[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 14 of about 14
1. Pecori Giraldi F, Andrioli M, De Marinis L, Bianchi A, Giampietro A, De Martin M, Sacco E, Scacchi M, Pontecorvi A, Cavagnini F: Significant GH deficiency after long-term cure by surgery in adult patients with Cushing's disease. Eur J Endocrinol; 2007 Feb;156(2):233-9
Hazardous Substances Data Bank. (L)-ARGININE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Impaired GH secretion usually accompanies Cushing's syndrome and a variable proportion of patients reportedly fail to recover normal GH secretion after successful treatment.
  • This wide variability is most probably due to differences in the treatment (i.e. surgery and/or radiotherapy), timing of patient re-evaluation after surgery and dynamic tests employed to challenge GH secretion, and hinders a precise assessment of risk of GH deficiency after cure.
  • The aim of the present study is to evaluate GH secretory status after long-term cure of Cushing's disease achieved by surgery alone.
  • Patients were studied 2-20 years (median 3.3 years) following remission of hypercortisolism; all patients underwent transsphenoidal surgery with the removal of an ACTH-secreting adenoma; repeat pituitary surgery for relapse was performed in two patients while bilateral adrenalectomy was necessary in two patients.
  • At the time of testing, 13 patients were still on steroid replacement therapy.
  • Studies on the clinical impact of GH deficiency and the use of GH replacement therapy seem warranted in patients cured from Cushing's disease.

  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17287413.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9034-39-3 / Growth Hormone-Releasing Hormone; 94ZLA3W45F / Arginine
  •  go-up   go-down


2. Petrossians P, Thonnard AS, Beckers A: Medical treatment in Cushing's syndrome: dopamine agonists and cabergoline. Neuroendocrinology; 2010;92 Suppl 1:116-9
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).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical treatment in Cushing's syndrome: dopamine agonists and cabergoline.
  • Since this action may also appear in a number of secretory tumors in various locations, DA agonists have elicited some interest as a medical treatment for hypercorticism.
  • Non-iatrogenic Cushing's syndromes are due in 70% of the cases to a pituitary adrenocorticotropic hormone (ACTH)-producing adenoma, and, less frequently, to an adrenal adenoma or an ectopic ACTH secretion by a neuroendocrine tumor.
  • First-line treatment in Cushing's syndrome consists of the surgical removal of the secreting tumor.
  • However, surgery may not achieve a complete cure in a number of cases, hence emphasizing the potential benefit of a medical complementary treatment, which could also benefit patients as an alternative approach, either when waiting for, or when the patient is not eligible for surgery.
  • Clinical trials of DA agonists in Cushing's disease have shown an inhibitory effect of these drugs with an inhibition of ACTH secretion and/or a decrease of tumor size.
  • There are only a few cases of documented use of DA agonists in ectopic ACTH secretion, but when the tumor expresses DA receptors, DA agonists may represent a useful complementary treatment.
  • In conclusion, DA agonists represent a potential preparatory or complementary treatment for endogenous Cushing's syndrome, especially in Cushing's disease.
  • In the future, association of these drugs with somatostatin analogs may also prove beneficial.
  • [MeSH-major] Cushing Syndrome / drug therapy. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use

  • 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
  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829631.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


3. Biermasz NR, Smit JW, Pereira AM, Frölich M, Romijn JA, Roelfsema F: Acromegaly caused by growth hormone-releasing hormone-producing tumors: long-term observational studies in three patients. Pituitary; 2007;10(3):237-49
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • During medical treatment basal GH secretion remained (slightly) elevated and secretory regularity was decreased in 24 h blood sampling studies.
  • We did not observe development of tachyphylaxis towards the drug or radiological evidence of (growing) metastases.
  • We propose life-long suppressive therapy with somatostatin analogs in cases with persisting elevated serum GHRH concentrations after removal of the primary tumor.
  • Independent parameters of residual disease are elevated basal (nonpulsatile) GH secretion and decreased GH secretory regularity.
  • [MeSH-major] Acromegaly / etiology. Adenoma / secretion. Carcinoid Tumor / secretion. Human Growth Hormone / secretion. Lung Neoplasms / secretion. Pancreatic Neoplasms / secretion. Paraneoplastic Endocrine Syndromes / metabolism. Parathyroid Neoplasms / secretion
  • [MeSH-minor] Adult. Entropy. Female. Hormones / blood. Humans. Longitudinal Studies. Magnetic Resonance Imaging. Male. Middle Aged. Octreotide. Pituitary Gland / pathology. Positron-Emission Tomography. Tomography, X-Ray Computed. Treatment Outcome

