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)

This study compares the efficacy of intravenous adrenocorticotropic hormone (ACTH) with intravenous hydrocortisone in the treatment of patients with symptomatic inflammatory bowel disease. Drug doses were pharmacologically equivalent on the basis of achieved plasma cortisol levels and continuously monitored urinary corticoid excretion rates. Drug selection and patient evaluation were accomplished with a random double blind technique. Evaluation of 22 consecutive hospital patients indicates that ACTH and hydrocortisone, when administered intravenously in pharmacologically equivalent dosage, are therapeutically equivalent, that response to ACTH is rapid, with no therapeutic lag, and that differences in therapeutic responses cannont be corrrelated with differences in systemic steroid levels.
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PMID:A controlled evaluation of intravenous adrenocorticotropic hormone and hydrocortisone in the treatment of acute colitis. 16 21

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.
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PMID:ACTH-induced adrenal hemorrhage: a complication of therapy masquerading as an acute abdomen. 184 72

Steroid enemas are widely used in distal inflammatory bowel disease (IBD). They are partly absorbed and suppress adrenocortical function. Beclomethasone dipropionate (BD) is a topically active steroid that undergoes rapid first-pass inactivation in the liver and is practically devoid of systemic side effects. We treated 32 consecutive patients with active distal ulcerative colitis (40 attacks) with 0.5 mg BD and/or 5 mg betamethasone phosphate (BP) enemas for 28 days. Clinical, laboratory, sigmoidoscopic, and histologic data were recorded before, during, and after the trial. The clinical efficacy of both treatments was similar. Betamethasone was slightly more effective in relation to the histologic improvement and disappearance of blood from the stools. Clinical signs of steroid overdosage were noted in patients on BP but not in patients on BD. Mean fasting plasma cortisol at the end of the trial was 2.9 micrograms/dl in the BP group and 15.3 micrograms/dl in the BD group. The adrenocorticotropin test was markedly suppressed in the BP group but not in the BD group. The absence of systemic steroid side effects makes BD enemas a useful addition in the therapy of IBD. Its oral administration should also be considered.
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PMID:A controlled trial of beclomethasone versus betamethasone enemas in distal ulcerative colitis. 200 42

We report two patients with inflammatory bowel disease in whom intravenous corticotropin therapy was complicated by bilateral adrenal hemorrhage. In one, the initial presentation was acute and unilateral, simulating colonic perforation and/or abscess. The diagnosis was made only at exploratory laparotomy. In the second patient, the presentation was subacute; multiple episodes of adrenal hemorrhage occurred subsequent to the course of corticotropin, and ultimately, hypoadrenalinism developed. Pertinent clinical and computed tomographic findings are reviewed.
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PMID:Bilateral adrenal hemorrhage as a complication of intravenous ACTH infusion in two patients with inflammatory bowel disease. 255 96

Increased activation of lymphocytes in inflammatory bowel disease is reflected by alterations of various immunological functions including enhanced spontaneous secretion of rheumatoid factor by mononuclear cells. since in rheumatic diseases increased secretion of rheumatoid factor is associated with decreased levels of beta-endorphin in circulating blood mononuclear leukocytes, we investigated levels of leukocyte beta-endorphin in inflammatory bowel disease and compared them with those in hepatobiliary disorders and in healthy subjects. Levels of beta-endorphin were measured in extracts from peripheral blood mononuclear leukocytes by radioimmunoassay. beta-Endorphin levels ranged from 0 to 67 pg/10(6) cells. Mononuclear leukocytes from ulcerative colitis patients contained as much beta-endorphin as those from healthy control subjects. In patients with Crohn's disease, levels of beta-endorphin were reduced by as much as roughly 50%. An inverse relationship was found between leukocyte beta-endorphin on the one hand and erythrocyte sedimentation rate, blood granulocyte or thrombocyte counts, and C-reactive protein levels in plasma on the other. In patients with various hepatobiliary disorders including fatty liver disease, viral hepatitis, primary biliary cirrhosis, and cryptogenic or alcoholic cirrhosis, beta-endorphin levels were not significantly different from the normal range values. Data indicate that leukocyte beta-endorphin may be involved in regulation of the systemic inflammatory activity of Crohn's disease.
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PMID:Decreased beta-endorphin content in peripheral blood mononuclear leukocytes from patients with Crohn's disease. 786 97

