Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ovine and human corticotropin-releasing factors (CRF) have similar potencies in causing adrenocorticotropic hormone (ACTH) and cortisol secretion in normal humans. Using long-acting ovine CRF (1 microgram/kg body weight as an intravenous bolus), we tested patients with Cushing's syndrome, adrenal insufficiency, and psychiatric conditions with mild hypercortisolism. Over 95% of hypercortisolemic patients with a pituitary adenoma responded with increases in plasma ACTH and cortisol concentrations; patients with the ectopic ACTH syndrome had no ACTH or cortisol responses; patients with ACTH-independent hypercortisolism of adrenal origin had low or undetectable plasma ACTH concentrations before and after CRF without any cortisol response. The differences in responses of patients with adrenal insufficiency of primary, pituitary, or suprapituitary type likewise suggest value of the CFR test in their differential diagnosis. The responses in the psychiatric patients should permit differentiation between Cushing's syndrome and hypercortisolism of psychiatric origin.
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PMID:NIH conference. Clinical applications of corticotropin-releasing factor. 298 7

Cushing's disease has come full cycle. As originally asserted more than 50 years ago, modern diagnostic techniques now demonstrate an adrenocorticotropic hormone (ACTH) secreting pituitary adenoma in approximately 80% of such patients. At this historical juncture, we report a long-term follow-up of our 17 patients who underwent adrenalectomy (8) or later adrenalectomy plus adrenal autotransplantation (9) between 1955 and 1976. Two patients died soon after surgery and five others died later of "natural" causes. Four others moved away but were stable when last contacted. Of the six patients who remain available for current follow-up, three have undergone hypophyseal surgery. Another patient has evidence of pituitary enlargement, and the remaining two are yet to undergo computerized tomography (CT) scan. Four illustrative cases are reviewed in some detail. One case presented with Nelson's syndrome and acute onset blindness. The second represented multiple endocrine adenomatosis with hyperparathyroidism in addition to Cushing's disease. The third exhibited Cushing's syndrome from the autotransplants, finally cured by hypophysectomy. The fourth exhibited huge ACTH levels from a large pituitary adenoma that could not be totally resected and recurrent Cushing's syndrome associated with large autotransplant "adenomas." The initial surgical treatment of choice is pituitary adenectomy. Bilateral adrenalectomy will remain useful where curative pituitary surgery is not feasible. Neither pituitary irradiation nor medical therapy has been truly effective in our patients. Adrenal autotransplants survive, to some extent, in virtually all patients. However, the degree of function is variable, and the full function may not be achieved for many months or even years. Functioning autotransplants have not prevented Nelson's syndrome, and they would appear to offer little practical benefit at this time.
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PMID:Cushing's disease today. Late follow-up of 17 adrenalectomy patients with emphasis on eight with adrenal autotransplants. 298 64

Release of immunoreactive ACTH and beta-endorphin (beta-EP) in response to corticotrophin-releasing factor (CRF) and dopaminergic agents was studied in vivo and in vitro in a patient with Cushing's disease. Iv administration of synthetic ovine (o) CRF significantly stimulated plasma ACTH release, accompanied by increase of plasma cortisol levels. Oral administration of bromocriptine significantly suppressed plasma cortisol levels. Although reduced responses of plasma ACTH and cortisol to o-CRF was observed 1 month after removal of the pituitary adenoma, these normalized 6 months after operation. In vitro perifusion of the pituitary adenoma obtained by surgery revealed that o-CRF also stimulated ACTH and beta-EP release in a dose-responsive manner (10(-9)M 10(-5)M) and that dopamine suppressed their basal secretion. Gel exclusion chromatography of the perfusates showed that the predominant component of ACTH and beta-EP before and after o-CRF stimulation coeluted with standard ACTH and beta-EP, respectively. The present data suggest that o-CRF is a potent secretagogue for ACTH and beta-EP release from the human pituitary adenoma causing Cushing's disease and that ACTH secretion from certain adenomas, possibly originating from the intermediate lobe of the pituitary gland, is partly regulated by a dopaminergic mechanism.
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PMID:Effect of ovine corticotrophin releasing factor, bromocriptine, and dopamine on release of ACTH and beta-endorphin in a patient with Cushing's disease. 298 59