  • Genetic Alliance. consumer health - Acromegaly.
  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7686-90 [2823271.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Jul;75(1):281-4 [1619020.001]
  • [Cites] Endocr Rev. 1988 Aug;9(3):357-73 [3145190.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Feb;68(2):499-504 [2493033.001]
  • [Cites] Endocrinology. 1989 Nov;125(5):2710-8 [2507296.001]
  • [Cites] Proc Soc Exp Biol Med. 1990 Mar;193(3):232-5 [2106141.001]
  • [Cites] Clin Endocrinol (Oxf). 1990 Mar;32(3):315-21 [2111746.001]
  • [Cites] Endocrinology. 1990 Nov;127(5):2149-56 [2226307.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Sep;73(3):569-76 [1908480.001]
  • [Cites] Endocrinol Metab Clin North Am. 1992 Sep;21(3):575-95 [1521513.001]
  • [Cites] Endocr Rev. 1992 Aug;13(3):476-98 [1425484.001]
  • [Cites] J Endocrinol Invest. 1993 Jan;16(1):69-81 [8445159.001]
  • [Cites] Am J Physiol. 1994 Apr;266(4 Pt 2):H1643-56 [8184944.001]
  • [Cites] J Clin Invest. 1994 Sep;94(3):1277-88 [8083369.001]
  • [Cites] Eur J Endocrinol. 1995 Sep;133(3):320-4 [7581949.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Oct;81(10):3746-53 [8855833.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Feb;82(2):634-7 [9024267.001]
  • [Cites] Neurosurgery. 1997 Mar;40(3):611-4; discussion 614-5 [9055303.001]
  • [Cites] Eur J Endocrinol. 1997 Apr;136(4):394-400 [9150699.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Aug;47(2):123-35 [9302383.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):688-92 [9467594.001]
  • [Cites] Eur J Endocrinol. 1998 Feb;138(2):164-9 [9506860.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14894-8 [10611309.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):700-12 [11158034.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Mar;280(3):R721-9 [11171650.001]
  • [Cites] Arch Intern Med. 2001 Apr 9;161(7):1010-1 [11295968.001]
  • [Cites] J Clin Endocrinol Metab. 2001 May;86(5):2227-30 [11344231.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Jul;55(1):135-40 [11453963.001]
  • [Cites] Endocrinology. 2001 Sep;142(9):3764-73 [11517152.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Dec;281(6):R1975-85 [11705784.001]
  • [Cites] Ann Oncol. 2001;12 Suppl 2:S89-94 [11762359.001]
  • [Cites] Neurosurgery. 2002 Jun;50(6):1356-9; discussion 1360 [12015856.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2002 Jun;110(4):188-92 [12058343.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jul;57(1):131-4 [12100081.001]
  • [Cites] Eur J Endocrinol. 2002 Sep;147(3):381-6 [12213676.001]
  • [Cites] Ann Endocrinol (Paris). 2002 Dec;63(6 Pt 1):536-9 [12527856.001]
  • [Cites] J Endocrinol Invest. 2003 Feb;26(2):163-9 [12739745.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2004 Jan;286(1):E25-30 [14506078.001]
  • [Cites] J Thorac Cardiovasc Surg. 2004 Oct;128(4):631-2 [15457172.001]
  • [Cites] J Clin Endocrinol Metab. 1984 May;58(5):796-803 [6423659.001]
  • [Cites] Br Med J (Clin Res Ed). 1984 Aug 25;289(6443):453-5 [6432140.001]
  • [Cites] J Clin Endocrinol Metab. 1984 Nov;59(5):846-9 [6434585.001]
  • [Cites] Cancer. 1984 Nov 15;54(10):2097-108 [6435852.001]
  • [Cites] J Clin Invest. 1985 May;75(5):1584-90 [2860126.001]
  • [Cites] Presse Med. 1985 Dec 7;14(42):2129-34 [2868453.001]
  • [Cites] Am J Physiol. 1986 Apr;250(4 Pt 1):E486-93 [3008572.001]
  • [Cites] Acta Endocrinol (Copenh). 1986 Sep;113(1):23-8 [2876570.001]
  • [Cites] Am J Surg Pathol. 1987 Oct;11(10):810-9 [2889383.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Feb;48(2):243-50 [9579239.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3104-9 [9745411.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):582-9 [10022420.001]
  • [Cites] Eur J Endocrinol. 1999 Mar;140(3):192-200 [10216513.001]
  • [Cites] J Clin Endocrinol Metab. 1999 May;84(5):1761-2 [10323416.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Sep;84(9):3162-9 [10487681.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Sep;84(9):3241-7 [10487694.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Apr;90(4):2104-9 [15671091.001]
  • [Cites] Ir J Med Sci. 2004 Oct-Dec;173(4):215-6 [16323617.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4776-80 [16968791.001]
  • [Cites] Cancer. 1988 Jul 15;62(2):445-50 [2898285.001]
  • (PMID = 17541749.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ PMC2045692
  •  go-up   go-down


