is present in normal and adenomatous human corticotrophs.
  • OBJECTIVE: The aim of the present study was to corroborate this finding and to seek evidence for mutations in the TPIT coding sequence in human tumoral corticotrophs.
  • DESIGN AND METHODS: Eight human ACTH-secreting pituitary adenomas were collected during surgery, mRNA extracted from primary cultures and reverse transcribed.
  • RESULTS: TPIT mRNA was detected in all 8 ACTH-secreting pituitary adenomas without apparent mRNA variants.
  • Lastly, sequencing did not reveal differences in the nucleotide arrangement compared with the published sequence.
  • CONCLUSIONS: Aberrant TPIT is unlikely to play a role in corticotroph tumoral trasformation, ie, Cushing's disease, as the entire coding sequence is expressed without any mutation by human pituitary ACTH-secreting adenomas.
  • Conversely, the significance of this transcription factor in tumoral ACTH hypersecretion remains to be clarified.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Homeodomain Proteins / genetics. Mutation / genetics. Pituitary Neoplasms / genetics. Transcription Factors / genetics
  • [MeSH-minor] Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. T-Box Domain Proteins. Tumor Cells, Cultured

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  • (PMID = 16483181.001).
  • [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] 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / Transcription Factors; 9002-60-2 / Adrenocorticotropic Hormone
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45. Giacomini D, Páez-Pereda M, Theodoropoulou M, Labeur M, Refojo D, Gerez J, Chervin A, Berner S, Losa M, Buchfelder M, Renner U, Stalla GK, Arzt E: Bone morphogenetic protein-4 inhibits corticotroph tumor cells: involvement in the retinoic acid inhibitory action. Endocrinology; 2006 Jan;147(1):247-56
The Lens. Cited by Patents in .

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  • [Title] Bone morphogenetic protein-4 inhibits corticotroph tumor cells: involvement in the retinoic acid inhibitory action.
  • The molecular mechanisms governing the pathogenesis of ACTH-secreting pituitary adenomas are still obscure.
  • In this study, we report that bone morphogenetic protein-4 (BMP-4) is expressed in the corticotrophs of human normal adenohypophysis and its expression is reduced in corticotrophinomas obtained from Cushing's patients compared with the normal pituitary.
  • BMP-4 treatment of AtT-20 mouse corticotrophinoma cells has an inhibitory effect on ACTH secretion and cell proliferation.
  • AtT-20 cells stably transfected with a dominant-negative form of the BMP-4 signal cotransducer Smad-4 or the BMP-4 inhibitor noggin have increased tumorigenicity in nude mice, showing that BMP-4 has an inhibitory role on corticotroph tumorigenesis in vivo.
  • Because the activation of the retinoic acid receptor has an inhibitory action on Cushing's disease progression, we analyzed the putative interaction of these two pathways.
  • Indeed, retinoic acid induces both BMP-4 transcription and expression and its antiproliferative action is blocked in Smad-4dn- and noggin-transfected Att-20 cells that do not respond to BMP-4.
  • This new mechanism is a potential target for therapeutic approaches for Cushing's disease.
  • [MeSH-major] Adenoma / pathology. Bone Morphogenetic Proteins / pharmacology. Bone Morphogenetic Proteins / physiology. Cushing Syndrome / pathology. Pituitary Neoplasms / pathology. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Bone Morphogenetic Protein 4. Cell Division / drug effects. Cell Line, Tumor. Humans. Immunohistochemistry. Mice. Pituitary Gland / pathology. Pituitary Gland / physiology. Reference Values


46. Brzezińska B, Junik R, Kamińska A, Zieliński G: [Difficulties in the diagnosis of ACTH-dependent Cushing's syndrome in a patient after left adrenalectomy and treated with glucocorticoids]. Endokrynol Pol; 2009 Nov-Dec;60(6):484-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Difficulties in the diagnosis of ACTH-dependent Cushing's syndrome in a patient after left adrenalectomy and treated with glucocorticoids].
  • [Transliterated title] Trudności w diagnostyce ACTH-zaleznego zespołu Cushinga u chorej po lewostronnej adrenalektomii i leczonej glikokortykosteroidami.
  • Cushing's syndrome (CS), that is a consequence of chronic excess of corticosteroides, is most frequently of iatrogenic origin.
  • Corticotropin secreting pituitary adenomas are responsible for most cases of endogenous Cushing' s syndrome.
  • Difficulties in the diagnosis and treatment of ACTH-dependent Cushing's syndrome concern with localization of the source of pathological ACTH secretion, particularly when magnetic resonance imaging is unable to identify the pituitary microadenoma.
  • In this paper we present the case of a patient with symptoms of Cushing's syndrome and describe problems with localization of the source of hypercortisolemia.
  • This delayed the right diagnosis and treatment.
  • [MeSH-major] Adrenocorticotropic Hormone / metabolism. Cushing Syndrome / diagnosis. Cushing Syndrome / etiology
  • [MeSH-minor] Adrenalectomy. Adult. Delayed Diagnosis. Female. Glucocorticoids / adverse effects. Glucocorticoids / therapeutic use. Humans. Lumbar Vertebrae / injuries. Lumbar Vertebrae / surgery. Methylprednisolone / adverse effects. Methylprednisolone / therapeutic use. Prednisone / adverse effects. Prednisone / therapeutic use. Spinal Fractures / complications. Spinal Fractures / surgery. Thoracic Vertebrae / injuries. Thoracic Vertebrae / surgery

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  • (PMID = 20041367.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Glucocorticoids; 9002-60-2 / Adrenocorticotropic Hormone; VB0R961HZT / Prednisone; X4W7ZR7023 / Methylprednisolone
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47. Bademci G: Pitfalls in the management of Cushing's disease. J Clin Neurosci; 2007 May;14(5):401-8; discussion 409

  • [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

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  • (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
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48. van Aken MO, Feelders RA, van der Lely AJ, Romijn JA, Lamberts SW, de Herder WW: [Cushing's syndrome. II. New forms of treatment]. Ned Tijdschr Geneeskd; 2006 Oct 28;150(43):2365-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cushing's syndrome. II. New forms of treatment].
  • Several new therapeutic options both medicinal and surgical, have emerged for the treatment of Cushing's syndrome.
  • In Cushing's disease caused by an adrenocorticotropin (ACTH) secreting pituitary adenoma, the introduction ofendoscopic pituitary surgery offers better visualization of the sella than does the traditional explorative surgery.
  • These agents may also be effective for the medicinal treatment of ectopic ACTH-secretion.
  • The primary treatment for ACTH-independent Cushing's syndrome is laparoscopic adrenalectomy.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / therapy. Adenoma / therapy. Cushing Syndrome / therapy
  • [MeSH-minor] Adrenalectomy. Adrenergic Antagonists / therapeutic use. Humans. Pituitary Gland / surgery. Treatment Outcome

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  • [CommentIn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2345-9 [17100122.001]
  • [CommentIn] Ned Tijdschr Geneeskd. 2007 Feb 3;151(5):330; author reply 331 [17326480.001]
  • (PMID = 17100127.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenergic Antagonists
  • [Number-of-references] 24
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49. Sahin SB, Cetinkalp S, Erdogan M, Cavdar U, Duygulu G, Saygili F, Yilmaz C, Ozgen AG: Pituitary apoplexy in an adrenocorticotropin-producing pituitary macroadenoma. Endocrine; 2010 Oct;38(2):143-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary apoplexy in an adrenocorticotropin-producing pituitary macroadenoma.
  • Adrenocorticotropin (ACTH) producing macroadenomas and pituitary apoplexy are unusual in Cushing' s disease.
  • A 20-year-old man who had been diagnosed Cushing' s disease 2 months ago, presented with sudden headache, nausea, and vomiting.
  • His serum cortisol level was 0.4 μg/dl and ACTH level was 23.9 pg/ml.
  • Magnetic resonance imaging of the pituitary gland disclosed a hemorrhage in the pituitary macroadenoma (22×19 mm).
  • Impaired secretion of pituitary hormones may be seen after the pituitary apoplexy.
  • We communicate a case with pituitary apoplexy of an ACTH secreting pituitary macroadenoma, causing acute glucocorticoid insufficiency.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Pituitary Apoplexy / etiology
  • [MeSH-minor] Acute Disease. Humans. Magnetic Resonance Imaging. Male. Pituitary ACTH Hypersecretion / etiology. Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / surgery. Young Adult

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  • (PMID = 21046475.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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50. 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
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  • [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

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  • (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; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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51. Bezerra MG, Latronico AC, Fragoso MC: [Endocrine tumors associated to protein Gsalpha/Gi2alpha mutations]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):784-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Many oncogenic mutations promote tumor growth by inducing autonomous activity of proteins that normally transmit proliferative signal initiated by extracellular factors.
  • The G proteins couple an array of seven transmembrane receptors at the cell surface with a variety of intracellular effectors, which produce second messenger molecules.
  • A subset of endocrine tumors, such as GH- or ACTH-secreting pituitary adenomas, functioning thyroid adenomas, adrenocortical and gonadal tumors were associated with somatic activating mutations in the highly conserved codons of the Gs (Arg201 and Gln227) and Gi (Arg179 and Gln205) proteins.
  • [MeSH-major] Endocrine Gland Neoplasms / genetics. GTP-Binding Protein alpha Subunits, Gi-Go / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Mutation / genetics. Oncogenes / genetics

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  • (PMID = 16444361.001).
  • [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
  • [Chemical-registry-number] EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 64
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52. Kidambi S, Raff H, Findling JW: Limitations of nocturnal salivary cortisol and urine free cortisol in the diagnosis of mild Cushing's syndrome. Eur J Endocrinol; 2007 Dec;157(6):725-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Limitations of nocturnal salivary cortisol and urine free cortisol in the diagnosis of mild Cushing's syndrome.
  • OBJECTIVE: Cushing's syndrome (CS) is difficult to diagnose due to its nonspecific presentation.
  • However, its performance in mild CS has not been reported.
  • We present 11 cases of CS with normal or mildly elevated UFC in whom NSC was helpful in making a diagnosis.
  • Imaging studies included magnetic resonance imaging (MRI) of pituitary or computer tomography scan of abdomen.
  • Out of eleven patients, six had an abnormality in the pituitary gland found by MRI and two out of eleven had adrenal masses.
  • The remaining three had normal pituitary MRI but had inferior petrosal sinus (IPS) sampling indicating Cushing's disease.
  • All patients had appropriate surgery, and histopathology of all except one was suggestive of either a cortisol-producing adrenal adenoma or an ACTH-secreting pituitary adenoma.
  • Multiple samples (urine/saliva) and DST are needed to make the diagnosis of mild CS.