Regulatory neuropeptides are widely distributed in the gastrointestinal tract, where they play an important role in motility, secretion, and immune and inflammatory responses. In this study, the rectal mucosal content of somatostatin (SOM), substance P (SP), beta-endorphin (BE), and thyrotropin-releasing hormone (TRH) was measured by radioimmunoassay in 56 patients with ulcerative colitis (UC), 15 patients with Crohn's disease (CD), 15 patients with acute infectious colitis (AIC), and 11 controls, who showed no inflammation of the rectal mucosa, nor abnormal bowel movements. The content of immunoreactive (ir)-SOM was decreased in UC patients, especially in those with persistent disease activity, while the levels of ir-SP, BE, and TRH were increased in such patients. Some changes of ir-peptide levels were also observed in CD and AIC patients. The changes in neuropeptide levels were analyzed in relation to histological grades of inflammation in UC patients, grades 4-5 showing the most significant changes. The levels of ir-SOM, SP, BE, and TRH showed no significant change in chronic persistent UC when measured 6-12 months after the initial examination. In contrast, in patients with remitting intermittent UC, the levels of SP and BE decreased during remission. Abnormal intestinal neuropeptide content may be implicated in the continued mucosal immune and inflammatory responses that are manifested in patients with inflammatory bowel disease.
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PMID:Abnormal neuropeptide concentration in rectal mucosa of patients with inflammatory bowel disease. 884 73

The mechanisms underlying inflammatory bowel disease (IBD) remain obscure but the importance of inflammatory processes is clear and most pharmacological therapies inhibit inflammation. The search for more effective agents with low toxicity continues. To test the possibility that the antiinflammatory/anticytokine peptide alpha-MSH can be used to control IBD, the peptide was administered to a murine colitis model. The peptide treatment had marked salutary effects: it reduced the appearance of fecal blood by over 80%, inhibited weight loss, and prevented disintegration of the general condition of the animals. Mice given alpha-MSH showed markedly lower production of TNF alpha by tissues of the lower colon stimulated with concanavalin A; the inhibitory effect of alpha-MSH on production of inflammatory nitric oxide by lower bowel tissue was even greater. The combined results indicate that alpha-MSH modulates experimental IBD, perhaps by inhibiting production within the gut of the local proinflammatory agents TNF alpha and nitric oxide, or by inhibiting inflammatory processes closely linked to these mediators.
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PMID:alpha-MSH modulates experimental inflammatory bowel disease. 914 24

Somatostatin receptors have been identified in a variety of neuroendocrine tumors and activated leukocytes. A high density of somatostatin receptors is also present in most intestinal intramural veins of patients with inflammatory bowel disease. We present a case of a 25-yr-old female with severe Crohn's disease unresponsive to medical therapy, including adrenocorticotropic hormone (ACTH) administration. The patient underwent (111)In-DTPA octreotide scintigraphy to evaluate the potential role of somatostatin receptor imaging in inflammatory bowel disease. Despite the lack of significant somatostatin receptors in the affected bowel, an unexpected prominent activity of (111)In-DTPA octreotide was noted in the adrenal glands on the SPECT images, presumably resulting from excessive stimulation by ACTH. The expression of somatostatin receptors in the stimulated adrenals may be used to image other adrenal pathologies and could potentially indicate response to therapy.
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PMID:Adrenal glands imaging with indium-111-DTPA-D-Phe1-octreotide following ACTH therapy. 929 15

The antiinflammatory effects of alpha-melanocyte-stimulating hormone (alpha-MSH) molecules, specifically alpha-MSH(1-13) and its COOH-terminal tripeptide alpha-MSH(11-13), are well established. The peptides have been effective in tests of all major models of inflammation, and more recent tests have been extended to include experimental inflammatory bowel disease, CNS ischemia/reperfusion injury, and bacterial endotoxin-induced inflammation within the brain. The broad effectiveness of alpha-MSH molecules in all major types of inflammation indicates that the peptides exert actions that are very basic to the inflammatory process. Three general mechanisms of antiinflammatory action of alpha-MSH molecules have been identified: inhibition of production of inflammatory mediators by, or inhibition of inflammatory actions of, peripheral host cells; inhibition of peripheral inflammation induced by actions on melanocortin receptors within the brain; inhibition of CNS inflammation by local action of the peptides. It appears that alpha-MSH molecules have multiple actions that modulate the primitive inflammatory response.
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PMID:Mechanisms of antiinflammatory action of the neuroimmunomodulatory peptide alpha-MSH. 962 64

We investigated the responses of the hypothalamic-pituitary-adrenal (HPA) axis during experimental colitis induced by intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid in the rat. On days 3 and 7 after induction of colitis, the corticotropin-releasing hormone (CRH) mRNA level in the parvocellular paraventricular nucleus (pPVN) of the hypothalamus was reduced, the plasma ACTH level remained at the basal level, and the plasma corticosterone (Cort) level was high. Induction of colitis on day 3 after adrenalectomy with Cort pellet replacement (ADX + Cort) resulted in a marked increase in CRH mRNA on day 7 after induction of colitis compared with noncolitic ADX + Cort animals. Pair feeding to match the food intake of the colitic animals resulted in no significant change in CRH mRNA in the pPVN, plasma ACTH, and Cort compared with healthy control animals. These findings indicated that CRH mRNA expression in the pPVN was inhibited by glucocorticoid feedback during this experimental colitis, and the decrease in food intake during colitis was not simply responsible for the expression of CRH mRNA. It is inferred that the HPA axis including the CRH level in the pPVN is altered in patients with inflammatory bowel disease.
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PMID:HPA-axis responses during experimental colitis in the rat. 1195 75


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