Advertisement
4. Zatelli MC, Ambrosio MR, Bondanelli M, degli Uberti EC: In vitro testing of new somatostatin analogs on pituitary tumor cells. Mol Cell Endocrinol; 2008 May 14;286(1-2):187-91
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro testing of new somatostatin analogs on pituitary tumor cells.
  • Somatostatin has been discovered as a somatotroph release inhibitory factor (SRIF), and, indeed, it has been demonstrated that SRIF and its analogs can inhibit pituitary tumor hormone secretion and control neoplastic bulk.
  • Several in vitro studies have contributed to the current knowledge of the mechanisms by which SRIF and its analogs may influence pituitary adenomas, opening the way to new possible therapeutic strategies.
  • This review focuses on the results obtained by testing several SRIF analogs in vitro on pituitary adenomas, concerning both secretory activity and cell viability.
  • These studies provide the basis for further investigations, both at basic and clinical level, of the application of SRIF analogs in the pituitary field.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use
  • [MeSH-minor] Cell Survival / drug effects. Drug Resistance, Neoplasm. Humans. Tumor Cells, Cultured

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18243520.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin
  • [Number-of-references] 42
  •  go-up   go-down


5. Daems T, Verhelst J, Michotte A, Abrams P, De Ridder D, Abs R: Modification of hormonal secretion in clinically silent pituitary adenomas. Pituitary; 2009;12(1):80-6
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modification of hormonal secretion in clinically silent pituitary adenomas.
  • BACKGROUND: Silent pituitary adenomas are a subtype of adenomas characterized by positive immunoreactivity for one or more hormones classically secreted by normal pituitary cells but without clinical expression, although in some occasions enhanced or changed secretory activity can develop over time.
  • PATIENTS AND METHODS: A series of about 500 pituitary adenomas seen over a period of 20 years were screened for modification in hormonal secretion.
  • RESULTS: Two cases were retrieved, one silent somatotroph adenoma and one thyrotroph adenoma, both without specific clinical features or biochemical abnormalities, which presented 20 years after initial surgery with evidence of acromegaly and hyperthyroidism, respectively.
  • While the acromegaly was controlled by a combination of somatostatin analogs and growth hormone (GH) receptor antagonist therapy, neurosurgery was necessary to manage the thyrotroph adenoma.
  • Immunohistochemical examination demonstrated an increase in the number of thyroid stimulating hormone (TSH)-immunoreactive cells compared to the first tissue.
  • Apparently, the mechanisms responsible for the secretory modifications are different, being a change in secretory capacity in the silent somatotroph adenoma and a quantitative change in the silent thyrotroph adenoma.
  • CONCLUSIONS: These two cases, one somatotroph and one thyrotroph adenoma, are an illustration that clinically silent pituitary adenomas may in rare circumstances evolve over time and become active, as previously demonstrated in silent corticotroph adenomas.
  • [MeSH-major] Pituitary Neoplasms / metabolism
  • [MeSH-minor] Acromegaly / drug therapy. Acromegaly / metabolism. Acromegaly / surgery. Adult. Human Growth Hormone / secretion. Humans. Immunohistochemistry. Insulin-Like Growth Factor I / secretion. Male. Thyrotropin / secretion

