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Query: UNIPROT:P01189 (
beta-endorphin
)
21,003
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Adrenal function was evaluated in fourteen cancer patients receiving chemotherapy which included short-term high-dose courses of prednisone. 90 min
corticotropin
stimulation tests were performed before therapy and 1, 2, 4, and 7 days after steroids were discontinued. Responses were evaluated by standard criteria of adrenal function and by measurement of the intergrated cortisol response to
corticotropin
over 90 min. Thirteen of fourteen patients had suppressed adrenal function for at least 24 h. Although in most patients adrenal function had returned to normal between day 2 and 4, in five patients it remained suppressed for 7 days or more. Suppression did not correlate with either steroid dose or duration of therapy. Four of five patients receiving only 5 days' therapy showed evidence of adrenal suppression. Although overt clinical
adrenal insufficiency
after steroid administration is rare, these results indicate that adrenal function is suppressed more regularly after short-term high-dose steroid therapy than has been appreciated.
...
PMID:Adrenal suppression after short-term corticosteroid therapy. 8 70
Four cases of adrenoleukodystrophy (ALD) and one case of adrenomyeloneuropathy (AMN) have developed in a kindred over three generations demonstrating that AMN is a clinical variant of ALD. Pituitary-adrenal function studies were performed in 10 family members, including two affected males and four females identified as carriers of ALD/AMN. No pituitary-adrenal abnormality was found in the carriers. However, basal morning plasma
adrenocorticotropic hormone (ACTH)
levels were markedly elevated in the two males with ALD and AMN, despite the fact that they had no clinical signs of
adrenal insufficiency
and that morning plasma cortisol levels and their response to maximal exogenous ACTH stimulation appeared to be normal. In addition, the integrated 24-hour response to the administration were also subnormal in these two cases. Thus, people with ALD and AMN may have subclinical partial adrenocrotical insufficiency. No other endocrinologic dysfunction was identified.
...
PMID:Adrenoleukodystrophy and adrenomyeloneuropathy associated with partial adrenal insufficiency in three generations of a kindred. 21 53
In four patients who required maintenance glucocorticoid therapy after bilateral adrenalectomy for Cushing's disease, we compared the effects of im injection and oral ingestion of cortisone acetate and hydrocortisone hemisuccinate. By the former route of administration, cortisone acetate was not effective in elevating plasma cortisol levels or in suppressing plasma
adrenocorticotropin
, although hydrocortisone was. When given by mouth, no significant difference was found between the two steroids. Therefore, in the treatment of acute
adrenal insufficiency
or in the maintenance of patients with chronic
adrenal insufficiency
and in their preparation for surgery or other stressful situations, we advise against im injection of cortisone acetate. Oral ingestion, however, is appropriate for maintenance.
...
PMID:Comparison of absorption of cortisone acetate and hydrocortisone hemisuccinate. 23 90
We evaluated the effect of ovine
corticotropin
-releasing hormone (CRH) on plasma immunoreactive (IR) concentrations of ACTH,
alpha-melanocyte-stimulating hormone
, and cortisol in 8 dogs with naturally acquired adrenocortical insufficiency. Of the 7 dogs with primary
adrenal insufficiency
, 6 had markedly high basal plasma IR-ACTH concentrations and exaggerated ACTH responses to CRH administration, whereas 1 dog that was receiving replacement doses of prednisone at the time of testing had normal basal IR-ACTH concentrations and a nearly normal response to CRH. In contrast, the 1 dog with secondary adrenocortical insufficiency had undetectable basal plasma IR-ACTH concentrations, which failed to increase after administration of CRH. Basal plasma
alpha-melanocyte-stimulating hormone
concentrations in the dogs with
adrenal insufficiency
were within normal range and were unaffected by CRH administration. In all 8 dogs with
adrenal insufficiency
, plasma cortisol concentrations were low and did not increase after administration of CRH. Therefore, stimulation with CRH produced 2 patterns of plasma IR-ACTH response when administered to dogs with naturally acquired
adrenal insufficiency
. Dogs with primary
adrenal insufficiency
had high basal plasma IR-ACTH concentrations and exaggerated responses to CRH, whereas the dog with secondary
adrenal insufficiency
had undetectable basal plasma concentrations of IR-ACTH that did not increase after stimulation with CRH.
...
PMID:Effects of synthetic ovine corticotropin-releasing hormone on plasma concentrations of immunoreactive adrenocorticotropin, alpha-melanocyte-stimulating hormone, and cortisol in dogs with naturally acquired adrenocortical insufficiency. 131 90
In this study, we reviewed the diagnostic efficiency of laboratory tests that are performed for assessment of patients with Cushing's syndrome or
adrenal insufficiency
. Baseline laboratory data from patients subsequently diagnosed with adrenal dysfunction were analyzed for tests performed between 1987 and 1989 at our institution. Results were analyzed for 36 patients diagnosed with pituitary-dependent Cushing's syndrome, 15 with ectopic Cushing's syndrome, 12 with adrenal-dependent Cushing's syndrome, 20 with primary
adrenal insufficiency
, and 7 with secondary
adrenal insufficiency
. Tests reviewed were plasma cortisol, plasma
corticotropin
, urinary free cortisol, urinary 17-ketosteroids, urinary ketogenic steroids, low-dose and high-dose dexamethasone suppression, and metyrapone stimulation. Our findings suggest that a substantial proportion of diagnoses could be based on the results of three tests--plasma
corticotropin
, plasma cortisol, and urinary free cortisol. We present a nomogram that combines the results of plasma
corticotropin
and plasma cortisol testing to enhance the diagnostic efficiency of these tests.
...
