BioMedLib Search Engine [ goto HOMEPAGE ]

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] An ACTH-secreting pituitary adenoma within the sphenoid sinus.

She was found to have a markedly elevated plasma ACTH-cortisol level.

Magnetic resonance imaging (MRI) revealed a mass in the left sphenoidal sinus, which had become enlarged to a point where it could not be removed by transsphenoidal surgery.

We decided to proceed with radiation therapy to shrink the tumor.

We describe a rare case of an ACTH-secreting pituitary adenoma within the sphenoid sinus.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Paranasal Sinus Neoplasms / diagnosis. Sphenoid Sinus / pathology

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20424367.001).

[ISSN] 1349-7235

[Journal-full-title] Internal medicine (Tokyo, Japan)

[ISO-abbreviation] Intern. Med.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

[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.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 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

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

Advertisement

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

Hazardous Substances Data Bank. HYDROCORTISONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. GADOPENTETATE DIMEGLUMINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The diagnostic value of fused positron emission tomography/computed tomography in the localization of adrenocorticotropin-secreting pituitary adenoma in Cushing's disease.

Despite the high resolution of magnetic resonance imaging (MRI) of the pituitary gland, up to 40% of cases of Cushing's disease (CD) have normal MRI.

Objective of this study is to explore the diagnostic potential of PET-CT for localization of adrenocorticotropin-secreting pituitary adenomas in CD.

PET-CT was performed in 12 cases with de novo (7 cases) or persistent CD (5 cases) that were proven to have CD on biochemical, radiological and/or histopathological findings.

PET-CT was positive in 7 of the 12 cases of CD (58%) showing a focal area of uptake in the pituitary gland.

If these findings are confirmed in larger studies, PET-CT might become an important diagnostic technique, especially when the more invasive and technically demanding procedure of IPSS is not available or inconclusive.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Pituitary ACTH Hypersecretion / pathology. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods

[MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Pituitary Gland / metabolism. Pituitary Gland / pathology

MedlinePlus Health Information. consumer health - CT Scans.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Clin Nucl Med. 2002 Mar;27(3):176-8 [11852303.001]

[Cites] J Clin Endocrinol Metab. 2004 May;89(5):2214-21 [15126544.001]

[Cites] N Engl J Med. 1991 Sep 26;325(13):897-905 [1652686.001]

[Cites] AJR Am J Roentgenol. 1994 Sep;163(3):680-2 [8079867.001]

[Cites] Rinsho Hoshasen. 1990 Mar;35(3):407-10 [2161060.001]

[Cites] Clin Endocrinol (Oxf). 2006 Apr;64(4):371-4 [16584507.001]

[Cites] Ann Intern Med. 1994 May 15;120(10):817-20 [8154641.001]

[Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):418-22 [8106630.001]

[Cites] J Nucl Med. 2001 May;42(5 Suppl):1S-93S [11483694.001]

[Cites] Lancet. 2006 May 13;367(9522):1605-17 [16698415.001]

[Cites] J Clin Endocrinol Metab. 1997 Jun;82(6):1780-5 [9177382.001]

[Cites] Neurosurgery. 1991 Jun;28(6):826-33 [2067604.001]

[Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):440-8 [10022398.001]

[Cites] J Clin Endocrinol Metab. 2008 May;93(5):1526-40 [18334580.001]

[Cites] Clin Endocrinol (Oxf). 1993 Sep;39(3):307-13 [8222293.001]

[Cites] AJNR Am J Neuroradiol. 2000 Apr;21(4):690-6 [10782779.001]

[Cites] Radiology. 1990 Oct;177(1):39-44 [2399336.001]

(PMID = 19387839.001).

[ISSN] 1573-7403

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas.

Somatostatin analogs and dopamine agonists are clinically used for medical therapy of functioning pituitary tumors, such as growth hormone- and prolactin-secreting tumors, however, their effects on ACTH-secreting tumors are controversial.

This study was aimed to determine whether somatostatin receptor (SSTR) subtype (1-5) and dopamine receptor type 2 (D2R) are differentially expressed in pituitary tumors causing Cushing's disease (CD), silent corticotroph adenoma (SCA), and non-functioning pituitary tumor (NFT).

Tissue specimens were obtained from 35 pituitary tumors during transsphenoidal surgery.

Both SSTR1 and 2 mRNA levels in SCA were greater than CD, while SSTR1 mRNA levels, but not SSTR2, in SCA were also greater than NFT.

SSTR5 mRNA levels in CD were greater than SCA, but did not differ between NFT and SCA.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Pituitary ACTH Hypersecretion / metabolism. Pituitary Neoplasms / genetics. Receptors, Dopamine D2 / genetics. Receptors, Somatostatin / physiology

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19318729.001).

[ISSN] 1348-4540

[Journal-full-title] Endocrine journal

[ISO-abbreviation] Endocr. J.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 0 / somatostatin receptor type 1; 9002-60-2 / Adrenocorticotropic Hormone

   

[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.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of genes related to corticotropin production and glucocorticoid feedback in corticotroph adenomas of dogs with Cushing's disease.

Cushing's disease caused by pituitary corticotroph adenoma is a common endocrine disease in dogs.

A characteristic biochemical feature of corticotroph adenomas is their relative resistance to negative feedback by glucocorticoids.

In this study, we examined gene expression related to adrenocorticotropic hormone (ACTH) production and secretion, and the negative feedback by glucocorticoids in canine corticotroph adenoma.

We used resected corticotroph adenomas from 10 dogs with Cushing's disease.

In order to investigate the alteration of gene expression between corticotroph adenoma and normal corticotrophic cells, ACTH-positive cells in the anterior lobe were microdissected using a laser-capture microdissection system, and mRNA levels of proopiomelanocortin (POMC), corticotropin releasing hormone receptor 1 (CRHR1), glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and 11 beta hydroxysteroid dehydrogenase (11HSD) type 1 and type 2 were determined using real-time RT-PCR.

POMC, CRHR1, and 11HSD2 mRNA levels in corticotroph adenoma were greater than those in normal corticotrophic cells (POMC, 5.5-fold; CRHR1, 4.9-fold; 11HSD2, 4.2-fold, P<0.01, respectively).

MR and 11HSD1 mRNA levels in corticotroph adenoma were lower than those in normal corticotrophic cells (MR, 2.2-fold; 11HSD1, 2.9-fold, P<0.01, respectively).

GR mRNA levels did not differ between corticotroph adenoma and normal corticotrophic cells.

Our results may help to understand the increased ACTH production and the resistance to negative feedback suppression by glucocorticoids in canine corticotroph adenomas.