  • [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] Pituitary. 2000 Oct;3(2):117-22 [11141695.001]
  • [Cites] Neuropathology. 2001 Dec;21(4):288-93 [11837535.001]
  • [Cites] Am J Pathol. 1989 Feb;134(2):345-53 [2464941.001]
  • [Cites] Mod Pathol. 1988 May;1(3):212-5 [3237702.001]
  • [Cites] Endocr Pathol. 2005 Summer;16(2):107-14 [16199895.001]
  • [Cites] Pituitary. 2007;10 (1):35-45 [17410413.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Apr;90(4):2117-21 [15671111.001]
  • [Cites] Aust N Z J Med. 1987 Apr;17(2):249-51 [3039955.001]
  • [Cites] Neurosurgery. 1994 Jul;35(1):39-44 [7936150.001]
  • [Cites] Clin Endocrinol (Oxf). 1985 Feb;22(2):147-53 [2985300.001]
  • [Cites] Pathol Res Pract. 1991 Dec;187(8):943-9 [1792190.001]
  • [Cites] Acta Neuropathol. 2006 Jan;111(1):1-7 [16328527.001]
  • [Cites] Hum Pathol. 1992 Dec;23(12):1332-9 [1468769.001]
  • [Cites] Pituitary. 1999 May;1(3-4):233-41 [11081203.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Feb;76(2):352-6 [8432778.001]
  • [Cites] Endocr Pathol. 2006 Summer;17(2):191-9 [17159252.001]
  • [Cites] Hum Pathol. 2004 Sep;35(9):1137-47 [15343517.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):59-64 [12519413.001]
  • [Cites] Neurol India. 2000 Dec;48(4):374-7 [11146605.001]
  • [Cites] Br J Neurosurg. 2005 Feb;19(1):38-42 [16147581.001]
  • [Cites] Neurosurgery. 2003 Nov;53(5):1076-84; discussion 1084-5 [14580274.001]
  • [Cites] J Neurosurg. 1987 Jun;66(6):806-11 [3572509.001]
  • [Cites] Neurosurgery. 2005 May;56(5):E1154; discussion E1154 [15854264.001]
  • [Cites] Acta Neuropathol. 2001 Nov;102(5):435-40 [11699555.001]
  • [Cites] Acta Endocrinol (Copenh). 1988 Aug;118(4):533-7 [2840793.001]
  • [Cites] J Neurosurg. 1987 Feb;66(2):244-50 [3543255.001]
  • [Cites] Eur J Endocrinol. 2003 Jul;149(1):17-22 [12824861.001]
  • [Cites] J Clin Neurosci. 2005 Apr;12(3):318-20 [15851094.001]
  • (PMID = 18350381.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-71-5 / Thyrotropin
  • [Number-of-references] 30
  •  go-up   go-down


6. Stepień H, Lawnicka H, Mucha S, Wagrowska-Danilewicz M, Stepień B, Siejka A, Komorowski J: Inhibitory effect of thalidomide on the growth, secretory function and angiogenesis of estrogen-induced prolactinoma in Fischer 344 rats. Life Sci; 2006 Sep 27;79(18):1741-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effect of thalidomide on the growth, secretory function and angiogenesis of estrogen-induced prolactinoma in Fischer 344 rats.
  • The process of angiogenesis has been found to be essential for the development of estrogen-induced pituitary prolactinoma in Fischer 344 rats.
  • Thalidomide [(alpha-(N-phthalimido)-glutarimide] is known to be a potent immunomodulatory drug with antiangiogenic properties, but its effect on lactotroph cell secretory function and pituitary prolactinoma formation has not been described yet.
  • The purpose of this study was to examine the effects of thalidomide on secretion of prolactin (PRL) and vascular endothelial growth factor (VEGF), cell proliferation, apoptosis and angiogenesis within the anterior pituitary gland in long-term diethylstilboestrol (DES)-treated male F344 rats in vivo and in vitro.
  • It was found that DES sharply increased serum PRL and VEGF levels.
  • On the other hand, simultaneous treatment of F344 rats with thalidomide for the last 15 days of the experiment attenuated the stimulatory effect of DES on PRL and VEGF secretion.
  • It also diminished prolactin cell proliferation evaluated as the number of proliferating cell nuclear antigen (PCNA)-positive stained cell nuclei and increased the number of apoptotic bodies determined by the terminal deoxynucleotidyl-mediated dUTP nick-end labeling (TUNEL) method in sections of the DES-induced pituitary prolactinoma.
  • The density of pituitary microvessels evaluated by microscopic counting of CD-31-positive blood vessels was also diminished by the tested drug.
  • In addition, thalidomide (10(-4) to 10(-6) M) inhibited cell proliferation, prolactin and VEGF secretion from rat pituitary prolactinoma cells cultured in vitro.
  • In conclusion, our results provide strong evidence for the antiprolactin and antitumor activity of thalidomide in experimentally DES-induced pituitary adenoma.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neovascularization, Pathologic / drug therapy. Pituitary Neoplasms / drug therapy. Prolactin / metabolism. Prolactinoma / drug therapy. Thalidomide / therapeutic use
  • [MeSH-minor] Animals. Antigens, CD31 / analysis. Apoptosis. Cell Nucleus / chemistry. Cell Proliferation / drug effects. Diethylstilbestrol / toxicity. Estrogens / toxicity. Pituitary Gland / chemistry. Pituitary Gland / pathology. Proliferating Cell Nuclear Antigen / analysis. Rats. Rats, Inbred F344. Vascular Endothelial Growth Factor A