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  • (PMID = 18057379.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 7S5I7G3JQL / Dexamethasone; WI4X0X7BPJ / Hydrocortisone
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53. Jin L, Riss D, Ruebel K, Kajita S, Scheithauer BW, Horvath E, Kovacs K, Lloyd RV: Galectin-3 Expression in Functioning and Silent ACTH-Producing Adenomas. Endocr Pathol; 2005;16(2):107-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Galectin-3 Expression in Functioning and Silent ACTH-Producing Adenomas.
  • Galectin-3 (Gal-3), a beta galactoside-binding protein, has been implicated in a variety of biological functions including cell growth, differentiation, tumor cell adhesion, angiogenesis, tumor progression, and metastasis.
  • We recently reported that Gal-3 was expressed in a subset of normal pituitary cells and tumors including PRL, ACTH, and in folliculo-stellate (FS) cells and tumors and that Gal-3 had an important regulatory role in pituitary cell proliferation.
  • We further investigated the expression of Gal-3 protein in ACTH- and PRL-producing tumors and the expression of various galectin mRNAs by RT-PCR in pituitary adenomas and normal pituitary.
  • Most silent ACTH subtypes 1 and 2 adenomas were negative or only focally positive for Gal-3 expression compared to functioning ACTH tumors from patients with Cushing's disease and Nelson's syndrome.
  • In the normal pituitary, Gal-3 was expressed in less than 1% of the basophil-invading cells (ACTH cells present in the posterior pituitary) and in a subset of the anterior lobe ACTH-positive cells.
  • RT-PCR analyses showed that many members of the galectin family including galectins 1, 2, 3, 4, 5, 6, 7, 8, and 9 were expressed in normal pituitary and in functioning ACTH- and PRL-producing tumors.
  • These results indicate that Gal-3 is associated with functioning ACTH and PRL tumors and is expressed infrequently in silent ACTH adenomas, suggesting that Gal-3 protein and/or gene is altered in non-functioning ACTH tumors.
  • The use of ACTH and Gal-3 immunostaining should help in the diagnosis of silent ACTH adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Adrenocorticotropic Hormone / secretion. Galectin 3 / biosynthesis. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism

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  • (PMID = 16199895.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA90249
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Galectin 3; 0 / RNA, Messenger; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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54. Min HS, Lee SJ, Kim SK, Park SH: Pituitary adenoma with rich folliculo-stellate cells and mucin-producing epithelia arising in a 2-year-old girl. Pathol Int; 2007 Sep;57(9):600-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary adenoma with rich folliculo-stellate cells and mucin-producing epithelia arising in a 2-year-old girl.
  • Pituitary adenoma is a rare neoplasm in childhood, with prolactin and adrenocorticotropic hormone (ACTH)-secreting adenomas predominating in this age group.
  • Herein is reported a case of an ACTH-producing macroadenoma with an unusual histology that occurred in a 2-year-old girl.
  • Because of the patient's age and the macroadenoma's suprasellar location and large size (up to 4 cm in diameter), radical surgery was performed under the suspicion of craniopharyngioma or germ-cell tumor.
  • Pathologically, it was a unique pituitary adenoma composed of monotonous ACTH-producing cells, smaller folliculo-stellate cells (FSC), and mucin-producing cells.
  • The FSC, non-hormone-secreting pituitary cells of uncertain function, were confirmed by their S-100 protein, glial fibrillary acidic protein and cytokeratin expression immunoprofiles.
  • The abrupt transition between the prominent gland-forming mucin-producing epithelia and the FSC component suggested that the mucin-producing epithelia might be derived from the FSC.
  • This association might represent so-called 'retrodifferentiation' of adenoma cells to the FSC and the precursor cells of Rathke's pouch.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Mucins / secretion. Pituitary Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Child, Preschool. Cytoplasm / ultrastructure. Disease Progression. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Keratins / metabolism. Magnetic Resonance Imaging. S100 Proteins / metabolism. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17685932.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / Mucins; 0 / S100 Proteins; 68238-35-7 / Keratins
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55. Szappanos A, Patócs A, Tõke J, Boyle B, Sereg M, Majnik J, Borgulya G, Varga I, Likó I, Rácz K, Tóth M: BclI polymorphism of the glucocorticoid receptor gene is associated with decreased bone mineral density in patients with endogenous hypercortisolism. Clin Endocrinol (Oxf); 2009 Nov;71(5):636-43
MedlinePlus Health Information. consumer health - Cushing's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The hypothalamic-pituitary-adrenal axis setpoint and the glucocorticoid sensitivity of various tissues are at least partially genetically determined.
  • DESIGN: Sixty patients including 35 patients with ACTH producing pituitary adenoma (CD) and 25 patients with adrenal Cushing's syndrome (ACS) as well as 129 healthy subjects were genotyped.
  • CONCLUSIONS: The BclI, N363S, ER22/23EK and A3669G polymorphisms of the GR gene probably do not modify the risk for the development of CD or ACS.
  • [MeSH-minor] Adenoma / genetics. Adult. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Pituitary Neoplasms / genetics. Young Adult

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  • (PMID = 19207316.001).
  • [ISSN] 1365-2265
  • [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 / Receptors, Glucocorticoid
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56. Hernández I, Espinosa-de-los-Monteros AL, Mendoza V, Cheng S, Molina M, Sosa E, Mercado M: Ectopic ACTH-secreting syndrome: a single center experience report with a high prevalence of occult tumor. Arch Med Res; 2006 Nov;37(8):976-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic ACTH-secreting syndrome: a single center experience report with a high prevalence of occult tumor.
  • BACKGROUND: Differentiation between the two forms of ACTH-dependent Cushing's syndrome is a challenging task.
  • Although the majority of these cases will be diagnosed as Cushing's disease secondary to an ACTH-secreting pituitary adenoma, 10-15% result from the ectopic ACTH secretion syndrome (EAS), which is usually due to neuroendocrine tumors.
  • The latter included a standard biochemical assessment (urinary free cortisol, low- and high-dose dexamethasone suppression tests), petrosal sinus sampling when indicated and imaging techniques such as pituitary MRI, total body CT and somatostatin receptor scintigraphy.
  • RESULTS: The ectopic nature of the ACTH hypersecretion was confirmed with inferior petrosal sinus samplings in all cases.
  • CT scanning localized a putative tumor in 6/8 patients, whereas octreotide scintigraphy was positive in only five.
  • However, upon performing thoracotomy, a documented ACTH-secreting bronchial carcinoid tumor was found in only four patients.
  • CONCLUSIONS: EAS is a rare cause of ACTH-dependent Cushing's syndrome.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Adenoma / therapy
  • [MeSH-minor] Adrenalectomy. Cushing Syndrome / diagnosis. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17045113.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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57. 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
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  • [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

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  • (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
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58. Tóth M, Vajda Z, Görömbey Z, Molnár F, Major L, Toke J, Szabolcs I, Szücs N, Kovács L, Kiss R, Czirják S, Füto L, Gláz E, Góth M, Rácz K: [Evaluation of the accuracy of inferior petrosal sinus sampling in the differential diagnosis of ACTH-dependent Cushing's syndrome]. Orv Hetil; 2007 May 6;148(18):843-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Evaluation of the accuracy of inferior petrosal sinus sampling in the differential diagnosis of ACTH-dependent Cushing's syndrome].
  • The differentiation of adrenocorticotropic hormone producing pituitary adenoma (Cushing's disease) from the ectopic ACTH syndrome is always a complex and difficult task, and in rare cases it is not possible to differentiate between the two disorders, even with the use of dynamic endocrine tests and the most advanced imaging techniques.
  • Inferior petrosal sinus sampling (IPSS) with subsequent ACTH measurements became the gold-standard method of the differential diagnostic process.
  • 34 patients with ACTH dependent Cushing's syndrome in whom the source of ACTH secretion couldn't be identified unambiguously with imaging techniques and/or dynamic endocrine tests underwent altogether 41 IPSS between 1999 and 2005.
  • The sensitivity of the method was calculated on the basis of 31 samplings of 25 patients who had definite endocrinological diagnosis confirmed by the recovery from Cushing's syndrome after surgical intervention and/or by histological examinations (22 patients with ACTH-producing pituitary adenoma and 3 patients with ectopic ACTH syndrome).
  • As a result of IPSS, pituitary-dependent Cushing's disease was diagnosed with a baseline central to peripheral ACTH ratio of >2.0 or with a ratio of >3.0 after corticotropin releasing hormone (CRH) administration.
  • IPSS correctly identified ACTH-producing pituitary adenoma in 20 of 28 sampling procedures, with a sensitivity of 71.4%.
  • In patients with Cushing's disease having true positive interventions, the basal and 5 minutes post-CRH ACTH concentrations were diagnostic in 14 and 19 cases, respectively.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. Adenoma / diagnosis. Adrenocorticotropic Hormone / blood. Cushing Syndrome / blood. Cushing Syndrome / diagnosis. Petrosal Sinus Sampling. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. False Negative Reactions. Female. Humans. Hungary. Male. Middle Aged. Predictive Value of Tests. Sensitivity and Specificity