These changes in gene expression may have a role in the growth of canine corticotroph adenoma, and help elucidate the pathophysiology of dogs with Cushing's disease.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adrenocorticotropic Hormone / biosynthesis. Dog Diseases / genetics. Glucocorticoids / physiology. Pituitary ACTH Hypersecretion / veterinary. Pituitary Neoplasms / veterinary

[MeSH-minor] 11-beta-Hydroxysteroid Dehydrogenases / genetics. Animals. Dogs. Feedback, Physiological. Female. Gene Expression / genetics. Male. Pro-Opiomelanocortin / genetics. RNA, Messenger / analysis. Receptors, Corticotropin-Releasing Hormone / genetics. Receptors, Glucocorticoid / genetics. Receptors, Mineralocorticoid / genetics. Reverse Transcriptase Polymerase Chain Reaction

MedlinePlus Health Information. consumer health - Pituitary Tumors.

MedlinePlus Health Information. consumer health - Steroids.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18818046.001).

[ISSN] 1879-0054

[Journal-full-title] Domestic animal endocrinology

[ISO-abbreviation] Domest. Anim. Endocrinol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Glucocorticoid; 0 / Receptors, Mineralocorticoid; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases

   

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

Hazardous Substances Data Bank. Corticotropin .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma.

Most contributions include a pituitary adenoma or a cyst/cystic tumor, particularly a Rathke cleft cyst.

The association of craniopharyngioma with an adenoma is particularly rare.

Among reported cases, some have included secondary prolactin cell hyperplasia due to pituitary stalk section effect.

Herein, we report two collision lesions, including a gonadotroph adenoma with adamantinomatous craniopharyngioma and a corticotroph adenoma with Rathke's cleft cyst.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Central Nervous System Cysts / complications. Corticotrophs / pathology. Craniopharyngioma / complications. Gonadotrophs / pathology. Pituitary Neoplasms / complications. Sella Turcica / pathology

Genetic Alliance. consumer health - Craniopharyngioma.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] No Shinkei Geka. 2005 Aug;33(8):797-803 [16095210.001]

[Cites] J Neurol Neurosurg Psychiatry. 1986 Nov;49(11):1305-7 [3794737.001]

[Cites] No To Shinkei. 1969 Dec;21(12):1326-9 [5395295.001]

[Cites] Arch Pathol. 1970 Nov;90(5):444-50 [5476241.001]

[Cites] Am J Clin Pathol. 2003 Nov;120(5):732-6 [14608900.001]

[Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]

[Cites] Oral Surg Oral Med Oral Pathol. 1959 Feb;12(2):199-205 [13633216.001]

[Cites] Am J Pathol. 2002 Dec;161(6):1997-2001 [12466115.001]

[Cites] Arch Pathol Lab Med. 1994 May;118(5):562-5 [8192565.001]

[Cites] Arch Dis Child. 1987 Oct;62(10):1077-8 [2823728.001]

[Cites] Endocr Rev. 2006 Jun;27(4):371-97 [16543382.001]

[Cites] J Pathol. 2004 Jul;203(3):814-21 [15221941.001]

[Cites] JAMA. 1978 Aug 4;240(5):471-3 [660898.001]

[Cites] J Neurosurg. 1966 Aug;25(2):199-204 [5296495.001]

[Cites] Endocr Rev. 1998 Dec;19(6):798-827 [9861546.001]

[Cites] Intern Med J. 2004 Sep-Oct;34(9-10):573-6 [15482272.001]

[Cites] Cancer. 1978 Jan;41(1):337-43 [626939.001]

[Cites] No Shinkei Geka. 1984 Jun;12(7):833-8 [6483092.001]

[Cites] Anat Rec. 1951 Feb;109(2):217-31 [14811058.001]

[Cites] Virchows Arch A Pathol Anat Histopathol. 1983;399(1):49-59 [6299000.001]

[Cites] Acta Neuropathol. 2005 Jun;109(6):589-97 [15891929.001]

[Cites] No Shinkei Geka. 1987 Dec;15(12):1313-8 [3448501.001]

[Cites] Mayo Clin Proc. 1989 Sep;64(9):1077-84 [2811485.001]

[Cites] No Shinkei Geka. 1986 Mar;14 (3 Suppl):435-40 [3703147.001]

[Cites] Endocrinology. 2002 Nov;143(11):4429-36 [12399440.001]

[Cites] Neuroradiology. 2001 Sep;43(9):755-9 [11594426.001]

[Cites] Endocr Pathol. 2001 Summer;12(2):125-36 [11579678.001]

[Cites] J Neurosurg. 2004 Jan;100(1):33-40 [14743909.001]

[Cites] Oral Surg Oral Med Oral Pathol. 1983 Nov;56(5):502-11 [6196702.001]

[Cites] Surg Neurol. 1989 May;31(5):381-6 [2711312.001]

[Cites] J Neurosurg. 2003 Jan;98(1):162-4 [12546365.001]

[Cites] J Neurol Neurosurg Psychiatry. 1975 Aug;38(8):782-6 [1185198.001]

[Cites] Neurosurgery. 1987 Sep;21(3):371-7 [3670583.001]

[Cites] J Neurosurg. 1966 Jan;24(1):77-81 [5903300.001]

[Cites] Neurosurgery. 1985 Oct;17(4):657-9 [4058703.001]

[Cites] Clin Endocrinol (Oxf). 2005 Apr;62(4):397-409 [15807869.001]

[Cites] J Pathol. 1971 Mar;103(3):185-7 [5567175.001]

[Cites] Br J Neurosurg. 1995;9(1):51-5 [7786427.001]

[Cites] J Neurooncol. 2005 Jul;73(3):205-9 [15980970.001]

[Cites] Cancer. 1972 Feb;29(2):423-30 [5013542.001]

[Cites] J Clin Endocrinol Metab. 1997 Jul;82(7):2357-62 [9215319.001]

[Cites] Pediatr Neurosurg. 1994;21 Suppl 1:2-10 [7841074.001]

[Cites] J Neurosurg. 1994 Jun;80(6):1018-25 [8189257.001]

[Cites] J Neurosurg. 1998 Oct;89(4):547-51 [9761047.001]

[Cites] No Shinkei Geka. 1987 Sep;15(9):999-1003 [3320806.001]

[Cites] Zh Vopr Neirokhir Im N N Burdenko. 1981 Nov-Dec;(6):52-4 [7336839.001]

[Cites] J Neurosurg. 2005 Apr;102(3 Suppl):318-21 [15881759.001]

[Cites] J Pathol Bacteriol. 1955 Jan-Apr;69(1-2):141-5 [13243181.001]

[Cites] Arch Pathol. 1960 Sep;70:293-9 [13850582.001]

[Cites] Cancer. 1976 Apr;37(4):1944-52 [1260697.001]

[Cites] Neurosurgery. 2000 Feb;46(2):291-302; discussion 302-5 [10690718.001]

[Cites] Cancer Genet Cytogenet. 1992 Mar;59(1):12-9 [1313329.001]

[Cites] Surg Neurol. 1994 Aug;42(2):112-6 [8091286.001]

[Cites] Cancer Genet Cytogenet. 1992 Jun;60(2):212-3 [1606570.001]

[Cites] Pituitary. 2004;7(1):39-44 [15638297.001]

[Cites] Endocr Pathol. 2002 Summer;13(2):157-65 [12165665.001]

[Cites] Intern Med. 1997 Feb;36(2):107-12 [9099592.001]

[Cites] Acta Neuropathol. 1992;83(2):211-5 [1557952.001]

[Cites] J Neurosurg. 1988 Oct;69(4):620-3 [3418397.001]

[Cites] Neurosci Lett. 2001 Sep 7;310(1):5-8 [11524144.001]

[Cites] Neurol Med Chir (Tokyo). 1993 Sep;33(9):643-50 [7505406.001]

(PMID = 17917812.001).