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • Hazardous Substances Data Bank. DIETHYLSTILBESTROL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16846617.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Estrogens; 0 / Proliferating Cell Nuclear Antigen; 0 / Vascular Endothelial Growth Factor A; 4Z8R6ORS6L / Thalidomide; 731DCA35BT / Diethylstilbestrol; 9002-62-4 / Prolactin
  •  go-up   go-down


7. Andersen M, Bjerre P, Schrøder HD, Edal A, Høilund-Carlsen PF, Pedersen PH, Hagen C: In vivo secretory potential and the effect of combination therapy with octreotide and cabergoline in patients with clinically non-functioning pituitary adenomas. Clin Endocrinol (Oxf); 2001 Jan;54(1):23-30
Hazardous Substances Data Bank. MENOTROPINS .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo secretory potential and the effect of combination therapy with octreotide and cabergoline in patients with clinically non-functioning pituitary adenomas.
  • The secretory capacity, in vivo, of clinically non-functioning pituitary adenomas may possibly predict tumour volume reduction during intensive medical therapy.
  • Ten patients (mean (range) 53 years (26-73)) with clinically non-functioning macroadenomas, > or = 10 mm were studied.
  • The secretory capacity of the adenomas was examined using basal, NaCl and TRH-stimulated LH, FSH and alpha-subunit levels.
  • The effect on tumour volume of 6 months' therapy with the combination of a somatostatin analogue, octreotide 200 microg x 3/day and a dopamine-D2-agonist, cabergoline 0.5 mg x 1/day was studied.
  • The basal LH, FSH and alpha-subunit levels were determined before and during 6 months' therapy with octreotide and cabergoline, and MR scans were used to evaluate tumour volume before and during this period of therapy.
  • A reduction in tumour volume (mean +/- SEM (range); 30% +/- 4% (18-46%)) during 6 months of combination therapy with octreotide and cabergoline was recorded only in patients with in vivo secretory potential.
  • Of the six patients with pretherapy secretory capacity, one displayed a very high basal level of alpha-subunit (74 microg/l) despite unmeasurable levels of LH and TSH, and an FSH-level of 1 IU/l.
  • During six months of therapy with octreotide and cabergoline, the basal levels of LH, FSH and alpha-subunit were reduced by > or = 50% in seven patients - including the six patients with in vivo secretion prior to therapy.
  • No new visual field defects were detected during therapy and no deterioration of existing visual field defects was recorded.
  • The medical therapy was well tolerated.
  • The in vivo basal and TRH-stimulated secretory capacity of LH, FSH and alpha-subunit predicted tumour reduction following intensive medical therapy in all of our patients with non-functioning pituitary adenomas.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / secretion. Antineoplastic Agents, Hormonal / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / secretion
  • [MeSH-minor] Adult. Aged. Dopamine Agonists / therapeutic use. Drug Therapy, Combination. Ergolines / therapeutic use. Female. Follicle Stimulating Hormone / blood. Humans. Luteinizing Hormone / blood. Male. Middle Aged. Octreotide / therapeutic use. Prognosis. Thyrotropin / blood

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11167922.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Dopamine Agonists; 0 / Ergolines; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
  •  go-up   go-down