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  • (PMID = 17468067.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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59. Sahdev A, Reznek RH, Evanson J, Grossman AB: Imaging in Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1319-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imaging in Cushing's syndrome.
  • Once the diagnosis of Cushing's syndrome (CS) has been established, the main step is to differentiate between ACTH dependent and independent disease.
  • In adults, 80% of CS is due to ACTH-dependent causes and 20% due to adrenal causes.
  • ACTH-secreting neoplasms cause ACTH-dependent CS.
  • These are usually anterior pituitary microadenomas, which result in the classic Cushing's disease.
  • Non-pituitary ectopic sources of ACTH, such as a small-cell lung carcinoma or carcinoid tumours, are the source of the remainder of ACTH-dependent disease.
  • Imaging is essential for determining the source of ACTH in ectopic ACTH production, locating the pituitary tumours and distinguishing adrenal adenomas, carcinomas and hyperplasias.
  • In our chapter we review the adrenal appearances in ACTH-dependent and ACTH-independent CS.
  • We also include a discussion on the use of MRI and CT for the detection and management of pituitary ACTH secreting adenomas.
  • CT of the chest, abdomen and pelvis with intravenous injection of contrast medium is the most sensitive imaging modality for the identification of the ectopic ACTH source and detecting adrenal pathology.
  • MRI is used for characterising adrenal adenomas, problem solving in difficult cases and for detecting ACTH-secreting pituitary adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Cushing Syndrome / diagnosis. Pituitary Gland / pathology. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. Adenoma / diagnosis. Adenoma / radiography. Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / radiography. Carcinoma / diagnosis. Carcinoma / radiography. Humans. Hyperplasia / diagnosis. Hyperplasia / radiography. Lung Neoplasms / diagnosis. Lung Neoplasms / secretion. Magnetic Resonance Imaging. Tomography, X-Ray Computed

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  • (PMID = 18209870.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 36
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60. Cavagnini F, Scacchi M, Pecori Giraldi F: Hypopituitarism in Cushing's disease. J Endocrinol Invest; 2008 Sep;31(9 Suppl):44-7
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  • [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

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  • (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
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61. Utz A, Biller BM: The role of bilateral inferior petrosal sinus sampling in the diagnosis of Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1329-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of bilateral inferior petrosal sinus sampling in the diagnosis of Cushing's syndrome.
  • Adrenocorticotropin hormone (ACTH)-dependent Cushing's syndrome is most often due to a pituitary corticotroph adenoma, with ectopic ACTH-secreting tumors representing approximately 15% of cases.
  • BIPSS is an interventional radiology procedure in which ACTH levels obtained from venous drainage very near the pituitary gland are compared to peripheral blood levels before and after corticotropin hormone (CRH) stimulation.
  • A gradient between these two locations indicates pituitary Cushing's, whereas the absence of a gradient suggests ectopic Cushing's.
  • Accurate BIPSS results require hypercortisolemia to suppress normal corticotroph ACTH production and hypercortisolemia at the time of the BIPSS to assure excessive ACTH secretion.
  • In some cases, intrapituitary gradients from side-to-side can be helpful to localize small corticotroph adenomas within the sella.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. Cushing Syndrome / diagnosis. Petrosal Sinus Sampling
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / blood. ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / blood. Adenoma / diagnosis. Adenoma / secretion. Adrenocorticotropic Hormone / blood. Corticotropin-Releasing Hormone. Diagnosis, Differential. Humans. Pituitary Neoplasms / blood. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secretion. Sensitivity and Specificity

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  • (PMID = 18209871.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
  • [Number-of-references] 37
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62. Scheithauer BW, Kovacs K, Horvath E, Young WF Jr, Lloyd RV: The pituitary in Turner syndrome. Endocr Pathol; 2005;16(3):195-200
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pituitary in Turner syndrome.
  • Although Turner syndrome is not uncommon, studies of the pituitary in this condition are few.
  • No gonadotroph adenomas were encountered.
  • Instead, three silent corticotroph microadenomas were seen; their etiology remains unexplained.
  • The question of whether the simultaneous occurrence of Turner syndrome and silent corticotroph adenoma is causal or incidental cannot be answered on the basis of the study of our material.
  • For example, it is possible that (a) protracted stimulation of gonadotrophs leads to transdifferentiation to corticotrophs, a hypothesis supported by the fact that normal and neoplastic gonadotrophs can contain ACTH and that some corticotroph adenomas produce LH and/or alpha subunit, (b) corticotrophs develop gonadotropin-releasing hormone (GnRH) receptors and undergo neoplastic transformation when exposed to continuous elevation of GnRH, FSH, and/or LH levels, and (c) the genetic defect in Turner syndrome promotes the formation of corticotroph adenomas.
  • [MeSH-major] Adenoma / complications. Pituitary Neoplasms / complications. Turner Syndrome / complications
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Female. Humans. Immunoenzyme Techniques

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  • (PMID = 16299402.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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63. Alexandraki KI, Grossman AB: Medical therapy of Cushing's disease: where are we now? Front Horm Res; 2010;38:165-73
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  • [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

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  • [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
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64. Dam-Hieu P, Irthum B, Seizeur R, Roudaut N, Besson G: Management of ACTH-secreting supradiaphragmatic adenomas. Clin Neurol Neurosurg; 2007 Oct;109(8):698-704
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of ACTH-secreting supradiaphragmatic adenomas.
  • Supradiaphragmatic adrenocorticotropic hormone (ACTH) secreting pituitary adenomas are exceptionally encountered (14 cases previously described) and raise issues concerning their nosology and management.
  • To illustrate this issue, we presented two cases of supradiaphragmatic ACTH secreting pituitary adenomas successfully excised via a subfrontal approach.
  • Both patients were female (20 and 41 years) and had a typical Cushing's syndrome.
  • MRI revealed, in both cases, a suprasellar mass in contact with the pars tuberalis of the pituitary.
  • One year later, the patient was operated on again via a subfrontal approach, allowing excision of a supradiaphragmatic adenoma and a complete cure of Cushing's disease.
  • In both cases, the diaphragma sellae was found to be intact and the pituitary stalk could be preserved.
  • Postoperative MRI demonstrated a clearly visible intact pituitary stalk in conjunction with normal aspect of the pituitary.
  • Supradiaphragmatic pituitary adenomas are most likely adenomas of the pituitary stalk with extra-axial development.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / pathology. Adenoma / surgery

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  • (PMID = 17532556.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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65. Suzuki S, Uchida D, Koide H, Suyama K, Shibata T, Yoshida T, Tanaka T, Noguchi Y, Saito Y, Tatsuno I: A possible association between aldosterone response to vasopressin and circadian change of aldosterone in the patients with aldosterone-producing adenoma. Peptides; 2008 Dec;29(12):2225-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A possible association between aldosterone response to vasopressin and circadian change of aldosterone in the patients with aldosterone-producing adenoma.
  • Vasopressin was reported to stimulate secretion of both cortisol and aldosterone through eutopic V1a receptors in adrenal gland.
  • Recently, adrenal hyper-responsiveness of plasma cortisol to vasopressin with eutopic overexpession of V1a receptors has been reported in Cushing's syndrome, such as a majority of cases of ACTH-independent macronodular adrenal hyperplasia and some cases of Cushing's adenomas.
  • There were a few reports regarding the aldosterone response to vasopressin in aldosterone-producing adenoma.
  • The aim of our study was to investigate the aldosterone response to vasopressin and its pathophysiological roles in the patients with aldosterone-producing adenoma.
  • Vasopressin-loading test was performed in 10 patients with aldosterone-producing adenoma, and in 16 patients with non-functioning adrenal tumors.
  • The roles of the aldosterone response to vasopressin were analyzed in terms of hormonal secretion and the expression of V1a receptor mRNA on the operated adrenal gland in aldosterone-producing adenoma.
  • We found that (1) a varying aldosterone response to vasopressin was observed, (2) absolute response of plasma aldosterone in aldosterone-producing adenoma was significantly higher than that in non-functioning tumor, (3) aldosterone response rate to vasopressin was significantly and negatively correlated with the decline rate (%) in plasma aldosterone from morning to evening in aldosterone-producing adenoma, (4) V1a receptor mRNA was expressed at various values in aldosterone-producing adenoma, and (5) surgical removal of aldosterone-producing adenoma eliminated the aldosterone response to vasopressin observed in patients with aldosterone-producing adenoma.
  • These findings indicated that vasopressin might be involved in the coordination of aldosterone secretion through eutopic expression of V1a receptor in aldosterone-producing adenoma.
  • [MeSH-major] Adenoma / metabolism. Aldosterone / blood. Circadian Rhythm. Pituitary Neoplasms / metabolism. Vasopressins / pharmacology