[ISSN] 1386-341X

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 65

   

[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.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma.

CONTEXT: Methods for preoperative diagnosis of prohormone convertase 2 (PC2)-positive ACTH-producing pituitary adenomas (APPAs) have not been established.

Also, their characteristics are not evident.

OBJECTIVE: This study was designed to understand the meaning of plasma alphaMSH levels and the role of cell proliferation-signaling molecules in PC2-positive APPAs.

RESULTS: Nine adenomas (47.4%) were immunopositive for PC2 and were large and invasive in nature.

Eight adenomas (42.1%) were immunopositive for both PC2 and p-Akt, and seven others (36.8%) were immunonegative for both, suggesting significant coexpression of PC2 and p-Akt in tumors.

Quantitative RT-PCR revealed that PC2 expression is associated with phosphorylation of Akt but not with its gene expression.

Most APPAs expressed receptor tyrosine kinases, but membrane-bound receptors could not be identified.

CONCLUSIONS: Our study suggests that PC2 expression and Akt phosphorylation are related at the molecular level, resulting in a change in cell cycle and an increase in pituitary adenoma size.

An elevation of plasma alphaMSH could conjecture the activation of the phosphatidylinositol 3/Akt cascade in PC2-positive APPAs and may become a valuable clinical marker of tumor growth in Cushing's disease.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Proprotein Convertase 2 / metabolism. alpha-MSH / blood

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20501680.001).

[ISSN] 1945-7197

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / RNA, Messenger; 581-05-5 / alpha-MSH; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.21.94 / Proprotein Convertase 2

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Ghrelin is produced by and directly activates corticotrope cells from adrenocorticotropin-secreting adenomas.

CONTEXT: In Cushing's disease, ACTH hypersecretion by pituitary corticotrope adenoma cells and resulting hypercortisolism is accompanied by a severely blunted GH secretory response.

Interestingly, in Cushing's disease, ghrelin markedly increases plasma ACTH, whereas its stimulatory action on GH secretion is reduced.

Although the reported expression of ghrelin receptors (GHS-R) in corticotrope tumors offers a potential mechanism for ghrelin-induced ACTH hypersecretion, studies on the direct effects of synthetic GH secretagogues on corticotropinoma cells offered contradictory results.

OBJECTIVE AND DESIGN: To evaluate the direct action of ghrelin on corticotropinoma cells from two patients with Cushing's disease, we measured its effect on free cytosolic calcium concentration ([Ca(2+)](i)).

Additionally, expression of GHS-R and its ligand ghrelin was examined in these cells and in five additional corticotropinomas.

RESULTS: Ghrelin (10(-6) m) induced a marked [Ca(2+)](i) increase in 89.5% (case 1; n = 19 cells) and 85% (case 2; n = 13 cells) of corticotropinoma cells.

Moreover, RT-PCR showed that expression of GHS-R isoforms is accompanied by that of ghrelin in all seven corticotrope adenomas examined.

Importantly, double immunogold electron microscopy revealed that ghrelin is costored within ACTH secretory vesicles in densely granulated adenomatous corticotropes.

CONCLUSIONS: These results constitute the first demonstration that ghrelin acts directly on corticotrope tumor cells derived from patients with Cushing's disease.

The presence of ghrelin and GHS-R suggests that pituitary ghrelin may play an autocrine/paracrine role in regulating ACTH release in Cushing's disease.

Our findings provide a plausible cellular basis for the exaggerated ACTH response to ghrelin in Cushing's disease and suggest novel research strategies to develop medical treatments for this disease.

[MeSH-major] Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Peptide Hormones / physiology. Pituitary Neoplasms / secretion

MedlinePlus Health Information. consumer health - Pituitary Tumors.

Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16551736.001).

[ISSN] 0021-972X

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; SY7Q814VUP / Calcium

   

[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

Genetic Alliance. consumer health - X-linked adrenal hypoplasia congenita.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 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

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17280594.001).

[ISSN] 0953-8194

[Journal-full-title] Journal of neuroendocrinology

[ISO-abbreviation] J. Neuroendocrinol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Magnetic resonance imaging characteristics and surgical results of adrenocorticotropin-secreting pituitary adenomas.

OBJECTIVE: To evaluate magnetic resonance imaging (MRI) characteristics and surgical results of adrenocorticotropin (ACTH)-secreting pituitary adenomas.

METHODS: MRI characteristics and relationship between MRI positive rate and surgical results of 266 patients with pathologically confirmed Cushing's disease were analyzed retrospectively.

All patients underwent thin-section sagittal and coronal scans of the pituitary gland before and after administration of gadolinium-diethylene triamine pentaacetic acid (Gd-DTPA) on a 1.5 Tesla MRI scanner, and dynamic enhanced MRI was performed in 39 patients.

RESULTS: Preoperative MRI revealed normal results in 41 (15.4%) cases, microadenoma in 179 (67.3%), macroadenoma in 42 (15.8%), and huge adenoma in 4 (1.5%).

Pituitary apoplexy was found in 13 (4.9%) cases.

Positive rate of ACTH-secreting adenomas was 84.6% (225/266) on MRI scans, and that of small microadenomas was 87.2% (34/39) on dynamic enhanced MRI scans.

Preoperative endocrinological tests of 199 cases supported the diagnosis of typical Cushing's disease, while the other 67 cases had atypical endocrinological results.

CONCLUSIONS: Enhanced coronal pituitary MRI is helpful for preoperative localization of ACTH-secreting pituitary microadenoma.

MedlinePlus Health Information. consumer health - MRI Scans.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18437910.001).