PMID:Biochemical evaluation of adrenal dysfunction: the laboratory perspective. 133 28
A rate-sensitive fast-feedback inhibition of stress-induced
corticotropin
secretion by glucocorticoids is well documented in rats. Studies in patients with Cushing's disease or
adrenal insufficiency
have also supported the existence of fast feedback in humans. However, few studies exist in normal healthy subjects or depressed patients. This study compared fast-feedback inhibition of
beta-endorphin
/beta-lipotropin secretion by hydrocortisone in 16 control subjects and 16 depressed patients. A fast-feedback effect of hydrocortisone on
beta-endorphin
/beta-lipotropin secretion during the hour of the hydrocortisone infusion was demonstrated in control subjects. Depressed patients demonstrated no increase in
beta-endorphin
/beta-lipotropin concentrations during the infusion. These data suggest a decreased sensitivity to glucocorticoid fast feedback in depressed patients and complement existing studies demonstrating decreased sensitivity to proportional feedback by dexamethasone in depressed patients. We believe the data presented herein are the first demonstration that abnormal feedback occurs at the level of the brain rather than pituitary in depressed patients.
...
PMID:Loss of glucocorticoid fast feedback in depression. 838 66
Four patients developed adrenal hemorrhage during treatment with intravenous
adrenocorticotropic hormone (ACTH)
for severe inflammatory bowel disease (IBD). This complication presented suddenly with upper abdominal and flank pain mimicking an acute surgical abdomen. In each patient the symptoms of the underlying bowel disease had subsided under the ACTH therapy. In our first patient the diagnosis was not made until laparotomy, but in the subsequent three patients the diagnosis was suspected by the strikingly similar clinical presentation. In each of these three latter patients the diagnosis was confirmed by sonography or computed tomography (CT) scan, and surgery was avoided. All four of our patients are doing well at 1-58 months of follow-up. Signs of
adrenal insufficiency
occurred only in the one of our four patients, and in those six of 11 previously reported patients, who had bilateral adrenal hemorrhage. ACTH-induced adrenal hemorrhage requires stopping ACTH and maintaining corticosteroid support. The diagnosis of adrenal hemorrhage should be considered in the patient treated with ACTH who develops unexplained acute abdominal or flank pain. Failure to recognize this complication of ACTH therapy can lead to unnecessary surgery or the dangerous continuation of the offending agent.
...
PMID:ACTH-induced adrenal hemorrhage: a complication of therapy masquerading as an acute abdomen. 184 72
Suramin is a polyanionic compound which has been used in the treatment of trypanosomiasis and acquired immunodeficiency syndrome (AIDS), while preliminary success has been reported in the treatment of cancer. However, suramin also causes
adrenal insufficiency
. We have previously reported that suramin selectively inhibited
corticotropin
(ACTH)-stimulated corticosterone release by dispersed adrenal cells in a dose-dependent manner via a direct interaction with the ACTH molecule. The present study was undertaken in order to investigate the effect of suramin on hormone release by dispersed rat anterior pituitary cells. Suramin at a concentration of 100 microM inhibited both basal and secretagogue-stimulated ACTH release by cells cultured in minimal essential medium (MEM) only, while it had no effect on ACTH release by cells cultured in MEM + 10% fetal calf serum (FCS) or MEM + 0.1% bovine serum albumin (BSA). In addition, suramin also caused a parallel decrease of prolactin (PRL) and growth hormone (GH) release by cells cultured in MEM only, suggesting a toxic, rather than a selective effect of suramin on anterior pituitary cells cultured in MEM only. In addition, suramin potentiated the effect of thyrotropin-releasing hormone (TRH) on PRL release by cells cultured in MEM + 10% FCS and suppressed the inhibitory effect of dopamine (DA) on PRL release by cells cultured in MEM + 10% FCS and in MEM + 0.1% BSA. Comparable suppressive effects of suramin on growth hormone-releasing hormone (GHRH)-stimulated and somatostatin (SRIH)-inhibited GH release were found in cells cultured in MEM + 0.1% BSA but not in cells cultured in MEM + 10% FCS.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Effects of suramin on hormone release by cultured rat anterior pituitary cells. 198 Aug 98
Addison's disease is an uncommon endocrine condition manifested by a variety of nonspecific symptoms, such as malaise, anorexia and nausea. Symptoms usually do not occur until most of the adrenal gland has been destroyed. Autoimmune disease has surpassed tuberculosis as the primary cause of Addison's disease. Nevertheless, tuberculosis still accounts for a significant proportion of cases. The rapid
adrenocorticotropic hormone (ACTH)
stimulation test is useful for identifying
adrenal insufficiency
. Maintenance therapy consists of hydrocortisone and fludrocortisone.
...
PMID:Addison's disease. 200 21
Suppression of endogenous cortisol production was assessed by a
corticotropin
-releasing hormone (CRH) test 24 hours after the last dose of the glucocorticoid in 48 patients (27 women and 21 men; mean age 48.9 [21-69] years) who had been taking fluocortolone for inflammatory rheumatic disease. Both during a few weeks of treatment (9 patients) and after a year (39 patients) complete suppression of endogenous cortisol production occurred in 17 patients, partial suppression in 17. This suppression did not unequivocally correlate with the dosage or duration of treatment, but there was a tendency towards it at higher dose levels (15-30 mg). Cortisol response to the CRH test was unremarkable in 14 patients. These results suggest that secondary
adrenal insufficiency
is to a considerable extent dependent on individual factors. Correspondingly the degree of suppression of the adrenal axis cannot be predicted for an individual patient without suitable testing.
...
PMID:[Corticotropin-releasing hormone (CRH) test for monitoring glucocorticoid therapy]. 216 99
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