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  • (PMID = 18838094.001).
  • [ISSN] 0196-9781
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Vasopressin; 11000-17-2 / Vasopressins; 4964P6T9RB / Aldosterone
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66. Wagenmakers MA, Netea-Maier RT, van Lindert EJ, Timmers HJ, Grotenhuis JA, Hermus AR: Repeated transsphenoidal pituitary surgery (TS) via the endoscopic technique: a good therapeutic option for recurrent or persistent Cushing's disease (CD). Clin Endocrinol (Oxf); 2009 Feb;70(2):274-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Repeated transsphenoidal pituitary surgery (TS) via the endoscopic technique: a good therapeutic option for recurrent or persistent Cushing's disease (CD).
  • BACKGROUND: No data on results of repeated transsphenoidal surgery via the endoscopic technique for patients with persistent or recurrent Cushing's disease are available.
  • DESIGN AND PATIENTS: We retrospectively evaluated the remission rates and complications of repeated transsphenoidal surgery via the endoscopic technique in 14 patients with persistent (N = 6) or recurrent (N = 8) Cushing's disease treated in our centre between 1999 and 2007.
  • The success of repeated transsphenoidal surgery could not be predicted by visualization of an adenoma on MRI before first or second surgery, histopathological confirmation of an ACTH secreting adenoma after first or second surgery, treatment with cortisol lowering agents before first or second surgery, the operation technique used during the first surgery, persistent vs. recurrent disease after the first surgery, age, gender and interval between the two surgeries.
  • CONCLUSION: Repeated transsphenoidal surgery via the endoscopic technique is a good treatment option for selected patients with recurrent or persistent Cushing's disease following primary pituitary surgery.
  • [MeSH-major] Endoscopy / methods. Neurosurgical Procedures / methods. Pituitary ACTH Hypersecretion / surgery. Pituitary Gland / surgery

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  • (PMID = 18616702.001).
  • [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] WI4X0X7BPJ / Hydrocortisone
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67. 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
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  • [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

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  • (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
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68. Miyoshi T, Otsuka F, Suzuki J, Inagaki K, Takeda M, Kano Y, Yamashita T, Ogura T, Date I, Tanaka Y, Hashimoto K, Makino H: Periodic secretion of adrenocorticotropin in a patient with Cushing's disease manifested during pregnancy. Endocr J; 2005 Jun;52(3):287-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Periodic secretion of adrenocorticotropin in a patient with Cushing's disease manifested during pregnancy.
  • We report the case of 19-year-old woman with cyclical Cushing's disease, in whom plasma adrenocorticotropin (ACTH) was secreted periodically after her first pregnancy.
  • Her ACTH secretion lacked normal daily fluctuation but exhibited periodic change during 1-year observation, showing 119 pg/ml, 34.6 pg/ml and 115 pg/ml at the 4th, 7th and 13th months after delivery.
  • Plasma ACTH levels were increased by corticotropin releasing hormone and metyrapone, while low-dose dexamethasone suppressed cortisol secretion.
  • Gel filtration analysis of the patient's plasma detected big ACTH molecules being eluted with a peak of authentic 1-39 ACTH.
  • Cranial magnetic resonance imaging revealed a 1-cm pituitary mass in right cavernous sinus.
  • The pituitary tumor was removed by transsphenoidal surgery at 13th month after delivery and was pathologically compatible with ACTH-producing pituitary adenoma by immunohistochemistry.
  • This case includes clinically rare subsets of Cushing's syndrome showing periodic ACTH secretion and aberrant ACTH molecules.
  • [MeSH-major] Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Pituitary ACTH Hypersecretion / blood. Pituitary Neoplasms / secretion. Pregnancy Complications, Neoplastic / blood
  • [MeSH-minor] Adult. Corticotropin-Releasing Hormone / pharmacology. Female. Humans. Hydrocortisone / blood. Hydrocortisone / secretion. Metyrapone. Pregnancy

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  • (PMID = 16006722.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone; ZS9KD92H6V / Metyrapone
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69. AbdelMannan D, Selman WR, Arafah BM: Peri-operative management of Cushing's disease. Rev Endocr Metab Disord; 2010 Jun;11(2):127-34
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peri-operative management of Cushing's disease.
  • Management of patients with ACTH producing pituitary adenoma remains to be challenging.
  • Removal of the pituitary adenoma through transsphenoidal surgery is the main stay of treatment.
  • Complete resection of the adenoma is followed by the development of ACTH deficiency since the normal corticotrophs are suppressed by the pre-existing hypercortisolemia.
  • The concern for ACTH deficiency has led many centers to advocate the use glucocorticoids before, during and after surgery.
  • Serum cortisol continues to be the best determinant of disease activity after surgical adenomectomy.
  • These include the dexamethasone suppression test, CRH stimulation without dexamethasone, urinary free cortisol measurements, desmopressin stimulation test, the determination of salivary cortisol and / or plasma ACTH concentrations.
  • [MeSH-major] Pituitary ACTH Hypersecretion / surgery
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Cushing Syndrome / metabolism. Cushing Syndrome / surgery. Glucocorticoids / metabolism. Humans. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / surgery

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  • (PMID = 20556520.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 9002-60-2 / Adrenocorticotropic Hormone
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70. Teshima T, Hara Y, Takekoshi S, Nezu Y, Harada Y, Yogo T, Teramoto A, Osamura RY, Tagawa M: Trilostane-induced inhibition of cortisol secretion results in reduced negative feedback at the hypothalamic-pituitary axis. Domest Anim Endocrinol; 2009 Jan;36(1):32-44
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trilostane-induced inhibition of cortisol secretion results in reduced negative feedback at the hypothalamic-pituitary axis.
  • Cushing's disease caused by pituitary corticotroph adenoma in dogs is usually treated by medical treatment, and the efficacy of this treatment has been reported.
  • The purpose of this study was to investigate the effect of reduced negative feedback through the inhibition of cortisol secretion by daily trilostane administration on the pituitary-adrenal axis in clinically normal dogs.
  • After the initiation of trilostane administration, plasma adrenocorticotropic hormone (ACTH) concentrations were increased remarkably.
  • As assessed by magnetic resonance imaging (MRI) during administration, the pituitary became enlarged.
  • After trilostane administration, the cytoplasmic areas of the pituitary corticotrophs were increased and the ratio of pituitary corticotrophs to all cells in the anterior lobe was greater in the trilostane-treated dogs than that in untreated animals.
  • Using real-time PCR quantification, the expression of proopiomelanocortin (POMC) mRNA in the pituitary and ACTH receptor (ACTH-R) mRNA in the adrenal gland was greater in the dogs treated with trilostane than in untreated dogs.
  • These results indicate that reduced negative feedback induced hyperfunction of the pituitary corticotrophs and pituitary enlargement in healthy dogs.
  • These changes suggest that the inhibition of cortisol secretion by trilostane may increase the risk for accelerating the growth of corticotroph adenomas in dogs with Cushing's disease.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Dihydrotestosterone / analogs & derivatives. Dogs. Hydrocortisone / antagonists & inhibitors. Hypothalamus / drug effects. Pituitary Gland / drug effects
  • [MeSH-minor] Adrenal Glands / chemistry. Adrenal Glands / drug effects. Adrenal Glands / pathology. Adrenocorticotropic Hormone / blood. Animals. Corticotrophs / drug effects. Corticotrophs / ultrastructure. Feedback, Physiological / drug effects. Female. Hyperplasia. Magnetic Resonance Imaging. Male. Pro-Opiomelanocortin / genetics. RNA, Messenger / analysis. Receptors, Corticotropin / genetics

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  • (PMID = 19041802.001).
  • [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 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Receptors, Corticotropin; 08J2K08A3Y / Dihydrotestosterone; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; L0FPV48Q5R / trilostane; WI4X0X7BPJ / Hydrocortisone
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71. 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
Hazardous Substances Data Bank. Corticotropin .

  • [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

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  • (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
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72. Minniti G, Osti M, Jaffrain-Rea ML, Esposito V, Cantore G, Maurizi Enrici R: Long-term follow-up results of postoperative radiation therapy for Cushing's disease. J Neurooncol; 2007 Aug;84(1):79-84
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term follow-up results of postoperative radiation therapy for Cushing's disease.
  • OBJECTIVES: Radiotherapy is currently used in patients with residual or recurrent pituitary adenomas after surgery.
  • However, there is little information of long-term outcome of patients with Cushing's disease following radiotherapy.
  • We assessed the long-term efficacy and toxicity of conventional radiotherapy in the control of Cushing's disease after unsuccessful transsphenoidal surgery.
  • PATIENTS AND METHODS: Forty patients with Cushing's disease were treated with conventional external beam radiotherapy at our Institution between 1988 and 2002.
  • The persistence of active disease after surgery was diagnosed by the increased high plasma cortisol levels, high 24 h urinary cortisol levels and absence of cortisol suppression after administration of dexamethasone.
  • CONCLUSION: Radiotherapy is effective in the long-term tumour- and hormone hypersecretion control of ACTH-secreting pituitary adenomas, however with a high prevalence of hypopituitarism.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / radiotherapy. Adenoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy. Neoplasm, Residual / radiotherapy. Pituitary ACTH Hypersecretion / radiotherapy
  • [MeSH-minor] Adult. Disease-Free Survival. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Male. Middle Aged

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  • (PMID = 17356896.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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73. Alexandraki KI, Grossman AB: Pituitary-targeted medical therapy of Cushing's disease. Expert Opin Investig Drugs; 2008 May;17(5):669-77
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary-targeted medical therapy of Cushing's disease.
  • BACKGROUND: The goals of ideal medical therapy for Cushing's disease should be to target the aetiology of the disorder, as is the case for surgery, which is the current 'gold standard' treatment.
  • However, no effective drug that directly and reliably targets the adrenocorticotropin-secreting pituitary adenoma has yet been found.
  • OBJECTIVE: To summarise pituitary-targeted medical treatment of Cushing's disease.
  • METHODS: Compounds with neuromodulatory properties and ligands of different nuclear hormone receptors involved in hypothalamo-pituitary regulation have been investigated.
  • RESULTS: The somatostatin analogue pasireotide and the dopamine agonist cabergoline, as well as their combination, show some therapeutic promise in the medical therapy of Cushing's disease.
  • CONCLUSION: 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] Dopamine Agonists. Ergolines. Oligopeptides. Pituitary ACTH Hypersecretion / drug therapy. Pituitary Gland / drug effects. Somatostatin / analogs & derivatives