[ISSN] 1001-9294

[Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih

[ISO-abbreviation] Chin. Med. Sci. J.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] China

[Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Endocr Pathol. 2003 Winter;14(4):363-8 [14739492.001]

[Cites] Neuropathology. 2001 Dec;21(4):288-93 [11837535.001]

[Cites] Ultrastruct Pathol. 1994 Jan-Apr;18(1-2):171-9 [8191623.001]

[Cites] Am J Pathol. 1984 Dec;117(3):429-40 [6095670.001]

[Cites] Ultrastruct Pathol. 1990 Nov-Dec;14(6):475-82 [2281546.001]

[Cites] Mod Pathol. 2002 Oct;15(10):1102-5 [12379758.001]

[Cites] Endocrinol Jpn. 1991 Jun;38(3):271-8 [1665412.001]

[Cites] Clin Endocrinol (Oxf). 1997 Jun;46(6):669-79 [9274697.001]

[Cites] Clin Endocrinol (Oxf). 1998 Oct;49(4):433-9 [9876339.001]

[Cites] Acta Neuropathol. 2001 Nov;102(5):435-40 [11699555.001]

(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

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Craniofac Surg. 2003 Jan;14(1):13-28 [12544216.001]

[Cites] Am J Med Genet. 2002 Sep 1;111(4):388-91 [12210297.001]

[Cites] Horm Res. 2003;60(4):168-73 [14530604.001]

[Cites] Am J Phys Anthropol. 1974 Nov;41(3):423-9 [4473903.001]

[Cites] Am J Med Genet. 1980;7(1):47-74 [7211952.001]

[Cites] Am J Med Genet. 1983 Mar;14(3):557-65 [6859106.001]

[Cites] J Craniofac Genet Dev Biol. 1985;5(3):229-38 [4044786.001]

[Cites] Clin Genet. 1993 Sep;44(3):129-38 [8275570.001]

[Cites] J Clin Endocrinol Metab. 1994 Nov;79(5):1498-502 [7962349.001]

[Cites] Am J Med Genet. 1998 Oct 2;79(4):294-304 [9781911.001]

[Cites] Am J Phys Anthropol. 1953 Mar;11(1):121-40 [13040508.001]

[Cites] Horm Metab Res. 2005 Jun;37(6):347-54 [16001326.001]

[Cites] J Clin Endocrinol Metab. 2005 Sep;90(9):5134-40 [15941871.001]

[Cites] J Clin Endocrinol Metab. 2006 Jan;91(1):221-4 [16219718.001]

[Cites] Eur J Endocrinol. 2006 May;154(5):753-8 [16645024.001]

[Cites] J Endocrinol Invest. 2006 Mar;29(3):208-13 [16682832.001]

[Cites] J Clin Endocrinol Metab. 2006 Sep;91(9):3316-23 [16787992.001]

[Cites] Genes Dev. 2006 Oct 15;20(20):2871-86 [17043312.001]

[Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R73-9 [17613551.001]

[Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R80-7 [17613552.001]

[Cites] Pediatrics. 2007 Sep;120(3):e575-86 [17698579.001]

[Cites] J Clin Endocrinol Metab. 2000 Aug;85(8):2701-8 [10946868.001]

[Cites] J Clin Endocrinol Metab. 2000 Dec;85(12):4556-61 [11134108.001]

[Cites] J Pediatr. 2001 Aug;139(2):215-9 [11487746.001]

[Cites] J Neurooncol. 2001 Sep;54(2):95-110 [11761437.001]

[Cites] Ann Med. 2002;34(3):179-91 [12173688.001]

[Cites] Front Neuroendocrinol. 2003 Apr;24(2):94-127 [12763000.001]

(PMID = 19344074.001).

[ISSN] 0334-018X

[Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM

[ISO-abbreviation] J. Pediatr. Endocrinol. Metab.

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00001595

[Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13; United States / NICHD NIH HHS / HD / Z01-HD-000642-04

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] Germany

[Other-IDs] NLM/ NIHMS310299; NLM/ PMC3143028

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Mol Cell Biol. 1997 Nov;17(11):6673-82 [9343431.001]

[Cites] Res Vet Sci. 2008 Aug;85(1):26-34 [17910968.001]

[Cites] Vet Surg. 1998 May-Jun;27(3):246-61 [9605236.001]

[Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):775-80 [10022452.001]

[Cites] Vet Rec. 1999 Jan 2;144(1):12-7 [10028568.001]

[Cites] Eur J Endocrinol. 2005 Apr;152(4):645-54 [15817922.001]

[Cites] Am J Physiol Endocrinol Metab. 2005 Aug;289(2):E278-87 [15769796.001]

[Cites] J Vet Intern Med. 2005 Sep-Oct;19(5):687-94 [16231713.001]

[Cites] Clin Endocrinol (Oxf). 2005 Nov;63(5):549-59 [16268808.001]

[Cites] J Vet Intern Med. 2005 Nov-Dec;19(6):810-5 [16355673.001]

[Cites] Res Vet Sci. 2006 Aug;81(1):24-30 [16271735.001]

[Cites] Endocrinology. 2006 Sep;147(9):4438-44 [16740975.001]

[Cites] Anal Biochem. 2006 Sep 1;356(1):36-43 [16844072.001]

[Cites] J Endocrinol. 2006 Sep;190(3):601-9 [17003261.001]

[Cites] Mod Pathol. 2001 Sep;14(9):892-9 [11557786.001]

[Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):117-23 [11231987.001]

[Cites] J Clin Invest. 2001 Oct;108(8):1123-31 [11602619.001]

[Cites] Eur J Endocrinol. 2002 May;146(5):707-16 [11980628.001]

[Cites] Domest Anim Endocrinol. 2002 Jun;22(4):201-10 [12044610.001]

[Cites] Ann N Y Acad Sci. 2002 Sep;970:119-33 [12381547.001]

[Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]

[Cites] Mol Cell Endocrinol. 2002 Nov 29;197(1-2):81-7 [12431800.001]

[Cites] Mol Cell Endocrinol. 2002 Nov 29;197(1-2):89-96 [12431801.001]

[Cites] Nat Rev Cancer. 2004 Apr;4(4):285-95 [15057288.001]

[Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85 [15070915.001]

[Cites] J Clin Endocrinol Metab. 2004 May;89(5):2452-62 [15126577.001]

[Cites] J Endocrinol. 1968 Jul;41(3):397-406 [5250268.001]

[Cites] Vet Pathol. 1980 Mar;17(2):109-22 [6244687.001]

[Cites] J Endocrinol. 1983 Feb;96(2):303-9 [6298337.001]

[Cites] Res Vet Sci. 1983 Mar;34(2):141-4 [6856991.001]

[Cites] Vet Rec. 1988 Feb 20;122(8):178-80 [3358285.001]

[Cites] Ann Intern Med. 1988 Sep 15;109(6):445-6 [3415103.001]

[Cites] Am J Vet Res. 1990 Aug;51(8):1280-5 [2201231.001]

[Cites] Clin Endocrinol (Oxf). 1994 Apr;40(4):479-84 [8187313.001]

[Cites] N Engl J Med. 1995 Mar 23;332(12):791-803 [7862184.001]

[Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3114-20 [7593411.001]

[Cites] Domest Anim Endocrinol. 1997 Mar;14(2):81-97 [9063651.001]

[Cites] J Endocrinol. 1997 Mar;152(3):387-94 [9071959.001]

[Cites] Vet Surg. 1997 Jul-Aug;26(4):295-309 [9232788.001]

[Cites] Genes Dev. 2006 Oct 15;20(20):2871-86 [17043312.001]

[Cites] J Clin Endocrinol Metab. 2006 Nov;91(11):4482-8 [16940446.001]

[Cites] J Neurosurg. 2007 Oct;107(4):830-40 [17937231.001]

[Cites] Mol Cell Endocrinol. 2008 May 14;286(1-2):69-74 [17977644.001]

[Cites] J Clin Endocrinol Metab. 1998 May;83(5):1619-23 [9589666.001]

(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

   

[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

Genetic Alliance. consumer health - Cushing's Syndrome.

