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)

The purpose of this study was to assess the glucocorticoid agonist activity of the antiprogestin steroid RU-486 by examining its ability to exert a glucocorticoid-like negative feedback effect on pituitary adrenocorticotropic hormone secretion. 10 patients with nonpituitary Cushing's syndrome, from whom cortisol therapy had been withheld for 36 hours, were given an oral dose of either a placebo, cortisol, or 20mg/kg of RU-480. 2 hours later, they were given an intravenous injection of lug/Kg of ovine corticotropin-releasing hormone. Blood samples were taken 15 minutes before the injection, at the time of the injection, and 15, 30, 60, 90, 120, and 180 minutes afterwards to measure adrenocorticotropic hormone and cortisol levels. Blood samples from the patients who received the RU-486 showed that RU-486 had suppressed the ovine corticotropin-releasing hormone-stimulated secretion of adrenocorticotropic hormone. However, the RU-486-induced suppression of the secretion of adrenocorticotropic hormone was only 80% that of the suppression induced by .1 mg/kg of cortisol, i.e., RU-486 had only 1/250 the glucocorticoid agonist effect of cortisol. RU-486, therefore, is a partial glucocorticoid agonist, but the effect is not of sufficient magnitude to prevent adrenal insufficiency in patients with nonpituitary Cushing's syndrome.
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PMID:The antiglucocorticoid and antiprogestin steroid RU 486 suppresses the adrenocorticotropin response to ovine corticotropin releasing hormone in man. 282 6

In this report, a case of Cushing's syndrome due to primary multinodular corticotrope hyperplasia is described. The patient had typical features of Cushing's syndrome and dynamic pituitary-adrenal testing, which suggested an ectopic adrenocorticotropic hormone (ACTH) syndrome. Results of petrosal sinus catheterization indicated that the pituitary gland was the source of excess ACTH. Total hypophysectomy resulted in complete remission of Cushing's syndrome. Light microscopic and immunohistochemical studies revealed multinodular corticotrope hyperplasia. Plasma corticotropin releasing hormone (CRH) was undetectable, and computed tomography of the chest and abdomen disclosed no neoplastic source of CRH. We speculate that either an abnormality in hypothalamic CRH secretion or corticotrope hypersensitivity to CRH might have been responsible for Cushing's syndrome in this patient.
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PMID:Cushing's syndrome due to primary multinodular corticotrope hyperplasia. 283 Apr 41

Ketoconazole has been used as a palliative treatment of Cushing's syndrome, due to its ability to lower cortisol production. We evaluated the effects of ovine Corticotropin Releasing Hormone (oCRH) 100 micrograms i.v. on ACTH and cortisol levels in 6 patients with Cushing's disease before and after treatment with ketoconazole 600 mg/day. Both hormones increased after oCRH. During ketoconazole, cortisol was lowered to normal levels and its response to oCRH was impaired. After treatment, basal ACTH showed variable changes while the response to oCRH was markedly enhanced compared to that before ketoconazole. In vitro: In a continuous perfusion system of isolated anterior pituitary cells from rats or human anterior pituitary adenoma, producing ACTH, ketoconazole 10(-5)-10(-6) M showed no inhibitory effects on both basal or lisine-vasopressin and oCRH stimulated ACTH secretion. Our findings confirm the inhibitory action of ketoconazole on basal and stimulated cortisol secretion. No inhibition of ACTH levels was observed both in vivo and in vitro.
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PMID:ACTH response to corticotropin releasing hormone in Cushing's disease before and after ketoconazole: in vivo and in vitro studies. 283 92

The experience with bilateral simultaneous inferior petrosal sinus catheterization and determination of the ACTH-concentration in 21 patients is reported. Venous blood sampling in the right and left inferior petrosal sinus was obtained before and after stimulation with Corticotropin-Releasing-Hormone (CRH). In 13 patients with Cushing's Syndrome a ACTH gradient (central versus peripheral) was measured. In all patients who were operated (11/13) a microadenoma was confirmed. In all patients with a central/peripheral gradient of the ACTH-levels at the same time an ipsi versus contralateral gradient between the two sides could be established after administration of CRH, which allowed a correct localization of the microadenoma. In 11 of 13 patients the site of the microadenoma was confirmed intraoperatively.
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PMID:[Localization of an ACTH-producing pituitary microadenoma using bilateral and simultaneous catheterization of the inferior petrosal sinus]. 283 91