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  • [ErratumIn] Expert Opin Investig Drugs. 2008 Jul;17(7):1141
  • (PMID = 18447593.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 0 / Neurotransmitter Agents; 0 / Oligopeptides; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; LL60K9J05T / cabergoline
  • [Number-of-references] 100
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74. Pecori Giraldi F, Scaroni C, Arvat E, Martin M, Giordano R, Albiger N, Leao AA, Picu A, Mantero F, Cavagnini F: Effect of protracted treatment with rosiglitazone, a PPARgamma agonist, in patients with Cushing's disease. Clin Endocrinol (Oxf); 2006 Feb;64(2):219-24
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of protracted treatment with rosiglitazone, a PPARgamma agonist, in patients with Cushing's disease.
  • OBJECTIVE: Cushing's disease, hypercortisolism due to a pituitary ACTH-secreting tumour, is a highly morbid illness as yet without effective medical therapy.
  • Recent studies have demonstrated that peroxisome proliferator-activated receptor gamma (PPARgamma) agonists effectively suppress ACTH secretion in a murine tumoral corticotroph cell line, but the few studies conducted so far in patients with ACTH-secreting pituitary adenomas have yielded variable results.
  • DESIGN: Ten patients with Cushing's disease were treated with 4-16 mg rosiglitazone p.o. daily for 1-8 months (median 3 months) and plasma ACTH and cortisol, urinary free cortisol (UFC), as well as parameters of insulin sensitivity, were recorded.
  • RESULTS: The acute challenge with rosiglitazone did not significantly modify plasma ACTH and cortisol levels.
  • In the others, UFC as well as plasma ACTH and cortisol decrements were inscribed within wide, random oscillations indicating that disease activity was substantially unchanged.
  • Insulin sensitivity was ameliorated in most patients, without relation to ACTH or cortisol secretion.
  • CONCLUSIONS: Although effective in a subset of patients, protracted rosiglitazone administration did not consistently restrain ACTH and cortisol secretion in patients with Cushing's disease.
  • Further investigations are needed to fully define the therapeutic potential of PPARgamma agonists in this disorder.
  • [MeSH-major] Peroxisome Proliferator-Activated Receptors / agonists. Pituitary ACTH Hypersecretion / drug therapy. Thiazolidinediones / administration & dosage

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  • (PMID = 16430724.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Peroxisome Proliferator-Activated Receptors; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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75. Pawlikowski M, Kunert-Radek J, Radek M: "Silent"corticotropinoma. Neuro Endocrinol Lett; 2008 Jun;29(3):347-50
Hazardous Substances Data Bank. Corticotropin .

  • [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

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  • (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
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76. Tauchmanovà L, Pivonello R, De Martino MC, Rusciano A, De Leo M, Ruosi C, Mainolfi C, Lombardi G, Salvatore M, Colao A: Effects of sex steroids on bone in women with subclinical or overt endogenous hypercortisolism. Eur J Endocrinol; 2007 Sep;157(3):359-66
Hazardous Substances Data Bank. MENOTROPINS .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PATIENTS: Seventy-one consecutive women were enrolled: 36 with overt hypercortisolism (26 with ACTH-secreting pituitary adenoma and 10 with cortisol-secreting adrenal tumor) and 35 with subclinical hypercortisolism due to adrenal incidentalomas.
  • METHODS: At diagnosis, we measured serum cortisol, FSH, LH, estradiol, testosterone, androstenedione and DHEAS, and urinary cortisol excretion.
  • RESULTS: Between women with overt and subclinical hypercortisolism BMD values and prevalence of any vertebral (69 vs 57%, P = 0.56), clinical (28 vs 11.4%, P = 0.22), and multiple vertebral fractures (36 vs 31%, P = 0.92) did not differ.
  • The deleterious effects of hypercortisolism on the spine may be partly counterbalanced by DHEAS increase at any degree of cortisol excess, and by preserved menstrual cycles in women with subclinical but not in those with overt hypercortisolism.

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  • (PMID = 17766720.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione; 4TI98Z838E / Estradiol; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 9002-68-0 / Follicle Stimulating Hormone; WI4X0X7BPJ / Hydrocortisone
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77. Mishra AK, Agarwal A, Gupta S, Agarwal G, Verma AK, Mishra SK: Outcome of adrenalectomy for Cushing's syndrome: experience from a tertiary care center. World J Surg; 2007 Jul;31(7):1425-32
MedlinePlus Health Information. consumer health - Cushing's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of adrenalectomy for Cushing's syndrome: experience from a tertiary care center.
  • Adrenalectomy continues to play an important role in the management of Cushing's syndrome (CS).
  • There were various etiologies--unilateral adrenocortical adenoma (n = 11), adrenocortical carcinoma (n = 13), pituitary ACTH-secreting adenoma with failed transsphenoidal surgery (n = 4), ectopic unidentified ACTH source (n = 7), bilateral adrenal macronodular hyperplasia (n = 1), primary pigmented nodular adrenal hyperplasia (n = 1) --for which the patients underwent adrenalectomy: unilateral (n = 22), bilateral (n = 13), or adrenonephrectomy (n = 2).
  • The hypothalamic-pituitary-adrenal axis recovered as shown by normalization of the short synacthen-stimulated cortisol level (peak level > or = 20 microg/dl) after a median follow-up of 9 months (range 6-18 months).
  • Surgery for adrenocortical adenoma is safe and effective; however, survival of patients with CS due to adrenocortical carcinoma remains poor.
  • Bilateral adrenalectomy provides early control of hypercortisolism in selected cases of unlocalized ectopic ACTH syndrome or failed transsphenoidal surgery.
  • [MeSH-minor] Adolescent. Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / complications. Adrenocortical Adenoma / surgery. Adult. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged. Retrospective Studies. Treatment Outcome

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  • (PMID = 17534556.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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78. Kovacs K, Horvath E, Coire C, Cusimano M, Smyth H, Scheithauer BW, Lloyd RV: Pituitary corticotroph hyperplasia preceding adenoma in a patient with Nelson's syndrome. Clin Neuropathol; 2006 Mar-Apr;25(2):74-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary corticotroph hyperplasia preceding adenoma in a patient with Nelson's syndrome.
  • We report the case of a 42-year-old woman with Cushing's disease and Nelson's syndrome.
  • A detailed morphologic study demonstrated nodular hyperplasia of corticotroph cells but no adenoma.
  • Following a long-lasting remission (14 years), Cushing's disease recurred.
  • After an unsuccessful second transsphenoidal surgery, Cushing's disease persisted and both adrenals were removed (at the age of 34).
  • The pituitary tumor proved to be a corticotroph adenoma; it was removed by the transsphenoidal approach (at the age of 42).
  • Although in most patients Cushing's disease is due to an ACTH-secreting pituitary corticotroph adenoma which precedes the manifestation of Nelson's syndrome, our case indicates not only that corticotroph hyperplasia may cause Cushing's disease but that it may exist before the development of Nelson's syndrome after the removal of both adrenals.
  • Our study supports the view that protracted stimulation of corticotrophs resulting from the elimination of the negative inhibitory feedback effect by corticosteroids plays a role in adenoma initiation.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / etiology. Adenoma / etiology. Hyperplasia / complications. Nelson Syndrome / etiology. Pituitary ACTH Hypersecretion / complications

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  • (PMID = 16550740.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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79. 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
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  • [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

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  • (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
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80. Parenti G, Nassi R, Silvestri S, Bianchi S, Valeri A, Manca G, Mangiafico S, Ammannati F, Serio M, Mannelli M, Peri A: Multi-step approach in a complex case of Cushing's syndrome and medullary thyroid carcinoma. J Endocrinol Invest; 2006 Feb;29(2):177-81
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  • [Title] Multi-step approach in a complex case of Cushing's syndrome and medullary thyroid carcinoma.
  • The diagnosis of Cushing's syndrome (CS) may sometimes be cumbersome.
  • In particular, in ACTH-dependent CS it may be difficult to distinguish between the presence of an ACTH-secreting pituitary adenoma and ectopic ACTH and/or CRH secretion.
  • We report here the case of a 54-yr-old man affected by ACTH-dependent CS in association with a left adrenal adenoma and medullary thyroid carcinoma (MTC).
  • It was then decided to remove the left adenomatous adrenal gland.
  • This case well depicts the complexity of the diagnostic workout, which is needed sometimes to correctly diagnose and treat CS, and suggests that monolateral adrenalectomy may represent, at least temporarily, a reasonable therapeutic option in occult ACTH-dependent hypercortisolism.
  • [MeSH-major] Carcinoma, Medullary / diagnosis. Cushing Syndrome / diagnosis. Thyroid Neoplasms / diagnosis

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  • (PMID = 16610247.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 9007-12-9 / Calcitonin
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81. 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
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  • [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.