MedlinePlus Health Information. consumer health - Cushing's Syndrome.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas.

OBJECTIVE: Galectin-3 (Gal-3) belongs to the family of carbohydrate-binding proteins with high affinity for galactoside and is involved in many biological processes including cell growth and differentiation, cell adhesion, tumor progression, apoptosis and metastasis.

The aim of this study was to disclose differences in the expression of Gal-3 in silent and functioning corticotroph pituitary adenomas.

DESIGN: We examined 30 pituitary adenomas (19 functioning corticotroph, 11 silent corticotroph adenomas).

Two prolactinomas and 2 functioning somatotroph adenomas served as positive controls.

The independent variables t-test was used for comparison of the mean expression of Gal-3 in the two different corticotroph adenoma subgroups.

RESULTS: Eighteen of the functioning corticotroph adenomas (94.73%) were positive for Gal-3 with a cytoplasmic and focally membranous distribution; two cases also exhibited nuclear expression, whereas 9 of the silent corticotroph adenomas (81.81%) had zero or<1% expression of Gal-3 (p=0.001).

CONCLUSIONS: Gal-3 is highly expressed in functioning corticotroph adenomas of the pituitary gland, while silent adenomas exhibit very focal to null expression of Gal-3.

This observation can be used in the pathological diagnosis to separate functioning from silent corticotroph adenomas of the pituitary.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / metabolism. Galectin 3 / metabolism

[MeSH-minor] Humans. Immunohistochemistry. Pituitary Gland / metabolism

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17724007.001).

[ISSN] 1109-3099

[Journal-full-title] Hormones (Athens, Greece)

[ISO-abbreviation] Hormones (Athens)

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3

   

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

Hazardous Substances Data Bank. Corticotropin .

Hazardous Substances Data Bank. MENOTROPINS .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Mod Pathol. 1998 Mar;11(3):232-8 [9521468.001]

[Cites] Neurosurgery. 2000 Sep;47(3):723-9; discussion 729-30 [10981760.001]

[Cites] Virchows Arch A Pathol Anat Histopathol. 1991;419(2):107-13 [1651583.001]

[Cites] Curr Med Chem. 2004 Oct;11(20):2651-65 [15544467.001]

[Cites] Pituitary. 2000 Oct;3(2):117-22 [11141695.001]

[Cites] Pituitary. 2001 Sep;4(4):215-21 [12501971.001]

[Cites] J Neurosurg. 2004 Nov;101(5):874-7 [15540932.001]

[Cites] J Neurosurg. 1990 Feb;72(2):262-7 [2153197.001]

[Cites] Pituitary. 2000 Oct;3(2):67-75 [11141698.001]

[Cites] Pituitary. 2001 Aug;4(3):127-8 [12138984.001]

[Cites] Neurosurg Clin N Am. 2003 Jan;14(1):25-39, vi [12690977.001]

[Cites] Mod Pathol. 2002 Oct;15(10):1102-5 [12379758.001]

[Cites] Am J Pathol. 1980 Mar;98(3):617-38 [6244736.001]

[Cites] Endocr J. 1993 Oct;40(5):571-9 [7951523.001]

[Cites] Brain Res. 1999 Nov 27;848(1-2):45-62 [10701998.001]

[Cites] Am J Pathol. 1995 May;146(5):1188-98 [7747813.001]

[Cites] Hum Pathol. 2004 Sep;35(9):1137-47 [15343517.001]

[Cites] J Clin Endocrinol Metab. 1988 Jun;66(6):1111-8 [3372677.001]

[Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):59-64 [12519413.001]

[Cites] J Histochem Cytochem. 2004 Jul;52(7):943-57 [15208361.001]

[Cites] Neurosurgery. 2003 Nov;53(5):1076-84; discussion 1084-5 [14580274.001]

[Cites] Endocrinology. 1994 Sep;135(3):854-62 [8070378.001]

[Cites] Pituitary. 2002;5(4):221-3 [14558669.001]

[Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3050-6 [12843142.001]

[Cites] Cell Tissue Res. 2001 Apr;304(1):43-9 [11383885.001]

[Cites] Science. 2002 Mar 22;295(5563):2231-5 [11910101.001]

[Cites] Pituitary. 1999 May;1(3-4):187-95 [11081197.001]

[Cites] Folia Histochem Cytobiol. 2004;42(4):245-7 [15704652.001]

[Cites] Zoolog Sci. 2003 Oct;20(10):1183-98 [14569141.001]

[Cites] Endocr Pathol. 1996 Summer;7(2):145-150 [12114642.001]

[Cites] Virchows Arch A Pathol Anat Histopathol. 1988;413(1):61-8 [2453972.001]

[Cites] J Neurosurg. 1998 Jun;88(6):1111-5 [9609310.001]

[Cites] Am J Med. 1978 Mar;64(3):492-9 [76447.001]

(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 3.4.21.- / Proprotein Convertases

   

[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

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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.

Hazardous Substances Data Bank. HYDROCORTISONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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

MedlinePlus Health Information. consumer health - Cushing's Syndrome.

Hazardous Substances Data Bank. HYDROCORTISONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Ann Intern Med. 1990 May 15;112(10):738-42 [2158760.001]

[Cites] N Engl J Med. 1991 Sep 26;325(13):897-905 [1652686.001]

[Cites] J Endocrinol Invest. 1996 Feb;19(2):131-5 [8778166.001]

[Cites] Acta Endocrinol (Copenh). 1985 Nov;110(3):302-7 [3000119.001]

[Cites] Acta Endocrinol (Copenh). 1986 Jul;112(3):323-8 [3751453.001]

[Cites] Am J Med. 1981 Aug;71(2):302-6 [6266251.001]

[Cites] J Clin Endocrinol Metab. 1990 Jun;70(6):1637-43 [2161425.001]

[Cites] J Clin Endocrinol Metab. 1984 Jun;58(6):1106-10 [6327752.001]

[Cites] N Engl J Med. 1988 Apr 14;318(15):966-70 [2832758.001]

[Cites] J Clin Endocrinol Metab. 1980 May;50(5):961-6 [6246139.001]

[Cites] J Clin Endocrinol Metab. 1984 Jan;58(1):25-31 [6315761.001]

[Cites] Lancet. 1986 Sep 6;2(8506):540-4 [2875282.001]

[Cites] Recent Prog Horm Res. 1969;25:283-314 [4310919.001]

(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

   

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

Hazardous Substances Data Bank. HYDROCORTISONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[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

Genetic Alliance. consumer health - Cushing's Syndrome.