A comparison was made with the data of 62 cases of pituitary adenoma, evaluated pre- and postoperatively, including as well the results of immunohistochemical hormone examination (also for calcitonin). Prolactin was found in 18 of the 21 adenomas carrying the preoperative diagnosis of prolactinoma, whereas cells containing other hormones (growth hormone, LH, FSH, TSH, ACTH, beta-endorphin), were only occasionally present. The growth hormone was strongly positive in the adenoma tissue in 16 of the 17 cases of acromegaly. 5 of these adenomas were accompanied by a marked hyperprolactinemia and also contained many prolactin cells. 6 of the 19 adenomas diagnosed as being 'inactive' contained hormone-positive cells, but only a very small number of cells. ACTH was found in 3 of the 4 pituitary adenomas of patients with Cushing's disease. 2 of these were also positive for beta-endorphin. The tissue of 1 gonadotrophic adenoma (with elevated FSH in serum) gave positive results with an anti-LH antiserum. Calcitonin was not found in any adenoma. The preoperative serum prolactin levels did not quantitatively correlate with the percentage of prolactin-positive cells.
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PMID:Immunohistochemical examination of pituitary adenomas. Comparison to clinical and endocrinological findings. 298 43

Electron-immunocytochemical staining with lectin (concanavalin A: Con A) binding sites analysis was applied to study secretory granules of human pituitary adenomas and surrounding normal pituitary tissue using post-embedded serial ultrathin sections. Twelve cases of human pituitary adenoma and three specimens of normal pituitary tissue surrounding adenomas were studied: the cases were operated on between 1982 and 1984. The tumors consisted of four prolactin (PRL)-, six growth hormone (GH)-, and two adrenocorticotropic hormone (ACTH)-producing adenomas. In parallel with the detection of Con A binding sites of secretory granules, their secreting hormones were characterized electron-microscopically with the immunocytochemical horseradish peroxidase (HRP) labeling using the avidin-biotin technique. The two cases of ACTH-producing adenomas showed either weak or negative reactions with Con A on secretory granules, while normal ACTH-producing pituitary cells showed strong reactions with Con A on every secretory granule observed. Large secretory granules of PRL- or GH-producing cells showed negative reactions with Con A both in the pituitary adenoma and normal pituitary, while some small granulated or sparsely granulated adenoma cells also showed strong reactions with Con A. The complexity of human pituitary adenomas is illustrated as well as the difference in biochemical structure of normal pituitary cells and pituitary adenoma cells secreting the same specific hormone.
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PMID:Difference of lectin binding sites of secretory granules between normal pituitary and adenoma cells. 299 Jan 44

Advances in radioimmunoassay procedures, immunocytochemistry, neuroradiologic imaging, and the surgical and medical treatment of pituitary adenomas have led to reappraisal of their classification as well as refinements in the diagnostic approaches used by pathologists. Sixty-two pituitary adenomas are described, and recent advances in this field are reviewed. Most of the patients were adults, but one of the adrenocorticotropic hormone (ACTH)-producing adenomas occurred in an 11-month-old infant. Endocrine-inactive tumors (43.5 per cent) were less common than hormone-producing tumors (56.5 per cent). Local invasion was most common in the former group, followed by ACTH-producing and other hormone-producing tumors. Ultrastructural features correlated with hormonal levels in the growth hormone(GH)-secreting tumors but not in the prolactin(LTH)- or ACTH-producing tumors. The formation of 7-nm filaments in the cytoplasm of tumor cells, corresponding to Crooke's hyaline change on light microscopy, was characteristic of ACTH-producing tumors. Ultrastructural changes in the ACTH granules suggested that the filaments may be derived from the feedback action of cortisol. Prior to surgery, a Rathke's cleft cyst and a chordoma were mistaken for endocrine-inactive pituitary adenomas. In two additional cases ectopic ACTH-producing tumors of lung clinically mimicked pituitary adenoma. Conversely, one pituitary adenoma mimicked sphenoid wing meningioma. Clinical, hormonal, and radiologic data and immunocytochemical and electron microscopic studies are needed for accurate pathologic interpretation and classification of pituitary adenomas.
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PMID:Pathobiologic study of pituitary tumors: report of 62 cases with a review of the recent literature. 299 52

In this paper, initial work on MSH at Dr. Lerner's laboratory in Portland, Oregon, from 1952 to 1954 is presented. The development of an in vitro bioassay method enabled us to show increased urinary excretion of MSH in Addison's disease. The ability of MSH to increase skin pigmentation in man was also demonstrated. Subsequent work on MSH during the past thirty years is reviewed, such as characterization of alpha- and beta-MSH and their precursors in the pituitary gland and localization of MSH-like peptides in various regions of the brain. Finally there are presented the characterization of gamma-MSH, the hypothermic effect of intracisternal administration of gamma-MSH, the effect of corticortropin releasing factor on increased secretion of alpha-MSH from rat pituitary, and the effect of arginine vasopressin on secretion of alpha-MSH from pituitary adenoma.
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PMID:Thirty-five years of progress in the study of MSH. 300 50

