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

The effectiveness of ketoconazole for the therapy of Cushing's syndrome, both of adrenal and pituitary origin, was retrospectively evaluated. To this end, the clinical and hormonal results in 5 patients were assessed. There were 4 females and one male, with ages ranging between 17 and 64 years. Three of them, who had Cushing's disease, received sustained treatment with ketoconazole when other therapeutic measures had failed. The two remaining patients (one with Cushing's disease and the other with adrenal adenoma) were treated with this drug in the preoperative period to alleviate the deterioration in the clinical condition caused by hypercortisolism. The clinical evolution of the patients is described, as well as the plasma adrenocorticotropin (ACTH) and the free cortisol in 24 hour urine in the subsequent controls. In view of the study results, we feel that ketoconazole is an effective treatment for the long term control of Cushing's syndrome. In addition, it may be also useful as preoperative therapy in those patients severely deteriorated by the sustained hypercortisolism.
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PMID:[Evaluation of the treatment of Cushing's syndrome using ketoconazole]. 269 99

Computed tomographic (CT) scans of the adrenal glands were obtained in nine patients with Cushing disease as a result of an adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma and macronodular hyperplasia of the adrenal glands. The findings were compared retrospectively with those in six patients with Cushing syndrome as a result of an autonomous adrenal adenoma and 16 with Cushing syndrome as a result of ectopic ACTH production. Seven of nine patients with macronodular adrenal hyperplasia had hyperplastic adrenal glands in addition to single or multiple focal adrenal nodules. The six patients with hypercortisolism caused by an autonomous adrenal adenoma showed atrophic (four patients) or normal (two patients) ipsilateral and contralateral adrenal glands. Fourteen of 16 patients with the ectopic ACTH syndrome had hyperplasia of the adrenal glands without nodularity, and only two had focal nodules.
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PMID:Macronodular adrenal hyperplasia in Cushing disease. 282 31

Adrenocorticotropic hormone (ACTH) levels from the inferior petrosal sinuses and peripheral veins were measured in 10 patients with Cushing's disease. All patients had normal or indeterminate computed tomography scans. In 9 of the 10 patients the petrosal vein sampling showed a gradient between pituitary ACTH and peripheral ACTH verifying the supposition of pituitary dependent hypercortisolism. In seven cases preoperative ACTH levels lateralized tumor to one side of the gland. In six of these cases tumor was found at that location at surgery. In the seventh case, no tumor was identified at surgery and that half of the gland was resected. Nine patients were cured following transsphenoidal excision of tumor.
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PMID:Usefulness of preoperative inferior petrosal vein sampling in Cushing's disease. 282 30

The authors administered 100 micrograms human corticotropin-releasing hormone (h-CRH) to alcohol-dependent subjects after short-term abstention from alcohol abuse and observed that these patients released significantly less adrenocorticotrophic hormone (ACTH) than a control group. Cortisol responses were also blunted, but this effect was less pronounced. These findings indicate that hypercortisolism in alcohol withdrawal is driven by a central neurotransmitter/receptor disturbance rather than by peripheral alterations.
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PMID:Response of ACTH and cortisol to human corticotropin-releasing hormone after short-term abstention from alcohol abuse. 284 Sep 77

The current article suggests that the neuroendocrine system constitutes a bidirectional link between the brain and humoral homeostasis in the periphery. Any change of neuronal activity in the brain--regardless whether induced by external stimuli or endogenous errors of metabolism--may result in altered composition of gene products. Among these are peptides which directly or indirectly alter endocrine activity and may concomitantly induce a variety of behavioral effects. This has been experimentally demonstrated by neuropeptidergic manipulation of sleep-electroencephalographic (EEG) measures and behavioral studies in animals. An integral part of the neuroendocrine communication are effects of peripheral hormones upon brain structures and their interactions with the immune system. Within this framework all hormones of the limbic-hypothalamic- pituitary-adrenocortical (LHPA)-axis play a dominant role, because: (1) corticotropin-releasing hormone (CRH) was shown to integrate centrally behavioral and metabolic responses to stress; and (2) corticosteroids exert a host of neurochemical changes within the CNS which by far exceed their primary endocrine feedback action. As a corollary, hyperexposure to corticosteroids induces widespread changes of neuronal cell biology which are of clinical significance for depression research (e.g. neuronal cell loss in the hippocampus, down-regulation of glucocorticoid receptors within monoaminergic neurons). Clinical neuroendocrine research over the past years focussed upon evaluation of pathophysiology underlying dexamethasone resistant cortisol levels or hypercortisolism linked to depression and utilized advanced methods for multihormonal analysis and newly synthesized neuropeptides (e.g. CRH) for challenge studies in combination with neurophysiological assessments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Implications of altered limbic-hypothalamic-pituitary-adrenocortical (LHPA)-function for neurobiology of depression. 284 59