MedlinePlus Health Information. consumer health - Cushing's Syndrome.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16618978.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

Hazardous Substances Data Bank. HYDROCORTISONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[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.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

Hazardous Substances Data Bank. Corticotropin .

ORBi (University of Liege). Free full Text at ORBi .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15817922.001).

[ISSN] 0804-4643

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease.

Cushing's syndrome can present a complex problem of differential diagnosis.

Of cases in which hypercortisolemia results from an adrenocorticotropic hormone (ACTH)-dependent process, approximately 80% are due to a pituitary adenoma (Cushing's disease [CD]), 10% are due to adrenal lesions, and the remaining 10% are secondary to ectopic ACTH secretion.

For patients with CD, surgical removal of the pituitary adenoma is the treatment of choice.

Thus, localization of the source of ACTH secretion is critical in guiding timely treatment decisions.

Inferior petrosal sinus sampling (IPSS) is considered to be the gold standard for confirming the origin of ACTH secretion in patients with Cushing's syndrome.

A number of other techniques are discussed including sampling from the cavernous sinus, the jugular vein, and multiple sites to aid the diagnosis and lateralization of ACTH-producing pituitary adenomas.

[MeSH-major] Petrosal Sinus Sampling / methods. Pituitary ACTH Hypersecretion / diagnosis

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17961020.001).

[ISSN] 1092-0684

[Journal-full-title] Neurosurgical focus

[ISO-abbreviation] Neurosurg Focus

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone

[Number-of-references] 46

   

[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

Genetic Alliance. consumer health - Cushing's Syndrome.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas.

OBJECTIVE: The prevalence of silent corticotroph adenomas (SCAs) is not rare among nonfunctioning pituitary adenomas (NFPAs); however, it is unknown whether the clinical significance of SCAs differs from that of NFPAs without ACTH immunoreactivity (non-SCAs).

MEASUREMENTS: We analysed whether clinical manifestations at diagnosis, postoperative recurrence rate and recurrence characteristics differed between SCA and non-SCA patients.

The mean age at the time of diagnosis was 44 years (range, 13-67 years) in the SCA group and 50 years (18-79 years) in the non-SCA group (P = 0.026), with respective follow-up periods of 5.2 (range, 1.0-16.0 years) and 4.2 years (0.5-16.1 years) (P = 0.255).

[MeSH-major] Adenoma / pathology. Adrenocorticotropic Hormone / analysis. Neoplasm Recurrence, Local. Pituitary Neoplasms / pathology

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19650787.001).

[ISSN] 1365-2265

[Journal-full-title] Clinical endocrinology

[ISO-abbreviation] Clin. Endocrinol. (Oxf)

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] England

[Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Current state of the art in the diagnosis and surgical treatment of Cushing disease: early experience with a purely endoscopic endonasal technique.

OBJECT: Transsphenoidal pituitary surgery is the primary therapy for Cushing disease because of its potential to produce lasting remission without the need for long-term drug or hormone replacement therapy.

The authors evaluated the current role of pure endoscopic endonasal pituitary surgery in the treatment of Cushing disease.

METHODS: Twenty-five patients underwent pure endoscopic surgery for confirmed Cushing disease.

Final histological results were consistent with adrenocorticotropin hormone (ACTH)-secreting adenoma in 20 patients.

Three patients presented with new anterior pituitary deficiency, but no one had permanent diabetes insipidus.

Treatment failure was attributable to involvement of the cavernous sinus in two patients, incomplete tumor removal in one, negative exploration in one, and nodular corticotroph hyperplasia of the pituitary gland in one.

CONCLUSIONS: Early results indicated that endoscopic endonasal surgery is a safe and effective treatment for ACTH-producing adenomas.

Further studies with a larger number of patients and longer follow-ups are required to determine whether this more minimally invasive pure endoscopic approach should become the standard of care for the surgical treatment of Cushing disease.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Endoscopy. Paranasal Sinuses / surgery. Pituitary ACTH Hypersecretion / diagnosis. Pituitary ACTH Hypersecretion / surgery

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17961027.001).

[ISSN] 1092-0684

[Journal-full-title] Neurosurgical focus

[ISO-abbreviation] Neurosurg Focus

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The effects of SOM230 on cell proliferation and adrenocorticotropin secretion in human corticotroph pituitary adenomas.

CONTEXT: There is no tumor-directed medical therapy available for Cushing's disease.

OBJECTIVE: The objective was to determine the in vitro effect of the somatostatin analog pasireotide (SOM230) on cell proliferation in human corticotroph tumors.

DESIGN/METHODS: Expression of somatostatin receptors (SSTR 1-5) was determined by quantitative RT-PCR in 13 human corticotroph tumors and by immunohistochemistry (IHC) in 12 of the 13 tumors.

SOM230 effects on cell proliferation and ACTH release were evaluated in vitro using primary cultures of six of the 13 human corticotroph adenomas.

RESULTS: In our series, we found expression of SSTR subtypes 1, 2, 4, and 5 in human corticotroph tumors by quantitative RT-PCR.

Significant suppression of cell proliferation was observed in all tumors cultured (percent suppression range: 10-70%; P = 0.045-0.001).

SOM230 inhibited ACTH secretion in five of the six tumors cultured (percent suppression range: 23-56%; P = 0.042-0.001).

CONCLUSION: Corticotroph tumors express multiple SSTR subtypes.

SOM230 significantly suppressed cell proliferation and ACTH secretion in primary cultures of human corticotroph tumors.

These in vitro results support the hypothesis that SOM230 may have a role in the medical therapy of corticotroph tumors.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenocorticotropic Hormone / secretion. Cell Proliferation / drug effects. Somatostatin / analogs & derivatives

[MeSH-minor] Adolescent. Adult. Child. Female. Humans. Immunohistochemistry. In Vitro Techniques. Male. Middle Aged. Pituitary ACTH Hypersecretion / drug therapy. RNA, Messenger / metabolism. Receptors, Somatostatin / metabolism. Tumor Cells, Cultured

COS Scholar Universe. author profiles.

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

Hazardous Substances Data Bank. Corticotropin .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16940446.001).

[ISSN] 0021-972X

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Grant] United States / Intramural NIH HHS / /

[Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

Genetic Alliance. consumer health - Cushing's Syndrome.

Hazardous Substances Data Bank. ROSIGLITAZONE .

