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)

Human corticotropin-releasing hormone (hCRH) test was performed in 57 normal volunteers and 102 patients with hypothalamic, pituitary and adrenocortical diseases. Intravenous bolus injection of synthetic hCRH, 100 micrograms for adults or 1.5 micrograms/kg for children, increased plasma ACTH and cortisol levels in about 90% of normal subjects. In 47 patients with Cushing's disease, plasma ACTH tended to show an exaggerated response to hCRH and peak ACTH was the most frequent abnormal component among the several reaction parameters. Poor responders among normal subjects and patients with Cushing's disease had significantly higher plasma cortisol levels before CRH administration. Patients with hypothalamic hypopituitarism showed exaggerated response, whereas patients with primary pituitary lesion, isolated ACTH deficiency or adrenal Cushing's syndrome showed no ACTH response. These differences in the response of patients suggest the value of the hCRH test in their differential diagnosis.
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PMID:Human corticotropin-releasing hormone test in normal subjects and patients with hypothalamic, pituitary or adrenocortical disorders. 284 92

Abnormalities in hypothalamic-pituitary adrenal axis function were demonstrated by measuring plasma adrenocorticotropin abnormal concentrations following Vasoactive Intestinal Peptide (VIP) and Corticotropin Releasing Hormone (CRH) administration during a phase of remission of Cushing's disease in a 45-year-old female patient. When observed 80 days after the first examination, the patient no longer showed cushingoid features and serum cortisol and plasma ACTH were not abnormally high. VIP infusion (75 micrograms during 12 min) induced a significant increase in serum cortisol and ACTH plasma levels with respect to the normal unresponsiveness. Exaggerated plasma ACTH response to CRH (50 micrograms iv) was also observed. We conclude that the study of ACTH and cortisol response to VIP and CRH may be useful in revealing Cushing's disease even during a remission phase of the disorder.
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PMID:Abnormal responses to vasoactive intestinal peptide and corticotropin releasing hormone during the spontaneous remission of Cushing's disease. 285 Mar 11

The results of investigation of the secretion of hypophyseal, adrenal and renal hormones resulting from parlodel administration in 44 patients with Itsenko-Cushing disease were discussed. Concentrations of corticotropin (ACTH), prolactin, somatotropin (STH), thyrotropin (TSH), cortisol, aldosterone, adrenalin, noradrenaline, dopamine and blood renin activity were determined by radioimmunoassays and radioenzymatic methods on an empty stomach and 30, 60 min., 2, 4 and 24 h after parlodel administration (2.5 mg) per os. Parlodel administration in Itsenko-Cushing disease was shown to cause a decrease in the secretion of hypophyseal hormones (ACTH, prolactin and STH). The level of cortisol raised before the start of the investigation was gradually decreased after the drug administration and reached its minimum in 2-4 h. Correlation of the basal level of aldosterone and blood renin activity, and a response of the renin-angiotensin-aldosterone system to parlodel administration was revealed. Changes in the secretion of catecholamines were of diverse nature: a decrease in the blood concentration of noradrenaline in the absence of adrenalin and dopamine shifts.
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PMID:[Effect of a single dose of parlodel on the secretion of various hormones in Itsenko-Cushing disease]. 285 Nov 39

The precursor of ACTH and beta-LPH is a glycoprotein with a molecular weight of more than 30 000. Its gene consists of three exons with two intervening sequences and most of the protein coding sequence is in exon 3. The gene is expressed not only in the pituitary gland but also in extrapituitary tissues. The gene expression in the anterior pituitary gland is regulated by CRF and glucocorticoids, but it is regulated differently in other tissues. The processing of the ACTH/beta-LPH precursor yields several peptides, but final products vary in tissues due to differential processing. The processing is abnormal in ACTH-producing tumours, especially in ectopic ACTH-producing tumours. Some abnormalities may also occur at the transcriptional or post-transcriptional level as well. Peptides derived from the same precursor are secreted concomitantly from the pituitary gland. CRF is the major stimulating factor, but vasopressin and some other factors are also involved in stimulating ACTH release. On the other hand, glucocorticoids inhibit ACTH release by acting at the hypothalamic and pituitary levels. In the pituitary ACTH-producing adenomas of Cushing's disease, CRF, vasopressin as well as other non-physiological factors stimulate ACTH secretion. Such abnormal receptor mechanisms are also seen in ectopic ACTH-producing tumours.
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PMID:ACTH and related peptides: molecular biology, biochemistry and regulation of secretion. 286 40

