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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reliability of the beta 1-24 corticotropin test, which is both cheap and safe, in the assessment of the hypothalamic-pituitary-adrenocortical function was re-evaluated by comparing its results with those of the metyrapone test in 71 subjects: 30 controls and 51 patients with suspected pituitary-adrenal dysfunction. Response to a 500 micrograms intramuscular injection of beta 1-24 corticotropin was evaluated by measuring the 60 min plasma cortisol levels; 4.5 g of metyrapone divided into 6 doses were then administered orally and response was evaluated by measuring plasma 11-desoxycortisol levels. A highly significant correlation (r = 0.79; p less than 0.001) was observed between plasma cortisol and plasma 11-desoxycortisol levels. The results were best interpreted by expressing the values obtained as plasma cortisol concentrations which, in normal subjects are at least 21 micrograms/100 ml. The rapid beta 1-24 corticotropin test was found to be very reliable (sensitivity 90%, specificity 100%) to detect adrenal insufficiency, irrespective of the organs affected on the hypothalamic-adrenocortical axis.
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PMID:[Rapid beta 1-24-corticotropin test in the exploration of the corticotropic axis. 71 cases]. 609 44

The signs and symptoms of adrenal insufficiency in the postoperative patient are generally nonspecific, and the diagnosis is usually made at postmortem examination. Two patients in whom adrenal insufficiency developed in the postoperative period are reported on (one had metastatic carcinoma to the adrenal glands and in the other bilateral adrenal hemorrhage developed during anticoagulant treatment). Both patients survived multiple, successive stressful episodes before the diagnosis of adrenal insufficiency was established by the alpha1-24 corticotropin stimulation test.
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PMID:Recognition of adrenal insufficiency in the postoperative patient. 624 51

Chronic oversecretion of adrenocorticotropin (ACTH) in Cushing's disease and partial adrenal insufficiency results in a plasma pattern of mineralocorticoid hormones (MCHs) in which deoxycorticosterone, 18-hydroxycorticosterone and aldosterone remain within normal limits. In patients with deficiencies of 17 alpha- and 21-hydroxylation, the entire MCH pathway may be initially stimulated by ACTH alone in the presence of reduced cortisol production. An ACTH-induced intra-adrenal factor reflected by levels of cortisol production, or cortisol itself, may determine MCH levels by its inhibition (high) or lack of inhibition (low) of 11 beta- and 18-hydroxylation.
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PMID:Clinical manifestation of adrenocorticotropin-determined plasma concentrations of mineralocorticoid hormones. 625 60

Increased adrenocorticotropic hormone (ACTH) levels after bilateral adrenalectomy could be secondary to a pituitary tumor, under replacement with cortisol, or an abnormality in the hypothalamic-pituitary-adrenal feedback loop. To distinguish between these possibilities, ACTH levels were measured before and after cortisol infusion (20 mg/h for 4 hours) in five groups: normal volunteers; patients with idiopathic adrenal insufficiency; and with bilateral adrenalectomy for Cushing's syndrome with no roentgenographic evidence of pituitary tumor, with pituitary tumors, and with equivocal roentgenographic studies (suspect pituitary tumors). Control ACTH levels in all groups of patients were higher than in normal volunteers but there was overlapping. Cortisol infusion suppressed ACTH in all subjects but the reductions in the last two groups were less than in the first three. The cortisol suppression test appears to be useful in determining whether increased ACTH level after adrenalectomy is due to a pituitary tumor.
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PMID:Cortisol suppression test in patients with elevated adrenocorticotropic hormone levels. 627 20

A 38-year-old man developed secondary adrenal insufficiency as a consequence of intrathecal methylprednisolone administration. Evidence in support of this diagnosis included an absent plasma cortisol response to insulin-induced hypoglycemia, an inadequate adrenal response to exogenous corticotropin stimulation, a typical delayed response to prolonged corticotropin infusion over 3 days, and the findings of an elevated level of prednisolone in the cerebrospinal fluid a full 2 months after its administration. It is therefore recommended that patients receiving intrathecal steroids be carefully observed for the possible development of secondary adrenal insufficiency.
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PMID:Secondary adrenal insufficiency after intrathecal steroid administration. 627 7