Hazardous Substances Data Bank. HYDROCORTISONE .

Hazardous Substances Data Bank. Corticotropin .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 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

   

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Neurosurgery. 2000 Sep;47(3):723-9; discussion 729-30 [10981760.001]

[Cites] J Clin Endocrinol Metab. 2004 Nov;89(11):5649-54 [15531524.001]

[Cites] Rev Med Chil. 1998 Dec;126(12 ):1497-501 [10349165.001]

[Cites] Endocrinol Metab Clin North Am. 1993 Jun;22(2):291-302 [8325288.001]

[Cites] Neurosurgery. 1993 Oct;33(4):602-8; discussion 608-9 [8232799.001]

[Cites] Clin Endocrinol (Oxf). 2003 May;58(5):545-9 [12699434.001]

[Cites] J Clin Endocrinol Metab. 2000 May;85(5):1789-93 [10843153.001]

[Cites] J Clin Endocrinol Metab. 1986 Jun;62(6):1173-9 [3009521.001]

[Cites] Neurosurg Focus. 2004 Apr 15;16(4):E6 [15191335.001]

[Cites] J Clin Endocrinol Metab. 2002 Jun;87(6):2745-50 [12050244.001]

[Cites] Eur J Endocrinol. 2003 Sep;149(3):195-200 [12943521.001]

[Cites] J Clin Endocrinol Metab. 1990 Aug;71(2):323-8 [2166068.001]

[Cites] Neurosurg Focus. 2007;23(3):E6 [17961022.001]

[Cites] Endocr Rev. 1980 Winter;1(1):100-7 [6785084.001]

[Cites] Arch Intern Med. 1992 Sep;152(9):1893-9 [1520058.001]

[Cites] Neurosurgery. 2005;56(1):65-72; discussion 72-3 [15617587.001]

[Cites] Clin Neurol Neurosurg. 2007 Jan;109(1):63-70 [16488532.001]

[Cites] Pituitary. 2004;7(3):157-163 [16010459.001]

[Cites] J Clin Endocrinol Metab. 1994 Aug;79(2):348-54 [8045946.001]

[Cites] J Intensive Care Med. 2008 Mar-Apr;23(2):75-90 [18372348.001]

[Cites] Acta Neurochir (Wien). 1993;120(3-4):118-22 [8460561.001]

[Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4963-9 [15886242.001]

[Cites] Pituitary. 2008;11(4):391-401 [18320327.001]

[Cites] Clin Endocrinol (Oxf). 2006 Mar;64(3):319-22 [16487443.001]

[Cites] Clin Endocrinol (Oxf). 1999 Aug;51(2):181-8 [10468988.001]

(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

   

[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

MedlinePlus Health Information. consumer health - After Surgery.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Indian Pediatr. 1981 Dec;18(12):918-21 [7343489.001]

[Cites] Neurol Neurochir Pol. 1993 Nov-Dec;27(6):839-42 [8164779.001]

[Cites] Pediatr Neurosurg. 1991-1992;17(6):284-303 [1668642.001]

[Cites] Acta Endocrinol (Copenh). 1990 Oct;123(4):423-30 [2173325.001]

[Cites] Eur J Pediatr. 1985 Jan;143(3):221-3 [3987721.001]

[Cites] Ann Intern Med. 1988 Sep 15;109(6):487-93 [2843068.001]

[Cites] Pediatr Neurosurg. 1999 Jul;31(1):7-11 [10545816.001]

[Cites] Eur J Pediatr. 1983 Dec;141(2):101-8 [6662137.001]

[Cites] Acta Neurochir Suppl (Wien). 1985;35:101-5 [3004116.001]

[Cites] Pediatr Radiol. 1996;26(1):48-50 [8598995.001]

[Cites] J Clin Endocrinol Metab. 1979 Jun;48(6):1017-25 [221523.001]

[Cites] J Clin Endocrinol Metab. 1999 Dec;84(12):4385-9 [10599692.001]

[Cites] Neurosurgery. 1991 Oct;29(4):509-14 [1944830.001]

[Cites] Am J Dis Child. 1982 Jul;136(7):605-7 [7091088.001]

[Cites] Pediatr Radiol. 1982;12 (2):81-3 [7099745.001]

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Medical therapy of Cushing's disease: where are we now?

The goals of ideal medical therapy for Cushing's disease should be to target the aetiology of the disorder, and thus surgery is the current 'gold standard' treatment.

However, no effective drug that directly and effectively targets the adrenocorticotropin-secreting pituitary adenoma has been found to date, and treatments to control the hypercortisolaemic state by adrenal-based therapy are frequently used.

Inhibitors of adrenal steroidogenesis, adrenolytic agents, compounds with neuromodulatory properties, and ligands of different nuclear hormone receptors involved in hypothalamo-pituitary regulation currently used have been reviewed.

The somatostatin analogue pasireotide and the dopamine agonist cabergoline, as well as their combination, show some therapeutic promise, while retinoic acid analogues should be further investigated in the pituitary-targeted medical therapy of Cushing's disease.

Since a percentage of patients treated with surgery are not cured, or improve and subsequently relapse, there is an urgent need for effective medical therapies for this disorder.

[MeSH-major] Pituitary ACTH Hypersecretion / drug therapy

Hazardous Substances Data Bank. HYDROCORTISONE .

Hazardous Substances Data Bank. MITOTANE .

Hazardous Substances Data Bank. METYRAPONE .

Hazardous Substances Data Bank. KETOCONAZOLE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2010 S. Karger AG, Basel.

(PMID = 20616508.001).

[ISSN] 0301-3073

[Journal-full-title] Frontiers of hormone research

[ISO-abbreviation] Front Horm Res

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Dopamine Agonists; 320T6RNW1F / Mifepristone; 51110-01-1 / Somatostatin; 78E4J5IB5J / Mitotane; R9400W927I / Ketoconazole; WI4X0X7BPJ / Hydrocortisone; ZS9KD92H6V / Metyrapone

[Number-of-references] 50

   

[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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Endocrinol Metab. 1999 Apr;84(4):1414-9 [10199788.001]

[Cites] Mol Cell Biol. 1997 Nov;17(11):6673-82 [9343431.001]

[Cites] Mol Cell Endocrinol. 2001 Dec 20;185(1-2):1-16 [11738789.001]

[Cites] J Clin Endocrinol Metab. 1999 Apr;84(4):1351-6 [10199778.001]

[Cites] Genes Dev. 2003 Mar 15;17(6):711-6 [12651888.001]

[Cites] J Biol Chem. 2003 Nov 21;278(47):46523-32 [12970370.001]

[Cites] Mod Pathol. 2002 Jan;15(1):11-7 [11796836.001]

[Cites] J Clin Endocrinol Metab. 1999 Jun;84(6):2212-20 [10372733.001]

[Cites] Mod Pathol. 2002 Oct;15(10):1102-5 [12379758.001]

[Cites] Mol Cell Biol. 2000 Jul;20(13):4826-37 [10848608.001]

[Cites] Mod Pathol. 2001 Sep;14(9):892-9 [11557786.001]

[Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1323-31 [15613420.001]

[Cites] Cell. 2001 Mar 23;104(6):849-59 [11290323.001]

[Cites] J Clin Endocrinol Metab. 2000 Jul;85(7):2537-42 [10902805.001]

[Cites] J Endocrinol Invest. 2003 Oct;26(10):957-65 [14759067.001]

[Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):3097-107 [11443173.001]

[Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3050-6 [12843142.001]

[Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):6080-7 [14671214.001]

[Cites] Mol Endocrinol. 2005 May;19(5):1329-42 [15695370.001]

[Cites] Pituitary. 1999 May;1(3-4):159-68 [11081194.001]

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Detection of adrenocorticotropin-secreting pituitary adenomas by magnetic resonance imaging in children and adolescents with cushing disease.