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  • (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
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82. Mauermann WJ, Sheehan JP, Chernavvsky DR, Laws ER, Steiner L, Vance ML: Gamma Knife surgery for adrenocorticotropic hormone-producing pituitary adenomas after bilateral adrenalectomy. J Neurosurg; 2007 Jun;106(6):988-93
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  • [Title] Gamma Knife surgery for adrenocorticotropic hormone-producing pituitary adenomas after bilateral adrenalectomy.
  • OBJECT: Patients with adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas may require a bilateral adrenalectomy to treat their Cushing's disease.
  • Approximately one third of these patients, however, will experience progressive enlargement of the residual pituitary adenoma, develop hyperpigmentation, and have an elevated level of serum ACTH.
  • METHODS: The prospectively collected University of Virginia Gamma Knife database of patients with pituitary adenomas was reviewed to identify all individuals with Nelson's syndrome who were treated with GKS.
  • These patients were assessed for tumor control (that is, lack of tumor growth over time) with neuroimaging studies (median follow-up duration 22 months) and for biochemical normalization of their ACTH levels (median follow-up duration 50 months).
  • Neuroimaging follow-up studies were available for 22 patients, and endocrine follow up was available for 15 patients in whom elevation of ACTH levels was documented prior to GKS.
  • In the 22 patients in whom neuroimaging follow-up studies were available, 12 had a decrease in tumor size, eight had no tumor growth, and two had an increase in tumor volume.
  • Ten of 15 patients with elevated ACTH levels prior to GKS showed a decrease in their ACTH levels at last follow up; three of these 10 patients achieved normal ACTH levels (< 50 pg/ml) and the other five patients with initially elevated values had an increase in ACTH levels.
  • Ten patients were thoroughly evaluated for post-GKS pituitary function; four were found to have new pituitary hormone deficiency and six did not have hypopituitarism after GKS.
  • CONCLUSIONS: Gamma Knife surgery may control the residual pituitary adenoma and decrease ACTH levels in patients with Nelson's syndrome.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Adrenalectomy. Nelson Syndrome / surgery. Radiosurgery

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  • (PMID = 17564169.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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83. de Bruin C, Meij BP, Kooistra HS, Hanson JM, Lamberts SW, Hofland LJ: Cushing's disease in dogs and humans. Horm Res; 2009 Jan;71 Suppl 1:140-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's disease in dogs and humans.
  • BACKGROUND: Cushing's disease (CD) is a common endocrinological disorder in dogs with an estimated incidence of 1 to 2 cases/1,000 dogs/year.
  • Canine CD may therefore serve as an animal model for human CD, especially since therapeutic canine hypophysectomy can generate substantial amounts of primary corticotroph adenoma tissue for in vitro research purposes.
  • In a recent study, we found that dopamine (DA) D(2) and somatostatin (SS) receptor subtypes are well expressed in canine corticotroph adenomas, but there are some distinct differences compared with the expression profile observed in human CD.
  • CASE REPORT: This case involves an 8-year-old female dog that developed signs of exercise intolerance, muscle weakness and polyuria/polydipsia due to an adrenocorticotropic hormone-secreting pituitary adenoma.
  • [MeSH-major] Dog Diseases / radiography. Pituitary ACTH Hypersecretion / radiography. Pituitary ACTH Hypersecretion / veterinary

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19153526.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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84. Roussel-Gervais A, Bilodeau S, Vallette S, Berthelet F, Lacroix A, Figarella-Branger D, Brue T, Drouin J: Cooperation between cyclin E and p27(Kip1) in pituitary tumorigenesis. Mol Endocrinol; 2010 Sep;24(9):1835-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cooperation between cyclin E and p27(Kip1) in pituitary tumorigenesis.
  • Cushing's disease is caused by glucocorticoid-resistant pituitary corticotroph adenomas.
  • We have previously identified the loss of nuclear Brg1 as one mechanism that may lead to partial glucocorticoid resistance: this loss is observed in about 33% of human corticotroph adenomas.
  • We now show that Brg1 loss of function correlates with cyclin E expression in corticotroph adenomas and with loss of the cell cycle inhibitor p27(Kip1) expression.
  • Because Brg1 is thought to have tumor suppressor activity, the present study was undertaken to understand the putative contribution of cyclin E derepression produced by loss of Brg1 expression on adenoma development.
  • Overexpression of cyclin E in pituitary proopiomelanocortin cells leads to abnormal reentry into cell cycle of differentiated proopiomelanocortin cells and to centrosome instability.
  • These alterations are consistent with the intermediate lobe hyperplasia and anterior lobe adenomas that were observed in these pituitaries.
  • When combined with the p27(Kip1) knockout, overexpression of cyclin E increased the incidence of pituitary tumors, their size, and their proliferation index.
  • These results suggest that cyclin E up-regulation and p27(Kip1) loss-of-function act cooperatively on pituitary adenoma development.
  • [MeSH-major] Cyclin E / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Pituitary Neoplasms / metabolism. Precancerous Conditions / metabolism
  • [MeSH-minor] Animals. Biomarkers / metabolism. Cell Differentiation. Cell Proliferation. Centrosome / metabolism. DNA Helicases / metabolism. Gene Knockdown Techniques. Hyperplasia. Mice. Mice, Transgenic. Nuclear Proteins / metabolism. Phenotype. Pituitary ACTH Hypersecretion / complications. Pituitary ACTH Hypersecretion / metabolism. Pituitary ACTH Hypersecretion / pathology. Pituitary Gland / metabolism. Pituitary Gland / pathology. Pro-Opiomelanocortin / metabolism. Repressor Proteins. Transcription Factors / metabolism

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  • (PMID = 20660298.001).
  • [ISSN] 1944-9917
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cyclin E; 0 / Nuclear Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 66796-54-1 / Pro-Opiomelanocortin; EC 3.6.1.- / Smarca4 protein, mouse; EC 3.6.4.- / DNA Helicases
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85. Drouin J, Bilodeau S, Vallette S: Of old and new diseases: genetics of pituitary ACTH excess (Cushing) and deficiency. Clin Genet; 2007 Sep;72(3):175-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Of old and new diseases: genetics of pituitary ACTH excess (Cushing) and deficiency.
  • The pituitary gland orchestrates our endocrine environment: it produces hormones in response to hypothalamic factors that integrate neural inputs and its activity is balanced by the feedback action of peripheral hormones.
  • Genetic analysis of pituitary function led to discovery of critical transcription factors that cause hormone deficiencies when mis-expressed.
  • This review will summarize recent findings that led to the first complete clinical description of inherited, isolated corticotropin (ACTH) deficiency (IAD) and to the first molecular mechanism for excessive ACTH production in Cushing's disease.
  • Indeed, mutations in TPIT, a positive or negative regulator of cell fates for different pituitary lineages, cause neonatal IAD, a condition considered anecdotic before discovery of this transcription factor.
  • Cushing's disease is caused by corticotroph adenomas that produce excess ACTH as a result of resistance to glucocorticoids (Gc).
  • Molecular investigation of the normal mechanism of Gc feedback led to identification of two essential proteins for pro-opiomelanocortin repression that are often mis-expressed in corticotroph adenomas thus providing a molecular explanation for Gc resistance.
  • These two proteins, Brg1 and histone deacetylase 2 (HDAC2), are involved in chromatin remodeling and may also participate in the tumorigenic process, as Brg1 is a tumor suppressor.
  • These recent advances have provided improved diagnosis and opened new perspectives for patient management and therapies.
  • [MeSH-major] Adrenocorticotropic Hormone / deficiency. Pituitary ACTH Hypersecretion / genetics
  • [MeSH-minor] Animals. DNA Helicases / physiology. Feedback, Physiological. Glucocorticoids / physiology. Histone Deacetylase 2. Histone Deacetylases / physiology. Homeodomain Proteins / genetics. Humans. Hypothalamo-Hypophyseal System / physiology. Nuclear Proteins / physiology. Pituitary-Adrenal System / physiology. Pro-Opiomelanocortin / metabolism. Receptors, Glucocorticoid / physiology. Repressor Proteins / physiology. T-Box Domain Proteins / genetics. Transcription Factors / physiology

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  • (PMID = 17718852.001).
  • [ISSN] 0009-9163
  • [Journal-full-title] Clinical genetics
  • [ISO-abbreviation] Clin. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Receptors, Glucocorticoid; 0 / Repressor Proteins; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / Transcription Factors; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.5.1.98 / Histone Deacetylase 2; EC 3.5.1.98 / Histone Deacetylases; EC 3.6.1.- / SMARCA4 protein, human; EC 3.6.4.- / DNA Helicases
  • [Number-of-references] 41
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86. 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
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  • [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

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  • (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
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87. Takeshita A, Inoshita N, Taguchi M, Okuda C, Fukuhara N, Oyama K, Ohashi K, Sano T, Takeuchi Y, Yamada S: High incidence of low O(6)-methylguanine DNA methyltransferase expression in invasive macroadenomas of Cushing's disease. Eur J Endocrinol; 2009 Oct;161(4):553-9
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  • [Title] High incidence of low O(6)-methylguanine DNA methyltransferase expression in invasive macroadenomas of Cushing's disease.
  • CONTEXT: Crooke's cell adenoma (CCA), characterized by massive Crooke's hyaline change in corticotroph adenoma, causes a rare subtype of Cushing's disease.
  • In contrast to ordinary corticotroph adenomas, CCAs are generally aggressive and present as invasive macroadenomas, which are refractory to both surgery and radiotherapy and have a high-recurrence rate.
  • OBJECTIVE: We report a patient with Crooke's cell carcinoma who presented with local invasion and liver metastases, which was refractory to conventional therapeutic modalities including transsphenoidal surgery, radiosurgery, medications, and hepatic transcatheter arterial embolization.
  • After all these treatments failed, the patient had monthly temozolomide administrations, resulting in gradual clinical improvement and biochemical data that were consistent with tumor shrinkage.
  • METHODS: We thus investigated MGMT expression, immunohistochemically, in seven CCAs (five invasive macroadenomas and two invasive microadenomas) and 17 ordinary-type adenomas (OTAs; three noninvasive macroadenomas, 12 noninvasive microadenomas, and two invasive microadenomas) from patients with Cushing's disease.
  • In 17 OTAs, only one adenoma showed low MGMT expression.
  • CONCLUSION: In Cushing's disease, invasive macroadenomas including CCA usually have low-MGMT expression.