The pituitary glands of 18 patients with untreated Addison's disease were studied by histologic and immunocytochemical methods. Adrenal destruction was caused by tuberculosis (13 cases) or autoimmune adrenalitis (five cases), and the duration of the adrenal insufficiency ranged from one to 16 years. Both diffuse and nodular hyperplasia of corticotropic cells were evident in each case, and the extent of hyperplasia correlated with the duration of disease. In five cases, nodular proliferations with morphologic features between those of hyperplasia and those of adenoma, termed tumorlets, were identified, as were two microadenomas, only one of which was available for study. In all instances, the proliferating corticotrophs stained positively with PAS and were immunoreactive for adrenocorticotropic hormone and beta-endorphin. We conclude that diffuse and nodular corticotroph hyperplasia are common in untreated Addison's disease, although frank adenoma formation seems to be rare. The latter may be related to the short duration of disease or may imply the absence of additional, unknown factors that are required for adenoma growth.
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PMID:The pituitary gland in untreated Addison's disease. A histologic and immunocytologic study of 18 adenohypophyses. 630 13

A normal plasma cortisol response to exogenous corticotropin has been advanced as a reliable indication of adequate hypothalamic-pituitary-adrenal function in patients suspected of having secondary adrenal failure. We have examined the validity of this diagnostic strategy in five patients who had undergone hypophysectomy and 27 patients recently treated with glucocorticoids. Eleven of the patients had normal adrenal responses to cosyntropin but had subnormal responses when the entire hypothalamic-pituitary-adrenal axis was examined using metyrapone; no patient who responded normally to metyrapone failed to respond to cosyntropin. Inducing hypoglycemia with insulin yielded results concordant with the results induced by metyrapone in four patients tested. A normal cortisol response to corticotropin alone should not be relied on to exclude secondary adrenal insufficiency. To do this it is necessary to demonstrate normal activity of the entire hypothalamic-pituitary-adrenal axis, which can be conveniently examined using metyrapone.
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PMID:Normal cortisol response to corticotropin in patients with secondary adrenal failure. 631 66

Ten patients with adrenal insufficiency receiving chronic glucocorticoid therapy were studied. All had subnormal plasma cortisol responses to ovine corticotropin-releasing hormone ( CRH ) (1 microgram/kg as an iv bolus) 12-60 h after discontinuation of steroid treatment. Plasma ACTH responses to CRH fell into three different patterns. The first three patients with primary adrenal insufficiency had high basal ACTH levels and augmented ACTH responses to CRH . A fourth such patient, however, treated with pharmacologic doses of prednisone, had a low normal ACTH response. Patients with secondary adrenal insufficiency had either low basal ACTH levels and diminished responses to CRH or low basal ACTH values but prolonged and augmented plasma ACTH responses to CRH with a delayed peak. We postulate that the group of patients with the former pattern have pituitary gland destruction whereas the patients with the latter pattern have hypothalamic CRH deficiency. Thus, CRH may be useful in differentiating between hypothalamic and pituitary causes of adrenal insufficiency.
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PMID:The corticotropin-releasing hormone stimulation test: a possible aid in the evaluation of patients with adrenal insufficiency. 632 50

In 22 patients undergoing elective surgery, adrenal function was assessed before and on the day of surgery. Patients receiving corticosteroid therapy but with a normal cortisol response to a corticotropin stimulation test (group II, n = 8) were not given hydrocortisone on the day of operation. Their cortisol concentration increased in a manner similar to patients (group I, n = 8) who had never had corticosteroid treatment. The plasma cortisol concentrations in these two groups were less than in subjects (group III), n = 6) with an impaired cortisol response to corticotropin stimulation, who were given hydrocortisone 25 mg at the induction of anaesthesia followed by a continuous infusion of hydrocortisone 100 mg during the next 24 h. There were no clinical signs of circulatory insufficiency in any group. The low-dose hydrocortisone therapy regimen is sufficient for substitution of adrenal function during surgery and in the early postoperative phase. It could lead to mild oversubstitution in patients with impaired adrenal insufficiency undergoing major surgery.
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PMID:Physiological cortisol substitution of long-term steroid-treated patients undergoing major surgery. 679 52

The best way to detect Cushing's syndrome is to measure urinary free cortisol and to conduct a 1-mg dexamethasone suppression test. The best way to distinguish among the varieties of Cushing's syndrome is to measure plasma adrenocorticotropic hormone (ACTH). Urinary 17-ketosteroid and plasma testosterone determinations are the most useful tests for finding the cause of virilization. Short ACTH stimulation is the test of choice to detect adrenal insufficiency.
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PMID:Adrenal dysfunction: test strategies for diagnosis. 746 50


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