The application of modern investigative techniques, particularly electron microscopy and immunohistochemistry, to the pituitary gland in Cushing's disease have confirmed that in the majority of cases (up to 90% in some series) the disease is due to a corticotroph microadenoma. It has also been shown that the tumours may produce not only ACTH, but also other peptides derived from the same precursor molecule, pro-opiomelanocortin and, in a small minority of cases, other pituitary hormones (e.g. prolactin). Since these peptides are known to have physiological actions they may account for some of the varied symptoms and signs of Cushing's disease. Because of the high incidence of single tumours the treatment of choice in many centres has become selective adenomectomy by the transsphenoidal route. However, a minority of cases appear to be the result of primary hypothalamic or central abnormalities and this may account for the identification of a normal pituitary gland or of corticotroph hyperplasia (with or without tumour formation). It is not possible at the present to identify these groups of patients on the basis of biochemical testing. It is hoped that detailed prospective studies correlating hormone secretion, responses to biochemical testing and detailed investigation of pathological tissue will provide further insight into the pathogenesis of particular variants of the disease.
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PMID:Current topics in neuropathology. Cushing's disease. 286 23

The diagnostic accuracy of the corticotropin-releasing-hormone (CRH) test was compared with that of the oral high-dose dexamethasone suppression test in the differential diagnosis of Cushing's syndrome. A false-negative response to CRH was present in 9% (2 of 22) of patients with pituitary-dependent Cushing's disease and to high-dose dexamethasone in 11% (2 of 18). All 3 patients with Cushing's syndrome due to an adrenal adenoma were unresponsive to both CRH and dexamethasone. The only patient with ectopic corticotropin secretion had a false-positive response of corticotropin to dexamethasone and no response of corticotropin to CRH. Simultaneous failure of both tests to indicate the cause of Cushing's syndrome did not occur in this series, except in 1 patient with Cushing's disease and overt macronodular hyperplasia. It is concluded that the diagnostic accuracy of the CRH test in patients with Cushing's syndrome is comparable to that of the high-dose dexamethasone test and that the highest discriminatory score in the differential diagnosis of Cushing's syndrome is achieved by using both a CRH test and a high-dose dexamethasone test.
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PMID:The corticotropin-releasing-hormone test versus the high-dose dexamethasone test in the differential diagnosis of Cushing's syndrome. 287 82

Circulating autoantibodies to human fetal pituitary cells were detected in 13 out of 51 patients who underwent transsphenoidal microsurgery for Cushing's disease. The absence of Fc receptors on human fetal pituitary corticotropin-producing cells allowed the detection of antibodies to these cells. In all the 13 patients, the antibodies were present before surgery, and 10 of them showed clinical and/or biochemical signs of incomplete cure of Cushing's disease after surgery. Only 3 out of 27 patients with a favourable outcome were antibody-positive. In all the antibody-positive patients, the antibodies were directed to corticotropin-producing cells and in 8 patients also to luteinising hormone or human growth hormone producing cells. A non-antigen-specific adherence of antibodies to Fc-receptors on corticotropin-cells was excluded by unchanged binding after preincubation of sections with purified rabbit Fc or Fc aggregates. The presence of pituitary corticotropin-cell antibodies in patients with Cushing's disease is associated with an unsuccessful outcome after transsphenoidal selective adenectomy.
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PMID:Autoantibodies to pituitary corticotropin-producing cells: possible marker for unfavourable outcome after pituitary microsurgery for Cushing's disease. 288 95