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  • (PMID = 19589911.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; WI4X0X7BPJ / Hydrocortisone
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88. Pecori Giraldi F, Andrioli M, De Marinis L, Bianchi A, Giampietro A, De Martin M, Sacco E, Scacchi M, Pontecorvi A, Cavagnini F: Significant GH deficiency after long-term cure by surgery in adult patients with Cushing's disease. Eur J Endocrinol; 2007 Feb;156(2):233-9
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  • [Title] Significant GH deficiency after long-term cure by surgery in adult patients with Cushing's disease.
  • OBJECTIVE: Impaired GH secretion usually accompanies Cushing's syndrome and a variable proportion of patients reportedly fail to recover normal GH secretion after successful treatment.
  • The aim of the present study is to evaluate GH secretory status after long-term cure of Cushing's disease achieved by surgery alone.
  • DESIGN AND METHODS: We studied 34 patients (27 females and 7 males, age range 21-68 years) formerly affected by Cushing's disease.
  • Patients were studied 2-20 years (median 3.3 years) following remission of hypercortisolism; all patients underwent transsphenoidal surgery with the removal of an ACTH-secreting adenoma; repeat pituitary surgery for relapse was performed in two patients while bilateral adrenalectomy was necessary in two patients.
  • CONCLUSIONS: This study demonstrates the presence of GH deficiency in a high percentage of patients with Cushing's disease after long-term remission of hypercortisolism obtained by surgery alone.
  • This finding is significant as it highlights that even the most favourable therapeutical course, i.e. remission achieved by surgery alone, is accompanied by impaired GH secretion.
  • Assessment of GH secretion is therefore recommended for all patients cured from Cushing's disease, even if not submitted to radiotherapy.
  • Studies on the clinical impact of GH deficiency and the use of GH replacement therapy seem warranted in patients cured from Cushing's disease.

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  • (PMID = 17287413.001).
  • [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] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9034-39-3 / Growth Hormone-Releasing Hormone; 94ZLA3W45F / Arginine
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89. Oyama K, Yamada S, Hukuhara N, Hiramatsu R, Taguchi M, Yazawa M, Matsuda A, Ohmura E, Imai Y: FSH-producing macroadenoma associated in a patient with Cushing's disease. Neuro Endocrinol Lett; 2006 Dec;27(6):733-6
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  • [Title] FSH-producing macroadenoma associated in a patient with Cushing's disease.
  • OBJECTIVE AND IMPORTANCE: We encountered a Cushing's disease patient whose surgically removed pituitary macroadenoma was not an ACTH-producing, but rather a gonadotroph adenoma.
  • Cure was obtained only after a tiny microadenoma, overlooked on preoperative studies, was removed by a 2nd operation from a compressed thin normal anterior pituitary gland.
  • Endocrinological examinations suggested Cushing's disease and MRI disclosed an invasive macroadenoma (22 mm in diameter) with suprasellar extension.
  • INTERVENTION: Despite total removal of the invasive macroadenoma by transsphenoidal surgery, her elevated serum cortisol- and ACTH levels failed to decrease.
  • Histologic study of the surgical specimen disclosed that the tumor was a silent FSH-producing, rather than an ACTH-producing adenoma.
  • Detailed re-evaluation of pre- and postoperative MRI suggested the presence of a 3-mm microadenoma on the left side of a thin compressed normal gland.
  • In a 2nd operation an ACTH-producing microadenoma was removed from inside the thin remaining compressed normal pituitary gland and endocrinological cure of Cushing's disease was achieved.
  • CONCLUSION: Although double adenomas, being a non-ACTH producing macroadenoma associated with an ACTH producing tiny microadenoma, are extremely rare in patients with Cushing's disease, detailed preoperative MRI evaluation is necessary to avoid missing tiny adenomas hidden in a compressed normal pituitary gland which is the cause of Cushing's disease, especially when a macroadenoma is found in patient with Cushing's disease.
  • [MeSH-major] Follicle Stimulating Hormone / secretion. Gonadotrophs / secretion. Neoplasms, Multiple Primary / pathology. Pituitary ACTH Hypersecretion / blood. Pituitary Neoplasms / pathology. Pituitary Neoplasms / secretion

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  • (PMID = 17187002.001).
  • [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] 9002-60-2 / Adrenocorticotropic Hormone; 9002-68-0 / Follicle Stimulating Hormone; WI4X0X7BPJ / Hydrocortisone
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90. 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
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  • [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.

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  • [Cites] Lancet. 1973 Aug 25;2(7826):418-21 [4124896.001]
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  • (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
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91. Czirják S: [Minimally invasive surgery of the pituitary and the sellar region]. Orv Hetil; 2006 Aug 20;147(33):1545-57
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  • [Title] [Minimally invasive surgery of the pituitary and the sellar region].
  • INTRODUCTION: New minimal invasive neurosurgical approaches for the treatment of diseases in the sellar and perisellar regions (superciliary and paraseptal approach, perioperative ACTH measurements, application of endoscopes and neuronavigation) were introduced by the author.
  • The study on perioperative plasma ACTH simultaneous measurements with rapid and standard methods revealed first in the literature that, during anaesthesia in patients with ACTH producing adenoma the plasma ACTH level changed individually.
  • There was no difference between arterial and venous plasma ACTH concentration in the same patient and the ACTH concentration in the bleedings from the peripituitary bony structures are individually variable, representing the network of the venous outflow of the pituitary.
  • The decrease in the plasma ACTH concentrations in the peripheral venous samples two hours after operation and next morning proved the radical removal of the adenoma.
  • The differences between concentrations in the left and right sides indicate the intrapituitary lateralization of the adenoma.
  • CONCLUSIONS: With the advent of the minimal invasive methods in surgery of the pituitary and the sellar region the mortality end the morbidity of the operations decreased.
  • [MeSH-major] Adenoma / surgery. Hypophysectomy / methods. Pituitary ACTH Hypersecretion / surgery. Pituitary Gland / surgery. Pituitary Neoplasms / surgery. Sella Turcica / surgery

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  • (PMID = 17037677.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 49
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92. Banasiak MJ, Malek AR: Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management. Neurosurg Focus; 2007;23(3):E13
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  • [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.

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  • (PMID = 17961028.001).
  • [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] 0 / Neurotransmitter Agents
  • [Number-of-references] 123
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93. Swords FM, Monson JP, Besser GM, Chew SL, Drake WM, Grossman AB, Plowman PN: Gamma knife radiosurgery: a safe and effective salvage treatment for pituitary tumours not controlled despite conventional radiotherapy. Eur J Endocrinol; 2009 Dec;161(6):819-28
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  • [Title] Gamma knife radiosurgery: a safe and effective salvage treatment for pituitary tumours not controlled despite conventional radiotherapy.
  • OBJECTIVE: We report the use of 'gamma knife' (GK) radiosurgery in 25 patients with pituitary adenomas not cured despite conventional therapy, including external beam radiotherapy.
  • PATIENTS AND METHODS: All patients had previously received conventional radiotherapy for a mean of 11.8 years prior to receiving GK; 23 out of 25 had also undergone pituitary surgery on at least one occasion.
  • Seventeen had hyperfunctioning adenomas that still required medical therapy without an adequate biochemical control--ten somatotroph adenomas, six corticotroph adenomas and one prolactinoma, while eight patients had non-functioning pituitary adenomas (NFPAs).
  • A total of 75% NFPAs showed disease stabilisation or shrinkage post GK.
  • The results in corticotroph adenomas were variable.
  • Prior to GK, 72% of the patients were panhypopituitary, and 42% of the remainder have developed new anterior pituitary hormone deficiencies to date.
  • CONCLUSIONS: These data indicate that GK is a safe and effective adjunctive treatment for patients with NFPAs and acromegaly not satisfactorily controlled with surgery and radiotherapy.

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  • (PMID = 19773368.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
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94. de Bruin C, Feelders RA, Lamberts SW, Hofland LJ: Somatostatin and dopamine receptors as targets for medical treatment of Cushing's Syndrome. Rev Endocr Metab Disord; 2009 Jun;10(2):91-102
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  • [Title] Somatostatin and dopamine receptors as targets for medical treatment of Cushing's Syndrome.
  • Somatostatin (SS) and dopamine (DA) receptors are widely expressed in neuroendocrine tumours that cause Cushing's Syndrome (CS).
  • In Cushing's disease, corticotroph adenomas mainly express dopamine receptor subtype 2 (D(2)) and somatostatin receptor subtype 5 (sst(5)), whereas sst(2) is expressed at lower levels.
  • Activation of these receptors can inhibit ACTH-release in primary cultured corticotroph adenomas and compounds that target either sst(5) (pasireotide, or SOM230) or D(2) (cabergoline) have shown significant efficacy in subsets of patients in recent clinical studies.
  • In selected cases of Ectopic ACTH-producing Syndrome (EAS), the sst(2)-preferring compound octreotide is able to reduce cortisol levels effectively.
  • In both normal adrenal tissue as well as in adrenal adenomas and carcinomas that cause CS, sst and DA receptor expression has been demonstrated.
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / drug therapy. Adrenocorticotropic Hormone / metabolism. Animals. Antineoplastic Agents / therapeutic use. Humans

