Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The structural features of 26 spontaneous pituitary tumors in aging female Long-Evans rats have been investigated by different morphologic techniques including immunoperoxidase staining and electron microscopy. By light microscopy, the tumors corresponded to chromophobic-sparsely granulated acidophilic adenomas, containing numerous pigment granules and showing congestion as well as focal hemorrhages. Positive cytoplasmic staining was obtained with Herlant's erythrosin as well as with Brookes' carmoisine methods, used to detect secretory granules of prolactin cells. Immunoperoxidase technique revealed the presence of immunoreactive prolactin in the cytoplasm of many adenoma cells. Growth hormone and TSH immuno-stainings were negative. By electron microscopy, the tumors were found to consist of prolactin cells exhibiting marked variability in subcellular morphology and differing considerably from non-tumorous resting prolactin cells. A decrease in size and number of secretory granules, proliferation of rough-surfaced endoplasmic reticulum, formation of "Nebenkerne", accumulation of free ribosomes, prominence of Golgi complex and the presence of misplaced exocytosis were characteristic features of the adenoma cells and were interpreted as indicating enhanced secretory activity. Crinophagy and transformation of secretory granules into pigment deposits were striking findings in many adenomas. Since all the adenomas seemed to derive from prolactin cells and belong to the same tumor class, it is assumed that prolactin cells in female Long-Evans rats are more susceptible to oncogenic stimuli than other hypophysial cell types.
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PMID:Spontaneous pituitary adenomas in aging rats. A light microscopic, immunocytological and fine structural study. 33 31

Growth hormone (GH) release was measured in 17 patients with active acromegaly following the administration of insulin, LH-RH and TRH given intravenously either combined or each separately. The simultaneous application of insulin and the hypothalamic releasing hormones resulted in a striking increase of plasma GH in 15 out of 17 patients. Inappropriate stimulation of GH release was found in 9 out of the 17 patients with acromegaly, when TRH was given as the only hormone; conversely this phenomenon due to LH-RH application was observed in 4 cases. In insulin-induced hypoglycemia GH release could be stimulated in 5 patients. After selective, transsphenoidal hypophysectomy, 4 of 13 patients still showed a definite stimulation of GH release after the combined use of test substances. Two of these also exhibited a comparable stimulation of GH after TRH, indicating adenoma cells remaining active after operation. The combined insulin-induced hypoglycemia/LH-RH/TRH-test is therefore advisable for patients with acromegaly, since GH release as well as other hypophyseal partial functions can be tested. The performance of individual tests is essential for evaluating selective stimulation of GH release.
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PMID:[Comparative studies of growth hormone secretion in acromegaly after isolated and combined application of insulin hypoglycemia, LH-RH- and TRH tests (author's transl)]. 34 58

A prolactin-secreting pituitary adenoma was removed trans-sphenoidally from a 37 years old man with gigantism (218 cm). Serum levels of prolactin (PRL) were elevated pre-operatively and decreased after administration of L-Dopa with no increase after TRH as is usually observed in PRL-secreting adenomas. Growth hormone (GH) and somatomedin serum levels were normal with no modification of GH after insulin hypoglycemia, oral glucose loading or L-Dopa. Morphological examination of the tumour demonstrated the presence of lactotrophs by light and electron microscopy and by immunofluorescense staining. No somatotrophs were found. In this unique case, the relationship between a PRL-secreting adenoma and gigantism is discussed.
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PMID:Prolactin-secreting pituitary adenoma in a man with gigantism: a case report. 39 52

Potassium depletion frequently occurs in primary aldosteronism and has been implicated as the cause of the impaired carbohydrate tolerance frequently associated with this syndrome. Glucose, insulin, and growth hormone regulation were studied in a 42-yr-old, male patient with an aldosterone-secreting adenoma when the patient was potassium-depleted and again after potassium repletion. Potassium repletion was documented by serial body potassium measurements, with an increase in body potassium from 2400 mEq to 2850 mEq after 400 mg spironolactone and 80 mEq supplemental potassium chloride were administered daily for 7 days. Potassium repletion resulted in improvement of the patient's glucose tolerance test, with a decrease in the peak glucose level from 184 mg/100ml to 130 mg/100ml and an increase in the peak insulin level from 46 muU/ml to 85 muU/ml. Intravenous administration of arginine resulted in a subnormal insulin response of 28 muU/ml in the base-line test and an increase to 59 muU/ml after potassium stores were repleted. Growth hormone response to arginine infusion was also initially minimal at 12.5 ng/ml, increasing markedly to 26 ng/ml after potassium replenishment. Insulin-induced hypoglycemia resulted in a depressed growth hormone response of 8 ng/ml when the patient was potassium-deficient, but a normal response of 30 ng/ml after potassium repletion. These observations demonstrate that impairment of both insulin and growth hormone responses to stimulation occur in primary aldosteronism with potassium depletion. These abnormalities may be reversed by potassium repletion.
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PMID:Improvement of growth hormone response to stimulation in primary aldosteronism with correction of potassium deficiency. 95 1