Four tumors consisting of pituitary adenomatous cells (AD) intricated with ganglion cells (GC) were studied. Each case was associated with a different clinical syndrome: acromegaly, amenorrhea-galactorrhea, Cushing's disease and isolated tumoral syndrome with no hormonal hypersecretion. (a) In the case with acromegaly, immunoreactive growth hormone (IR-GH) was present in 80% of AD. IR-vasoactive intestinal peptide (VIP) was found in 5%-10% of AD and in few GC. Rare GC and processes showed IR-GH-releasing hormone (GRH), -somatostatin (SRIH), -gonadotropin-releasing hormone and -adrenocorticotropin-releasing hormone. (b) In the case with amenorrhea-galactorrhea, IR-prolactin (PRL) was seen in 90% of AD. IR-PRL and -VIP were present in rare GC. (c) In the case with Cushing's disease, 60% of AD and very few GC contained IR-adrenocorticotropin (ACTH) and beta-lipotropin. Rare GC processes contained IR-SRIH. (d) In the case without pituitary hormone hypersecretion, PRL was localized in rare AD and GC. Pituitary hormone and neuropeptides were never colocalized in the same cells. No case displayed IR-neurophysins or -thyroliberin. Pituitary hormones were localized by ultrastructural immunogold labeling. These findings show that: (i) in three cases, pituitary hormones (PRL and ACTH), and, in one case, VIP could be localized in both adenomatous and ganglion cells; (ii) the pituitary hormone-containing cells in the tumors could be related to the hypersecretory syndromes; (iii) intratumoral IR-VIP and -GRH might be involved in GH and PRL hypersecretion in the cases with acromegaly and amenorrhea-galactorrhea.
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PMID:Immunocytochemistry of four mixed pituitary adenomas and intrasellar gangliocytomas associated with different clinical syndromes: acromegaly, amenorrhea-galactorrhea, Cushing's disease and isolated tumoral syndrome. 292 94

Immunoreactive beta-endorphin was determined in the plasma of 37 elderly subjects (73 +/- 7 years of age), in 3 young or young adult subjects without adrenal disease, in 4 women with clinical adrenogenital syndrome, in 1 man with Cushing's disease. Immunoreactive beta-endorphin in plasma was measured by radioimmunoassay in six samples of each subject collected at 4-hour intervals over a 24-hour span. The observation of a circadian rhythm in circulating immunoreactive beta-endorphin with highest values during the late night and early morning hours is extended to elderly subjects in the 8th decade. The beta-endorphin plasma concentrations in the few clinically healthy young adult subjects studied fell within the same range. The circadian variation of the group of elderly subjects was used as reference in the clinical evaluation of plasma beta-endorphin concentrations in patients with pituitary-adrenocortical disorders. The need for circadian rhythm qualified reference values is shown by the observation of the circadian variations of circulating immunoreactive beta-endorphins in the patients with adrenogenital syndrome and Cushing's disease in whom abnormalities in the concentration of circulating beta-endorphin were found at certain circadian stages but not at others.
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PMID:Circadian rhythm of beta-endorphin in the plasma of clinically healthy subjects and in patients with adrenocortical disorders. 294 69

Ovine corticotropin-releasing factor (oCRF) stimulates increased plasma immunoreactive adrenocorticotropin (IR-ACTH) and IR-cortisol at threshold, half-maximal, and maximal doses of 0.01-0.03, 0.3-1, and 3-10 micrograms/kg, respectively. Side effects occur with increasing frequency, severity, and duration at doses above 1 microgram/kg. oCRF has a prolonged duration of action, at least in part because of the long circulating half-life of intact oCRF in plasma. Increasing doses of oCRF given in late afternoon progressively diminish the next morning's circadian rise in plasma IR-ACTH in normal subjects, but not in Addisonian patients or subjects receiving metyrapone, indicating that prolonged oCRF-induced hypercortisolemia is the cause. Plasma IR-lipotropins and IR-beta-endorphin rise and fall concomitantly with IR-ACTH after oCRF injection. Arginine vasopressin increases the IR-ACTH response to oCRF fourfold when given simultaneously with oCRF. Cushing's disease patients respond variably, suggesting that oCRF may not be a very useful diagnostic agent in Cushing's syndrome. However, the combination of oCRF with growth hormone-releasing factor, gonadotropin-releasing hormone, and thyrotropin-releasing hormone appears to provide a rapid and useful test of combined anterior pituitary function.
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PMID:Clinical studies with synthetic ovine corticotropin-releasing factor. 298 41


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