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  • (PMID = 18642088.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 115
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95. Petit JH, Biller BM, Yock TI, Swearingen B, Coen JJ, Chapman P, Ancukiewicz M, Bussiere M, Klibanski A, Loeffler JS: Proton stereotactic radiotherapy for persistent adrenocorticotropin-producing adenomas. J Clin Endocrinol Metab; 2008 Feb;93(2):393-9
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  • [Title] Proton stereotactic radiotherapy for persistent adrenocorticotropin-producing adenomas.
  • CONTEXT: Radiation therapy is a potentially curative treatment for corticotroph adenomas refractory to surgery.
  • OBJECTIVE: Our objective was to evaluate the efficacy and safety of PSR for persistent Cushing's disease (CD) and Nelson's syndrome (NS).
  • CR in NS was based on normalization of plasma corticotropin.
  • No secondary tumors were noted on follow-up magnetic resonance imaging scans, and there was no clinical evidence of optic nerve damage, seizure, or brain injury.
  • There were 17 patients (52%) who developed new pituitary deficits.
  • CONCLUSIONS: PSR is effective for patients with persistent corticotroph adenomas with low morbidity after a median follow-up of 62 months; longer follow-up is warranted for late radiation-related sequelae.
  • [MeSH-major] Nelson Syndrome / surgery. Pituitary ACTH Hypersecretion / surgery. Protons / therapeutic use. Radiosurgery / methods

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  • (PMID = 18029460.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protons; WI4X0X7BPJ / Hydrocortisone
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96. Nigawara T, Iwasaki Y, Asai M, Yoshida M, Kambayashi M, Sashinami H, Hashimoto K, Suda T: Inhibition of 11beta-hydroxysteroid dehydrogenase eliminates impaired glucocorticoid suppression and induces apoptosis in corticotroph tumor cells. Endocrinology; 2006 Feb;147(2):769-72
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  • [Title] Inhibition of 11beta-hydroxysteroid dehydrogenase eliminates impaired glucocorticoid suppression and induces apoptosis in corticotroph tumor cells.
  • Cushing's disease is characterized by persistent ACTH secretion under hypercortisolemia.
  • In an attempt to clarify the molecular mechanism, we examined the effect of 11beta-hydroxysteroid dehydrogenase (HSD) inhibition on glucocorticoid suppression of ACTH release using murine corticotroph tumor cells.
  • We conclude that ectopic expression of 11beta-HSD2 is, at least in part, responsible for the impaired glucocorticoid suppression in corticotroph adenoma.
  • Inhibition of 11beta-HSD2 may be applicable to the medical therapy for Cushing's disease.
  • [MeSH-major] 11-beta-Hydroxysteroid Dehydrogenases / metabolism. Adenoma / enzymology. Apoptosis. Glucocorticoids / metabolism. Hydrocortisone / metabolism. Pituitary ACTH Hypersecretion / enzymology. Pituitary Neoplasms / enzymology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Carbenoxolone / pharmacology. Cell Line, Tumor. Feedback, Physiological. Mice

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  • (PMID = 16254034.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases; MM6384NG73 / Carbenoxolone; WI4X0X7BPJ / Hydrocortisone
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97. Matsuno A: [Recent trends in the pathophysiology and treatment of pituitary adenomas]. Brain Nerve; 2009 Aug;61(8):957-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Recent trends in the pathophysiology and treatment of pituitary adenomas].
  • Recent molecular pathological investigations have elucidated the cytodifferentiation of pituitary cells and identified several transcriptional factors that regulate this cytodifferentiation of pituitary cells.
  • The patterns of cytodifferentiation are closely related to the pathogenesis of pituitary adenomas.
  • Meanwhile, the role of hypothalamic hormones in the development of pituitary adenomas has recently attracted the attention of investigators.
  • The expression of growth hormone-releasing hormone and corticotrophin releasing hormone in corticotroph adenomas have been demonstrated in somatotroph adenomas and corticotropin adenomas, respectively.
  • This finding indicates that the endogenous expression of hypothalamic hormones and their receptors in human pituitary adenoma cells has ample significance in the autocrine or paracrine regulation of pituitary hormone production and tumor extension induced by hypothalamic hormones produced by adenoma cells.
  • The recent progress in surgical techniques for treatment of pituitary adenomas has provided several alternatives: transsphenoidal surgery vs. transcranial surgery, sublabial approach vs. endonasal approach, and microsurgery vs. endoscopic surgery.
  • There have also been developments in the medical treatment of pituitary adenomas.
  • The frequently used dopamine agonist, cabergoline, is very effective for treating prolactin-producing adenoma.
  • Long-acting octreotide and pegvisomant are now available for the treatment of growth hormone producing adenoma.
  • Cabergoline is also used for growth hormone producing adenoma.
  • Temozolomide has recently been used for atypical adenomas or pituitary carcinomas.
  • Adult growth hormone deficiency sometimes occurs in postoperative patients with pituitary adenomas.
  • [MeSH-major] Adenoma / etiology. Adenoma / therapy. Pituitary Neoplasms / etiology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Corticotropin-Releasing Hormone. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Ergolines / therapeutic use. Growth Hormone-Releasing Hormone. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / therapeutic use. Humans. Hypothalamic Hormones. Incidental Findings. Neurosurgical Procedures / methods. Neurosurgical Procedures / trends. Octreotide / therapeutic use. Prolactinoma. Receptors, Neuropeptide. Receptors, Pituitary Hormone-Regulating Hormone

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
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  • (PMID = 19697885.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; 0 / Hypothalamic Hormones; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / pegvisomant; 0 / somatotropin releasing hormone receptor; 12629-01-5 / Human Growth Hormone; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
  • [Number-of-references] 32
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98. van der Hoek J, Lamberts SW, Hofland LJ: The somatostatin receptor subtype 5 in neuroendocrine tumours. Expert Opin Investig Drugs; 2010 Mar;19(3):385-99

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AREAS COVERED IN THIS REVIEW: The scope of this review is primarily focused upon recent insights in sst(5)-receptor physiology, novel sst(5)-targeted treatment options predominantly directed towards pituitary adenomas, and gastroenteropancreatic neuroendocrine tumours.
  • WHAT THE READER WILL GAIN: An understanding of the potential that novel sst(5)-targeted SRIF analogues might have in the medical treatment of Cushing's disease and acromegaly, as demonstrated by translational research, based on pathophysiological data combined with results from clinical trials.
  • Finally, absence of sst(5) in corticotroph adenomas could be related to tumour aggressiveness in Cushing's disease.
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / physiopathology. Animals. Drug Design. Gastrointestinal Neoplasms / drug therapy. Gastrointestinal Neoplasms / physiopathology. Humans. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / physiopathology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / physiopathology

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  • (PMID = 20151855.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5
  • [Number-of-references] 101
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99. Vassiliadi D, Tsagarakis S: Unusual causes of Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1245-52
MedlinePlus Health Information. consumer health - Cushing's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual causes of Cushing's syndrome.
  • Although in the majority of the patients with Cushing's syndrome (CS), hypercortisolism is due to ACTH hypersecretion by a pituitary tumour or to ectopic ACTH secretion from an extrapituitary neoplastic lesion or to autonomous cortisol secretion by an adrenal tumour, in occasional patients a much rarer entity may be the cause of the syndrome.
  • The following unusual forms of CS were identified: (i) ACTH hyperesecretion due to ectopic corticotroph adenomas in the parasellar region or the neurohypophysis, or as part of double adenomas, or gangliocytomas;.
  • (ii) ACTH hypersecretion due to ectopic CRH or CRH-like peptide secretion by various neoplasms;.
  • (iii) ACTH-independent cortisol hypersecretion from ectopic or bilateral adrenal adenomas;.
  • Such unusual presentations of CS illustrate why Cushing's syndrome represents one of the most puzzling endocrine syndromes.
  • [MeSH-minor] ACTH Syndrome, Ectopic / complications. Adrenal Gland Neoplasms / complications. Female. Glucocorticoids / adverse effects. Humans. Liver Neoplasms / complications. Megestrol Acetate / adverse effects. Ovarian Neoplasms / complications. Pituitary Neoplasms / complications. Ritonavir / adverse effects

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  • (PMID = 18209862.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Glucocorticoids; O3J8G9O825 / Ritonavir; TJ2M0FR8ES / Megestrol Acetate
  • [Number-of-references] 58
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100. Rotondo F, Scheithauer BW, Kovacs K, Bell DC: Rab3B immunoexpression in human pituitary adenomas. Appl Immunohistochem Mol Morphol; 2009 May;17(3):185-8
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rab3B immunoexpression in human pituitary adenomas.
  • To shed light on its presence in the normal human pituitary and in adenomas, a detailed immunohistochemical study of 130 surgically removed human pituitary adenomas was undertaken, including 23 somatotroph, 32 lactotroph, 19 functional corticotroph, 10 silent subtype 1 and 8 silent subtype 2 corticotroph adenomas, 12 gonadotroph hormone producing, 10 thyrotroph, 7 silent subtype 3 adenomas, and 9 null cell adenomas, 5 of the latter being of oncocytic type.
  • Among the 32 prolactin lactotroph adenomas, 10 had been treated preoperatively with bromocriptine, a dopamine agonist.
  • Among the 23 somatotroph adenomas, 10 were pretreated with octreotide, a long acting somatostatin analog.
  • The results showed Rab3B immunopositivity to be strongest in corticotroph adenomas followed by thyrotroph, lactotroph, gonadotroph, null cell, and somatotroph adenomas.
  • No difference was noted between endocrinologically active and silent corticotroph adenomas.
  • Our results add new information to the view that Rab3B is involved in the regulation of pituitary hormone secretion.

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  • (PMID = 19384079.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3A64E3G5ZO / Bromocriptine; EC 3.6.1.- / RAB3B protein, human; EC 3.6.5.2 / rab3 GTP-Binding Proteins; RWM8CCW8GP / Octreotide
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