This study was designed to establish in vitro model systems in human hormone-producing pituitary adenomas that are analogous to the in vivo cellular environment. Mechanically dispersed cells composed of single cells and aggregates from 6 pituitary adenomas (3 GH producing adenomas and 3 prolactinomas) were cultured on microporous membrane cell culture inserts (Millicell-CM) coated with Basement Membrane Matrigel for up to 6 months. Growth hormone or prolactin in the medium was measured during the culture, and morphological feature in vitro was also compared with that of the original tumor at intervals. Not only single cells but also large aggregated cells which usually float in the medium when seeded on conventional plastic, were flattened and firmly attached to coated microporous membrane under the control of medium volume in culture. In both type adenomas, especially prolactinomas, surviving aggregated adenoma cells revealed preserved hormone activity and no dedifferentiation of cell characteristics after 6 months in culture. Particularly during the first 2 months in culture, close similarity existed between in vivo and in vitro conditions with regard to cell morphology and hormone release. These results indicate that this new culture method may further aid the investigation of in vitro cellular structure and function in human pituitary adenomas under conditions which closely mimic the in vivo cellular environment.
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PMID:[Inventions for preservation of hormonal function in long-term culture of human functioning pituitary adenoma]. 193 Dec 58

Approximately 25% of patients with pituitary adenomas have no clinical or biochemical evidence for excess hormone secretion and are classified as having null cell or nonfunctioning adenomas. To characterize the cell type of these tumors, we analyzed pituitary hormone gene expression in clinically nonfunctioning pituitary adenomas using specific oligonucleotide probes for the messenger (m)RNAs encoding growth hormone, prolactin, ACTH, and the glycoprotein hormone subunits, alpha, luteinizing hormone (LH)beta, follicle-stimulating hormone (FSH)beta, and thyroid-stimulating hormone (TSH)beta. Expression of one or more of the anterior pituitary hormone genes was found in 12/14 (86%) of the patients with clinically classified nonfunctioning adenomas. Expression of one or more of the glycoprotein hormone genes (alpha, LH beta, FSH beta, TSH beta) was identified most commonly (79%) with expression of multiple beta-subunit genes in many cases. Expression of alpha-subunit mRNA was found in each of the adenomas from patients expressing one of the beta-subunit mRNAs and in three patients with no detectable beta-subunit mRNA. Although FSH beta and LH beta mRNAs were found with similar frequencies in nonfunctioning adenomas, expression of FSH beta mRNA was generally much more abundant. TSH beta mRNA was detected in only one adenoma. The levels of glycoprotein hormone subunit mRNAs were variable in different adenomas, but the lengths of the mRNAs and transcriptional start sites for the alpha- and beta-subunit genes were the same in the pituitary adenomas and in normal pituitary. Growth hormone and prolactin gene expression were not observed in the nonfunctioning adenomas, but ACTH mRNA was found in a single case. Immunohistochemistry of the adenomas confirmed production of one or more pituitary hormones in 13/14 (93%) nonfunctioning tumors, with a distribution of hormone production similar to that of the hormone mRNAs. These data indicate that pituitary adenomas originating from cells producing glycoprotein hormones are common, but are difficult to recognize clinically because of the absence of characteristic endocrine syndromes and defective hormone biosynthesis and secretion.
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PMID:Glycoprotein hormone genes are expressed in clinically nonfunctioning pituitary adenomas. 282 61

Folliculo-stellate cells (FS cells) in 40 pituitary adenomas and portions of anterior pituitary adjacent to the tumor in 26 cases were investigated immunohistochemically, using polyclonal antisera to S-100 protein (S-100) and glial fibrillary acidic protein (GFAP). The objective was to clarify the histological behavior of the FS cells. In most pituitary adenomas there were few or no S-100- or GFAP-positive cells, in comparison with numerous positive cells in the parts of the adenohypophyses compressed by adenomas. However, positive FS cells were observed in some types of pituitary adenomas. Growth hormone and prolactin producing adenomas frequently contained significant amounts of FS cells. In non-functioning adenomas, an unique case of FS cell adenoma was present. The adenoma was composed mainly of FS cells and immature glandular cells. The FS cells were sometimes located around follicles containing Periodic acid Schiff-positive material. Therefore, the FS cell adenoma is characterized by S-100- and GFAP-positive FS cells and PAS-positive follicles. In this type of adenoma, FS cells seemed to be the main proliferating component. In parts of the adenohypophyses adjacent to the adenomas, GFAP-positive FS cells were numerous. In the pathological conditions FS cells may possess the potential of reactive proliferation.
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PMID:Proliferating potential of folliculo-stellate cells in human pituitary adenomas. Immunohistochemical and electron microscopic analysis. 302 33