8. Harms E, Siggelkow H, Buchfelder M, Saeger W, Hüfner M: [Macroadenoma of the pituitary gland with moderate hyperprolactinaemia]. Dtsch Med Wochenschr; 2003 Mar 28;128(13):667-70
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Macroadenoma of the pituitary gland with moderate hyperprolactinaemia].
  • [Transliterated title] Makroadenom der Hypophyse mit mässiger Hyperprolaktinämie.
  • HISTORY AND CLINICAL FINDINGS: A 46-year-old woman was referred to the neurosurgery department for treatment of a macroadenoma of the pituitary.
  • INVESTIGATIONS: The endocrinological work-up revealed a moderately elevated prolactin level of 3133 mU/l (147 ng/ml) with intact pituitary functions.
  • She had no visual impairment and the MRI depicted a pituitary tumor with a maximal diameter of 1.9 cm and both intra- and suprasellar extension.
  • DIAGNOSIS, TREATMENT AND CLINICAL COURSE: The diagnosis of a nonfunctioning macrodenoma with functional hyperprolactinemia was made and a selective transsphenoidal adenomectomy was performed.
  • The primary histology showed a chromophobe adenoma.
  • In the meantime, because of persistent galactorrhea and elevated prolactin levels, treatment with cabergolin 0.5 mg/week was started.
  • A follow-up MRI after 3 months of treatment showed a significant shrinkage of the residual tumor.
  • CONCLUSION: This case demonstrates that the differential diagnosis of macroprolactinoma with low secretory activity and functional hyperprolactinemia is very difficult preoperatively in individual cases.
  • This is relevant because macroprolactinomas with low secretory activity can also be treated successfully with dopamine agonists.
  • We therefore suggest a drug treatment trial with dopamine agonists in all macroadenoms with hyperprolactinemia, particularly in those with prolactin levels above 2000 mU/l (100 ng/ml).
  • [MeSH-major] Hyperprolactinemia / surgery. Pituitary Neoplasms / surgery. Prolactinoma / surgery
  • [MeSH-minor] Diagnosis, Differential. Ergolines / therapeutic use. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Middle Aged. Neoplasm, Residual / drug therapy. Pituitary Gland / pathology. Pituitary Gland / surgery. Postoperative Complications / drug therapy

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12660899.001).
  • [ISSN] 0012-0472
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


9. Chung TT, Evanson J, Walker D, Akker SA, Besser GM, Monson JP, Grossman AB, Drake WM: Safety of GH replacement in hypopituitary patients with nonirradiated pituitary and peripituitary tumours. Clin Endocrinol (Oxf); 2008 Jun;68(6):965-9
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Safety of GH replacement in hypopituitary patients with nonirradiated pituitary and peripituitary tumours.
  • BACKGROUND: Published data suggest that growth hormone replacement (GHR) may be given safely to patients with hypopituitarism consequent upon a pituitary/peripituitary tumour.
  • However, a preponderance of patients treated with external pituitary irradiation were included.
  • OBJECTIVE: To assess the safety of GHR in nonirradiated pituitary/peripituitary tumour.
  • PATIENTS: We imaged prospectively the pituitary glands of 48 patients (18 males; mean age 51.6 years range 21-77) who had adult onset growth hormone deficiency (AO-GHD) after appropriate treatment for a pituitary/peripituitary tumour but who did not receive external pituitary irradiation.
  • Pituitary surveillance imaging was performed prior to the commencement of GHR, at 6-12 months and then yearly.
  • For patients with secretory tumours, biochemical markers (cortisol and prolactin) were used as evidence of tumour recurrence.
  • Three patients were judged to have an apparent increase in tumour volume and/or marker, although only one was thought to be possibly GH related--a patient with a cystic chromophobe adenoma who demonstrated a marginal increase in residual tumour volume 4 years after commencement of GHR.
  • CONCLUSION: These data add to the growing body of evidence for the safety of GHR in hypopituitary patients consequent upon pituitary/peripituitary mass lesions and represents the first reported series in a heterogeneous group of nonirradiated patients.
  • [MeSH-major] Human Growth Hormone / adverse effects. Human Growth Hormone / therapeutic use. Hypopituitarism / drug therapy. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18031317.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
  •  go-up   go-down