Cushing's syndrome due to bronchial carcinoid tumors that secrete adrenocorticotropin (ACTH) may be difficult to distinguish from pituitary Cushing's disease, since the responses to dexamethasone and metyrapone are sometimes similar. Recently, the ACTH and cortisol responses to ovine corticotropin-releasing factor (oCRF) have been shown to be different in pituitary Cushing's disease than in Cushing's syndrome due to other causes. It is not known if the response to oCRF can distinguish pituitary Cushing's disease from those ACTH-secreting bronchial carcinoid tumors that respond to dexamethasone and metyrapone. A case of Cushing's syndrome due to an ACTH-secreting bronchial carcinoid is described in which the responses to dexamethasone, metyrapone, and oCRF were indistinguishable from the responses observed in pituitary Cushing's disease. A bronchial carcinoid tumor should be considered even when responses to dexamethasone, metyrapone, and oCRF suggest pituitary Cushing's disease.
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PMID:Ectopic ACTH syndrome caused by a bronchial carcinoid tumor responsive to dexamethasone, metyrapone, and corticotropin-releasing factor. 284 Aug 23

An extremely unusual case of adrenocorticotropin (ACTH)-producing Grawitz tumor is reported in a 56-year-old female. The clinical feature of the patient was compatible with Cushing's syndrome. The plasma levels of ACTH and cortisol were markedly elevated. At autopsy, a left renal tumor was demonstrated and its histopathological diagnosis was renal cell carcinoma (Grawitz tumor). The adrenal gland was bilaterally enlarged with diffuse hyperplasia of the fasciculate zone. The adenohypophyseal cells were atrophic and showed Crooke's degeneration. The tumor contained extremely high levels of ACTH, beta-lipotropin and beta-endorphin. The presence of large molecular weight forms of ACTH has also been demonstrated by a Sephadex G-50 gel filtration of the tumor extract. We authors believe that this is the first documented case of ACTH-producing Grawitz tumor in the literature.
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PMID:Ectopic ACTH syndrome due to Grawitz tumor. 284 40

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

The data on the status of the hypothalamic-pituitary-adrenal (HPA) axis in haemodialysis (HD) patients are conflicting. Moreover, a state reminiscent of Cushing's syndrome has been reported in this group of patients. Corticotropin-releasing hormone (CRH), that is produced by the hypothalamus and modulates the secretion of adrenocorticotropic hormone (ACTH), has been shown to be useful as a provocative test of the HPA axis. We investigated the effect of exogenous ovine CRH (oCRH) on plasma levels of ACTH and cortisol in 13 chronic HD patients. The plasma concentrations of immunoreactive CRH following oCRH administration were similar in patients and controls. In all patients, oCRH given intravenously as bolus injection caused a further increase in the already elevated levels of cortisol. The mean basal plasma levels of ACTH were within the normal range. There was, however, a blunted ACTH response to oCRH. We conclude that the HPA axis in chronic HD patients retains the ability to respond to exogenous oCRH. The patterns of the ACTH and cortisol response to this peptide resemble those observed in chronic stress (depression, anorexia nervosa). Besides, the kinetics of disappearance of oCRH indicate that the kidney may not be the major organ that metabolizes oCRH.
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PMID:Ovine corticotropin-releasing hormone stimulation test in patients with chronic renal failure: pharmacokinetic properties, and plasma adrenocorticotropic hormone and serum cortisol responses. 285 25

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

A male patient with corticotropin-releasing factor (CRF) and adrenocorticotropin (ACTH)-producing syndrome is described. Soon after being referred to us the patient developed pneumonia, anaemia, oedema and respiratory distress, and died on the 24th day after admission. Autopsy and histology revealed that he had a rare type of multiple endocrine neoplasia (type 1 + paraganglioma) with a mediastinal paraganglioma, parathyroidal hyperplasia, pancreatic islet cell adenoma, duodenal multiple carcinoid tumours and adrenocortical nodular hyperplasia. It was not possible to examine the pituitary. The paraganglioma contained a large amount of immunoreactive (IR)-CRF (606 ng/g wet weight), IR-ACTH (59.4 ng/g wet weight), IR-human proopiomelanocortin n-terminal (1-76) peptide (hNT, 156.8 ng/g wet weight) and IR-beta-lipotropin (beta-LPH, 146.9 ng/g wet weight). The major IR-ACTH, beta-LPH and IR-hNT were eluted at ACTH-(1-39), beta-LPH and hNT marker positions, respectively. Big ACTH was not detected. IR-CRF eluted at the human CRF marker position on Sephadex G-75 chromatography and high performance liquid chromatography (HPLC). The IR-CRF fraction from the HPLC showed CRF bioactivity which paralleled that of synthetic human CRF in monolayer cultured rat anterior pituitary cells. Our results suggest that not only ACTH but CRF produced by the paraganglioma was responsible for the patient's Cushing's syndrome.
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PMID:Multiple endocrine neoplasia with Cushing's syndrome due to paraganglioma producing corticotropin-releasing factor and adrenocorticotropin. 287 33


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