CONTEXT: We recently showed that pre- and postcontrast spoiled gradient-recalled acquisition in the steady-state (SPGR) was superior to conventional pre- and postcontrast T-1 weighted spin echo (SE) acquisition magnetic resonance imaging (MRI) for the diagnostic evaluation of pituitary tumors in adult patients.

OBJECTIVE: The present investigation assessed the use of SPGR vs. SE-MRI in the diagnostic evaluation of ACTH-secreting tumors in children and adolescents with Cushing disease.

PATIENTS: Thirty children with Cushing disease (13 females and 17 males with a mean age of 12 +/- 3 yr) were studied.

Postcontrast SPGR-MRI identified the location of the tumor in 18 of 28 patients, whereas postcontrast SE-MRI identified the location and accurately estimated the size of the tumor in only five patients (P < 0.001).

CONCLUSIONS: We conclude that conventional MRI, even with contrast enhancement, mostly failed to identify ACTH-secreting microadenomas in children and adolescents with Cushing disease.

Postcontrast SPGR-MRI was superior to SE-MRI and should be used in addition to conventional SE-MRI in the pituitary evaluation of children and adolescents with suspected Cushing disease.

[MeSH-major] Adenoma / diagnosis. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Cushing Syndrome / diagnosis. Magnetic Resonance Imaging. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secretion

MedlinePlus Health Information. consumer health - Cushing's Syndrome.

MedlinePlus Health Information. consumer health - MRI Scans.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15941871.001).

[ISSN] 0021-972X

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] United States

[Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone

   

[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

Genetic Alliance. consumer health - Cushing's Syndrome.

MedlinePlus Health Information. consumer health - Cushing's Syndrome.

Hazardous Substances Data Bank. PREDNISONE .

Hazardous Substances Data Bank. METHYLPREDNISOLONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

MedlinePlus Health Information. consumer health - Cushing's Syndrome.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16195406.001).

[ISSN] 0013-7227

[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 / BMP4 protein, human; 0 / Bmp4 protein, mouse; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 5688UTC01R / Tretinoin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical and biochemical characteristics of adrenocorticotropin-secreting macroadenomas.

CONTEXT: Cushing's disease as a result of a pituitary macroadenoma is an uncommon cause of Cushing's syndrome, and reports in the published literature are few and of limited size.

OBJECTIVE: Our objective was to establish the clinical and biochemical characteristics of macroadenomas associated with Cushing's disease compared with a large cohort of microadenomas and to assess their response to therapy.

PATIENTS: Patients had Cushing's disease presenting with a pituitary macroadenoma, in comparison with a large group of microadenoma patients.

MAIN OUTCOME MEASURES: Outcome measures included basal and dynamically responsive plasma ACTH and cortisol levels and response to treatment.

RESULTS: We identified 18 patients with Cushing's disease secondary to a macroadenoma; basal 0900 h plasma ACTH was 135.8 +/- 32.5 and 45.0 +/- 4.3 ng/liter (mean +/- SEM), respectively, in macroadenomas and microadenomas (P = 0.013).

Testing with high-dose dexamethasone showed less suppression in the macroadenomas (57.6 +/- 8.7% vs. 74.4 +/- 2.1%; P = 0.02) and an attenuated ACTH response to CRH.

CONCLUSIONS: Pituitary macroadenomas causing Cushing's disease have biochemical features largely distinct from patients harboring microadenomas but represent one end of a continuum.

[MeSH-major] Adenoma / metabolism. Adrenal Gland Neoplasms / metabolism. Adrenocorticotropic Hormone / secretion. Pituitary ACTH Hypersecretion / metabolism

[MeSH-minor] Adult. Combined Modality Therapy. Female. Humans. Hydrocortisone / blood. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Tomography, X-Ray Computed. Treatment Outcome

MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.

Hazardous Substances Data Bank. HYDROCORTISONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15886242.001).

[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] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pituitary tumor type affects the chance of biochemical remission after radiosurgery of hormone-secreting pituitary adenomas.

OBJECTIVE: Reported biochemical remission rates have ranged widely after stereotactic radiosurgery for patients with hormone-secreting pituitary adenomas.

Confounding variables include histology, radiation dose, use of pituitary-suppressive medications, and length of follow-up.

METHODS: A retrospective review of 46 patients with pituitary adenomas (growth hormone-secreting, n = 27; prolactin-secreting, n = 11; adrenocorticotropin-secreting, n = 8) undergoing radiosurgery between January 1990 and December 2003 was conducted.

All received a tumor margin dose of 18 Gy or more and were off pituitary-suppressive medications for at least 1 month before radiosurgery.

RESULTS: The 4-year remission rates were 87% for patients with Cushing's disease, 67% for patients with acromegaly, and 18% for patients with prolactinomas.

Patients with oversecretion of adrenocorticotropin or growth hormone were more likely to achieve remission after radiosurgery than patients with prolactinomas (hazard ratio, 4.4; 95% confidence interval, 1.1-18.2; P = 0.04).

Of 44 patients with normal or partial anterior pituitary function before radiosurgery, 16 (36%) developed one or more new anterior pituitary deficits.

The incidence of new anterior pituitary deficits was 26% at 4 years.

CONCLUSION: There seems to be a differential sensitivity after radiosurgery for hormone-secreting pituitary adenomas.

Remission rates are greater for patients with Cushing's disease and acromegaly, whereas radiosurgery is less effective in achieving biochemical remission for patients with prolactinomas.

[MeSH-major] Adenoma / metabolism. Adenoma / surgery. Pituitary Hormones / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / surgery. Radiosurgery

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Neurosurgery. 2010 May;66(5):E1030; author reply E1030 [20404679.001]

(PMID = 18824993.001).

[ISSN] 1524-4040

[Journal-full-title] Neurosurgery

[ISO-abbreviation] Neurosurgery

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Pituitary Hormones