10. Drimmie FM, MacLennan AC, Nicoll JA, Simpson E, McNeill E, Donaldson MD: Gigantism due to growth hormone excess in a boy with optic glioma. Clin Endocrinol (Oxf); 2000 Oct;53(4):535-8
Hazardous Substances Data Bank. GOSERELIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • True gigantism is rare in early childhood and is usually due to excess GH secretion from a pituitary adenoma.
  • There is no evidence of a direct secretory role for the tumour and we postulate that the tumour is affecting GH secretion through an effect on somatostatin tone.
  • Specific tumour therapy is not indicated for this patient in the absence of mass effect or visual disturbance.
  • The GH excess is being treated with somatostatin analogue (Octreotide) and as he has developed precocious puberty he is also receiving long acting GnRH analogue (Zoladex).
  • This boy appears likely to have neurofibromatosis type 1 (NF1) which raises the question of subtle GH excess in NF1 patients with tall stature.
  • [MeSH-minor] Adult. Child, Preschool. Gonadotropin-Releasing Hormone / analogs & derivatives. Goserelin / therapeutic use. Humans. Magnetic Resonance Imaging. Male. Neurofibromatosis 1 / complications. Neurofibromatosis 1 / diagnosis. Neurofibromatosis 1 / drug therapy. Octreotide / therapeutic use. Puberty, Precocious / complications. Puberty, Precocious / diagnosis. Puberty, Precocious / drug therapy. Somatostatin / analogs & derivatives

  • Genetic Alliance. consumer health - Gigantism.
  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11012581.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0F65R8P09N / Goserelin; 33515-09-2 / Gonadotropin-Releasing Hormone; 51110-01-1 / Somatostatin; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


11. Donangelo I, Rodacki M, Peixoto MC, Vaisman M, Caldas NR, Gadelha MR: Dependency and analgesia related to treatment with subcutaneous octreotide in patients with growth hormone-secreting tumors. Endocr Pract; 2004 Mar-Apr;10(2):107-11
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dependency and analgesia related to treatment with subcutaneous octreotide in patients with growth hormone-secreting tumors.
  • OBJECTIVE: To describe three patients diagnosed with somatotropinomas in whom the analgesic effect of octreotide was observed, along with dependency to the drug.
  • METHODS: These patients had pituitary macroadenomas treated with transphenoidal surgery and pituitary radiotherapy, and received high daily doses (>900 microg/day) of subcutaneous octreotide because of persistent high levels of growth hormone and insulin-like growth factor I (IGF-I).
  • RESULTS: Headache occurred prior to drug administration in all three cases, with relief soon after.
  • We also observed tolerance to octreotide's analgesic and anti-secretory actions (one patient), craving for the drug (two patients), withdrawal syndrome (one patient), and drug abuse (one patient).
  • CONCLUSION: Dependency syndrome may occur when high doses of octreotide are used, sometimes leading to drug abuse.
  • Tolerance to the growth hormone anti-secretory effect of the drug may encourage physicians to increase doses to levels at which drug dependency has been observed.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / secretion. Antineoplastic Agents, Hormonal / adverse effects. Human Growth Hormone / secretion. Octreotide / adverse effects. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / secretion. Substance-Related Disorders
  • [MeSH-minor] Adolescent. Adult. Combined Modality Therapy. Drug Tolerance. Female. Humans. Middle Aged

  • MedlinePlus Health Information. consumer health - Drug Abuse.
  • MedlinePlus Health Information. consumer health - Drugs and Young People.
  • MedlinePlus Health Information. consumer health - Opioid Abuse and Addiction.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15256326.001).
  • [ISSN] 1530-891X
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