Dogs with spontaneous pituitary-dependent hyperadrenocorticism were divided into two groups, one with normal plasma concentrations of alpha-MSH (normal alpha-MSH dogs, n = 26) and the other with high plasma concentrations of alpha-MSH (high alpha-MSH dogs, n = 14), on the presumption that high alpha-MSH concentrations indicated a parent cell of pars intermedia origin. The urinary corticoid/creatinine ratios of the high alpha-MSH dogs were significantly higher than those of the normal alpha-MSH dogs. The percentage decrease of the corticoid/creatinine ratios following dexamethasone administration was significantly higher in the normal alpha-MSH dogs than in the high alpha-MSH dogs. Dexamethasone resistance occurred in both the normal alpha-MSH dogs (4 out of 26) and the high alpha-MSH dogs (7 out of 14), indicating a relative rather than an absolute difference. The short-term effect of orally administered bromocriptine, at a dose (10 micrograms/kg body weight) known to be effective in lowering prolactin concentrations in dogs, was investigated by measuring concentrations of cortisol, ACTH and alpha-MSH in plasma at 4, 6 and 8 h after administration. Significant decreases were observed for cortisol in both groups and for alpha-MSH only in the high alpha-MSH dogs. The effect of 5 days of bromocriptine administration (10 micrograms at 12-h intervals) was assessed by measurements of urinary corticoid/creatinine ratios. Considering both groups as a whole, only the corticoid/creatinine ratios of the high alpha-MSH dogs decreased significantly on the first day of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of bromocriptine on corticotrophin, melanotrophin and corticosteroid secretion in dogs with pituitary-dependent hyperadrenocorticism. 284 49

A retrospective study on stored plasma from normal dogs and dogs with pituitary dependent hyperadrenocorticism (PDH), pituitary dependent hyperadrenocorticism controlled by mitotane (o,p'-DDD),* iatrogenic hyperadrenocorticism, and hypoadrenocorticism was conducted to determine if alterations in aldosterone production exist in these disorders. The plasma aldosterone concentration (PAC) was measured by radioimmunoassay immediately before and 1 hour after adrenocorticotropic hormone (ACTH) administration (0.5 IU/kg, intravenously [IV]). PACs increased significantly when ACTH was administered to normal dogs. Dogs with PDH had a lower baseline PAC, but their PAC increased to levels similar to that of normal dogs after ACTH administration. In dogs with PDH controlled by o,p'-DDD therapy, the response to ACTH was significantly less than that of normal dogs or dogs with untreated PDH. Dogs with iatrogenic hyperadrenocorticism had a lower baseline and post-ACTH PAC than normal dogs. Dogs with hypoadrenocorticism had a normal basal PAC, but showed no significant increase in PAC following ACTH administration. These findings suggest that PACs are significantly altered in a variety of adrenal diseases, and that the ACTH stimulation test may be useful when evaluating aldosterone secretion in adrenopathic disorders. In addition, at therapeutic dosages, o,p'-DDD treatment was associated with a decrease in basal and post-ACTH PACs in dogs with PDH.
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PMID:A retrospective study of aldosterone secretion in normal and adrenopathic dogs. 285 51

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

Fifty-nine patients with Cushing's syndrome, due to adrenocortical tumor, were studied and treated during the period 1953 through 1983 at Vanderbilt University Medical Center. Cushing's syndrome is caused by hypercortisolism that can be due to (1) medicinal use of steroids, (2) excess pituitary secretion of adrenocorticotropin (ACTH) (Cushing's disease), (3) adrenocortical tumor, benign or malignant, and (4) the ectopic ACTH syndrome. Clinical and endocrinologic features of Cushing's syndrome are described, and differential diagnosis of adrenocortical tumor by precise endocrinologic studies is detailed. Computerized axial tomographic (CAT) scan is currently the most accurate imaging modality for preoperative localization of tumors. Preoperative differential diagnosis between adrenocortical adenoma and carcinoma has become fairly accurate. Operative approaches in each category are described. Follow-up from 1 to 30 years has been completed for all patients, except for one who was lost after 7 years. Results of surgical treatment of adrenocortical adenomas are excellent, but the salvage from adrenocortical carcinomas is poor.
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PMID:Tumors of the adrenal cortex and Cushing's syndrome. 298 63

Adrenocorticotropic hormone (ACTH) administration increases cortisol synthesis but produces a biphasic aldosterone response. Some investigators believe that the hypercortisolism from prolonged ACTH administration is responsible for this aldosterone response. The present study evaluated the plasma aldosterone response to four acute single-dose ACTH regimens that produced only a transient increase in plasma cortisol. Fourteen normal adult men received (1) 1-18 ACTH intravenous bolus (IV), (2) 1-18 ACTH intramuscular (IM), (3) 1-39 ACTH (IM), and (4) 1-24 ACTH (IV). The plasma aldosterone increased within one hour and tended to parallel the cortisol increment with all four ACTH regimens. With all of these ACTH regimens, the plasma aldosterone level decreased below placebo with 1-24 ACTH (IV) (24 hours), 1-39 ACTH (IM) (24 hours), and 1-18 ACTH (IV) and (IM) (48 hours) at a time when the cortisol had returned to normal. These results suggest that the delayed ACTH-induced aldosterone inhibition production are not directly related to cortisol production and do not require prolonged ACTH administration. These observations are consistent with ACTH induction of a nonaldosterone mineralocorticoid, which is independently suppressing aldosterone production.
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PMID:Biphasic plasma aldosterone responses to four single-dose ACTH regimens. 299 73


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