Growth hormone (GH)-producing pituitary adenoma from a 50-year-old acromegalic female was studied histochemically, immunohistochemically and electron microscopically. The adenoma was characterized by numerous crystal-like amyloid bodies of 5 to 40 micron in diameter. In the periphery of the crystal-like amyloid, bundles of amyloid fibrils were closely associated with deep invaginations of adenoma cells. The adenoma cells had numerous vesicles and vacuoles filled with amyloid fibrils, some of which were continuous with extracellular space. The crystal-like amyloids, as well as the adenoma cells, were immunohistochemically positive for GH. It might be possible that disorder of hydrolysis of "prohormone," from which GH is elaborated, is responsible for the amyloid production, and that amyloid discharge is accompanied with immunoreactive GH.
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PMID:Growth hormone-producing pituitary adenoma with crystal-like amyloid immunohistochemically positive for growth hormone. 388 Jun 54

Growth hormone release inhibiting hormone (GHRIH) was administered by constant infusion over 75 minutes to eight acromegalic patients at different doses. 100 to 1,000 mug were equally effective in reducing circulating growth hormone (GH) levels; 25 mug lowered GH levels in only five patients, and at this dose the extent of the fall was smaller than from doses of 100 mug or more. 10 mug was ineffective. Injection of single doses of 500 mug by intravenous, subcutaneous, and intramuscular routes caused only small and transient reductions in GH levels, though the effect was improved by injecting the hormone intramuscularly in 2 ml of 16% gelatin. Injection of a suspension of 4 mg GHRIH in 1 ml of arachis oil lowered growth hormone levels for between three and four hours.In four acromegalic patients an oral 50-g glucose tolerance test was performed during a continuous infusion of either saline or 1,000 mug GHRIH. The "paradoxical" rise in growth hormone seen in these patients during the saline infusion was suppressed by GHRIH. The blood glucose responses were, moreover, modified by GHRIH in that the peak was delayed and occurred at the end of the infusion in each case. A "normal" glucose tolerance curve was converted to a "diabetic" type of response in two patients. This effect could be accounted for by the inhibition of insulin secretion known to occur with large doses of GHRIH.We speculate that acromegaly may be primarily a hypothalmic disease due to deficiency of GHRIH resulting in excessive secretion of growth hormone from the pituitary and adenoma formation due to inappropriate and prolonged stimulation of the pituitary.
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PMID:Growth hormone release inhibiting hormone in acromegaly. 459 81

Tumors from 42 surgically resected pituitaries and from 13 autopsy cases were studied immunohistochemically with polyclonal antisera to 7 anterior pituitary hormones and with a newly developed monoclonal antibody directed against human chromogranin for evaluation of the distribution of chromogranin in normal and neoplastic pituitaries. In addition, a prospective study was done for assessment of the prevalence, morphology, and endocrine cell types of pituitary tumors in 100 autopsy subjects. When these 55 pituitary adenomas were examined with monoclonal antibody (LK2H10) directed against human chromogranin, selective staining of normal adenohypophyseal cell types and pituitary tumors was observed. Most null-cell adenomas (12/14) were positive for chromogranin, whereas all prolactin (PRL)-producing adenomas (19/19) were negative. Growth hormone (GH) adenomas were focally positive (9/9). All oncocytomas (2/2), 1 thyrotropin (TSH) adenoma, and a follicle-stimulating hormone/luteinizing hormone adenoma were positive for chromogranin. One or more adenomas were present in 14% of the autopsy cases. The tumors occurred most frequently in patients in the fifth through the seventh decades of life. Immunohistochemical staining of 13 adenomas revealed 1 TSH, 1 ACTH, and 4 PRL-producing tumors, whereas 7 other tumors, which were null-cell or undifferentiated adenomas, failed to stain for any of the seven principle pituitary hormones. These results indicate that antibody LK2H10 to human chromogranin is useful in the immunohistochemical characterization of pituitary adenomas. Incidental pituitary microadenomas from autopsy-derived pituitaries most commonly produce PRL, or they belong to the null-cell or undifferentiated tumor group.
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PMID:Pituitary adenomas. An immunohistochemical study of hormone production and chromogranin localization. 608 68


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