12. Losa M, Mortini P, Giovanelli M: [The role of somatostatin analogues in the treatment of hypophyseal adenomas]. Minerva Endocrinol; 2003 Mar;28(1):39-51
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The role of somatostatin analogues in the treatment of hypophyseal adenomas].
  • Somatostatin analogues are widely employed in the treatment of hypophyseal adenomas.
  • The most widely used analogues at the present time are octreotide and lanreotide.
  • Both octreotide and lanreotide have proved their effectiveness in the treatment of GH- and TSH-secretory hypophyseal adenomas.
  • In those patients who respond to pharmacological treatment we often achieve not only the control of hormonal hypersecretion, but also a reduction in the volume of hypophyseal neoplasia.
  • In the other types of hypophyseal adenoma, on the other hand, somatostatin analogues have proved to have little effect: apart from isolated cases of effectiveness in non-functioning adenomas, the administration both of octreotide and lanreotide to patients with Cushing's disease or prolactinoma did not significantly modify the hormonal hypersecretion or tumoural volume.
  • The side-effects of somatostatin analogues are comparatively rare and of moderate entity: only a small percentage of patients requires the treatment to be suspended owing to the occurrence of side-effects.
  • Octreotide, bound to radioactive substances or to toxins, has also been utilised for the selective destruction of neoplastic tissues expressing the sst(2) receptor of somatostatin.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Acromegaly / drug therapy. Acromegaly / etiology. Adrenocorticotropic Hormone / secretion. Combined Modality Therapy. Cushing Syndrome / drug therapy. Cushing Syndrome / etiology. Forecasting. Human Growth Hormone / secretion. Humans. Insulin-Like Growth Factor I / secretion. Octreotide / adverse effects. Octreotide / pharmacology. Octreotide / therapeutic use. Peptides, Cyclic / adverse effects. Peptides, Cyclic / pharmacology. Peptides, Cyclic / therapeutic use. Prolactinoma / drug therapy. Radiopharmaceuticals / therapeutic use. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / physiology. Thyrotropin / secretion. Treatment Outcome. Yttrium Radioisotopes / therapeutic use

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12621362.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Peptides, Cyclic; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 0 / Yttrium Radioisotopes; 118992-92-0 / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; 9002-60-2 / Adrenocorticotropic Hormone; 9002-71-5 / Thyrotropin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 79
  •  go-up   go-down


13. Saveanu A, Gunz G, Dufour H, Caron P, Fina F, Ouafik L, Culler MD, Moreau JP, Enjalbert A, Jaquet P: Bim-23244, a somatostatin receptor subtype 2- and 5-selective analog with enhanced efficacy in suppressing growth hormone (GH) from octreotide-resistant human GH-secreting adenomas. J Clin Endocrinol Metab; 2001 Jan;86(1):140-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In addition, the SSTR5-preferring analog showed a slight additive effect when used in combination with SSTR2 preferential drugs at submaximal concentrations in octreotide partially sensitive adenomas.
  • The octreotide-sensitive GH secretory adenomas presented with a high level of both SSTR2 and SSTR5 mRNA expression [222 +/- 61 and 327 +/- 136 pg/pg glyceraldehyde-3-phosphate dehydrogenase (GAPDH), respectively].
  • [MeSH-major] Adenoma / secretion. Human Growth Hormone / antagonists & inhibitors. Human Growth Hormone / secretion. Octreotide / therapeutic use. Pituitary Neoplasms / secretion. Receptors, Somatostatin / therapeutic use. Somatostatin / analogs & derivatives
  • [MeSH-minor] Acromegaly / drug therapy. Acromegaly / metabolism. Adult. Drug Resistance. Female. Hormones / therapeutic use. Humans. Male. Middle Aged. Prolactin / secretion. RNA, Messenger / metabolism. 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
  • (PMID = 11231991.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIM-23244; 0 / Hormones; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


14. Guerra Y, Lacuesta E, Marquez F, Raksin PB, Utset M, Fogelfeld L: Apoplexy in non functioning pituitary adenoma after one dose of leuprolide as treatment for prostate cancer. Pituitary; 2010;13(1):54-9
Hazardous Substances Data Bank. LEUPROLIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoplexy in non functioning pituitary adenoma after one dose of leuprolide as treatment for prostate cancer.
  • We report the case of a 60 year old male who complained of headache and blurry vision--that progressed to left ophthalmoplegia and ptosis--after receiving a dose of leuprolide for Prostate cancer therapy.
  • The patient underwent transsphenoidal debulking, and the tissue obtained demonstrated immunohistochemical staining for LH.
  • A literature review revealed nine previously reported cases of pituitary apoplexy after GnRH agonist therapy for prostate cancer.
  • In most cases, the sellar tissues stained for LH, consistent with a gonadotropinoma.
  • Particular attention to clinical findings suggestive of a non functioning pituitary tumor in patients receiving GnRH agonist therapy is critical as routine screening with MRI is not practical.
  • [MeSH-major] Adenoma / complications. Leuprolide / adverse effects. Pituitary Neoplasms / complications. Stroke / chemically induced
  • [MeSH-minor] Antineoplastic Agents, Hormonal / adverse effects. Gonadotropin-Releasing Hormone / agonists. Humans. Male. Middle Aged. Prostatic Neoplasms / complications. Prostatic Neoplasms / drug therapy. Sella Turcica






Advertisement