Molecular forms of immunoreactive adrenocorticotropin (ACTH), beta-lipotropin (beta-LPH) (beta-endorphin (beta-END), human NH-2-terminal (hNT) of pro-opiomelanocortin (POMC), and gamma-3-melanotropin (gamma-3-MSCH) were studied in plasma, CSF and urine of a patient with Nelson's syndrome by molecular sieving and concanavalin A (Con A)-sepharose chromatography. In the culture tumor medium of the tumor cells, and in the plasma and CSF, these compounds were found mainly in forms corresponding in molecular weight to the authentic peptides, with the exception of gamma-3-MSH. Stimulation of the pituitary tumor by synthetic ovine corticotropin-releasing factor (CRF 1-41) caused a 171-468% increase in vivo (60 min) and 453-953% increase in vitro (3h incubation) in the levels of POMC derived peptides; it increased the relative amount of beta-END in vivo, and that of beta-LPH in vitro. Molecular sieving chromatography of urine samples revealed that beta-LPH and hNT are extensively degraded by the kidney. By contrast, ACTH showed no significant renal degradation before the removal of the pituitary adenoma. However, following pituitary surgery, only smaller fragments of immunoreactive (IR) ACTH were detected in the urine. These results suggest no major abnormal metabolic pathway for POMC in Nelson's syndrome, although the proportions of various peptides derived from the precursor could be different in vivo from those after in vitro incubation under basal conditions and during CRF stimulation. The results also indicate differences in the renal handling of ACTH in POMC hypersecretory states.
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PMID:Characterization of peptides derived from pro-opiomelanocortin in the biological fluids of a patient with Nelson's syndrome. 300 68

Neurophysins have been recognized as the carrier proteins of vasopressin and oxytocin. The distribution of neurophysins is immunohistochemically confirmed in the hypothalamus, median eminence, and posterior lobe of the pituitary gland. The authors detected neurophysins in the human corticotrophs and pituitary adenomas with the use of the immunohistochemical method with antiserum to human neurophysins, which did not cross-react with adrenocorticotropic hormone (ACTH), beta-endorphin, and corticotropin-releasing factor. All of ten pituitary glands obtained by autopsy revealed the presence of neurophysin-positive cells in the anterior, intermediate, and the posterior lobes. The neurophysin-positive cells were similar to the corticotrophs in shape and distribution. Simultaneous staining for ACTH and neurophysins in the serial sections revealed that neurophysin-positive cells were also ACTH-positive. One hundred twenty-four cases of pituitary adenoma operated upon were investigated. All of 7 Cushing's adenomas were composed of neurophysin-positive cells. Six tumors with giantism showed sparsely distributed neurophysin-positive cells. No neurophysin-positive cells were observed in any other cases. This study is the first reported evidence of the presence of neurophysins in the human corticotrophs and pituitary adenomas.
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PMID:Presence of neurophysins in the human pituitary corticotrophs, Cushing's adenomas, and growth hormone-producing adenomas detected by immunohistochemical study. 302 92

The addition of orally administered bromocriptine mesylate to cyproheptadine hydrochloride therapy completely normalized urinary-free cortisol levels for three months in a 21-year-old woman with Cushing's syndrome in whom results from standard dexamethasone suppression and metyrapone stimulation tests as well as baseline corticotropin levels were originally compatible with a diagnosis of an occult pituitary adenoma. When transsphenoidal exploration of the sella turcica was unsuccessful and hypercortisolism persisted, the source of corticotropin was discovered using petrosal sinus and venal caval catheterization. A 1 X 1.5-cm carcinoid tumor of the lung was identified and removed, thereby correcting the hypercortisolism. The tumor was demonstrated by immunoperoxidase staining to contain corticotropin. Orally administered bromocriptine, with or without cyproheptadine therapy, may be useful in the palliative treatment of some patients with carcinoid or other ectopic corticotropin-producing tumors. We postulate that bromocriptine therapy acted directly on carcinoid tumor cells to directly inhibit corticotropin production by a dopaminergic mechanism.
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PMID:Prolonged suppression of a corticotropin-producing bronchial carcinoid by oral bromocriptine. 303 81


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