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)

In a group of 160 patients with Crohn's disease involving the colon, there were seven patients with toxic dilatation, four with granulomatous colitis and three with ileocolitis, all successfully treated without mortality. This complications is more common than previously recognized in Crohn's colitis. In Crohn's disease, toxic dilatation is less likely to proceed to perforation of the bowel, because of the nature of the pathology and is more likely to respond to conservative measures: intubation, with decompression, corticotropin, steroids and high-dose antibiotic administration. Although patients do recover from this life-threatening complication with conservative management, the majority of patients, if not all, will ultimately come to surgical excision of the colon. If surgery is mandatory, it should be carried out early, rather than late, in the patient who is failing to respond to medical therapy, certainly before the development of perforation, massive hemorrhage, or gram negative sepsis with shock. The surgical therapy will depend upon the state of the bowel at laparotomy. Thus, an intact bowel in a young patient, would favor subtotal colectomy or proctocolectomy; a sealed perforation, a diverting ileostomy with skin level colostomy decompression as suggested by Turnbull and a free perforation, the minimum adequate procedure which will tide the patient over the early postoperative period. Diverting ileostomy alone has been effective in two of our patients but should be avoided in ulcerative colitis. The critically ill patient with the ominous finding of "disintegrating colitis" and multiple leaks, will require nothing less than total radical excision of the diseased bowel in the hope of immediate salvage.
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PMID:Crohn's disease of the colon. III. Toxic dilatation of the colon in Crohn's colitis. 16 16

We investigated the effect of a known T cell mitogen, phytohemagglutinin (PHA) and the neuropeptide beta-endorphin on the in vitro lymphocyte proliferative response in patients with ulcerative colitis and in health persons. We found that patients with ulcerative colitis show enhanced reactivity to PHA, when incubated in the presence of beta-endorphin. The activity of the disease during the period of the investigation seemed to play no role, since lymphocytes from both patients in exacerbation or remission reacted in a similar manner.
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PMID:Enhanced proliferative response to beta-endorphin of phytohemagglutinin-activated lymphocytes from patients with ulcerative colitis. 192 60

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

Abnormal content and proportion of leucin-and methionine-enkephalins and beta-endorphin were found in blood plasma of chronic colitis sufferers. Nonspecific ulcerative colitis was associated with relevant peptides deficiency varying with the disease gravity, whereas in catarrhal colitis the peptides concentration was significantly elevated. Endogenous opioid peptides seem to play a role in pathogenesis of various colitis forms.
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PMID:[Plasma levels of endogenous opioid peptides in patients with chronic colitis]. 253 4

A yin-yang hypothesis is presented linking noradrenergic activity, thromboxane, melatonin, left hemisphere functioning, and cyclic AMP on the one hand, and dopamine, beta-endorphin, calcium, right hemisphere functioning, and cyclic GMP on the other. It is further suggested that there is a yoking of NA, TXA2, serotonin and melatonin in the left hemisphere, and a similar yoking of DA, BE, calcium and cGMP in the right. Evidence is presented to support the hypothesis that each element (NA, TXA2, etc.) on one side can modulate or balance a corresponding element (DA, BE, etc.) on the other. It is suggested that thromboxane is the key element in noradrenergic overactivity and that not taking this into consideration has confounded much prior research. This theory takes into account information processing models as well as pharmacological data and neurochemical theory on coupling of adenylate cyclase to its hormone receptors. Inhibiting noradrenergic overactivity can be obtained by inhibiting thromboxane and concomitantly activating opiate receptors. This protocol may have clinical utility in treating a wide range of disorders such as: anxiety, depression, schizophrenia, sleeplessness, withdrawal states, enuresis, Gilles de la Tourette syndrome, Parkinsonism, Alzheimers, dementia, anorexia, infant ruminations, essential tremor, spasticity of spinal cord injury, diarrhoea, ulcerative colitis, extrapyramidal symptoms, akathisia, neuroleptic malignant syndrome, attention deficit disorder, hyperhidrosis, and possibly AIDS.
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PMID:Inhibiting noradrenergic overactivity by inhibition of thromboxane and concomitant activation of opiate receptors via dietary means. 254 22

We looked for factors predicting the therapeutic outcome in 66 patients with severe ulcerative colitis treated with intravenous hydrocortisone or corticotropin (ACTH) for 10 days. Patients were randomized before therapy within strata defined by whether they had received oral corticosteroids continuously before the study (group A, 35 patients) or not (group B, 31 patients). Comparisons were made between groups receiving what we considered optimal corticoid therapy, hydrocortisone for group A and ACTH for group B. Overall, therapeutic success was achieved in 28 (42%), with a median time of 7.5 days. Favorable factors measured on admission to the study were those suggesting less severe colitis activity: absence of fulminant disease, limited disease extent, a shorter duration of the present attack, fewer stools, a lower erythrocyte sedimentation rate (ESR), and a higher hemoglobin. Factors compatible with more severe colitis including fulminant activity, more extensive disease, a shorter total disease duration, bloody stools, and fewer bowel movements, favored an early response among those patients who were to achieve a remission. Prolonging therapy beyond 10 days by switching to the alternate corticoid drug did not improve the remission rate. Achieving remission during the initial therapy period, especially when it occurred early, was the most important predictive factor for a favorable clinical course during the following year. Prolonging therapy did not improve the 1-year remission rate. In fact, a higher proportion of patients who continued to require therapy underwent colectomy than those who received one treatment course.
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PMID:Predicting the outcome of corticoid therapy for acute ulcerative colitis. Results of a prospective, randomized, double-blind clinical trial. 303 Nov 50

Sixty-six patients hospitalized for ulcerative colitis were treated in a prospective, double-blind, clinical trial. They received either 120 U/day of intravenous corticotropin or 300 mg/day of intravenous hydrocortisone. Patients were randomized within strata defined by whether they had received oral corticosteroids continuously for at least 30 days before the study (group A, 35 patients), or whether they had received no such prior treatment (group B, 31 patients). Twenty-eight of the 66 patients (42%) achieved remission. In group B, the proportion of patients entering remission was greater with corticotropin than with hydrocortisone (63% vs. 27%, 0.025 less than p less than 0.05). The opposite trend was observed within group A, for whom hydrocortisone appeared more effective (53% vs. 25%, 0.05 less than p less than 0.10). Impaired adrenal responsiveness, as measured by serum cortisol and dehydroepiandosterone-sulfate levels, did not explain the different responses to therapy within the two study groups. Twenty of 28 patients whose acute therapy was successful were still in remission 1 yr after study. These data suggest that, at the doses used, intravenous corticotropin therapy of severe ulcerative colitis is the more effective choice for those patients not previously treated with corticosteroids, while intravenous hydrocortisone seems preferable for patients already receiving steroid treatment.
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PMID:Corticotropin versus hydrocortisone in the intravenous treatment of ulcerative colitis. A prospective, randomized, double-blind clinical trial. 630 58

Corticotropin releasing hormone (CRH) is a key hormone in integrated response to stress, acting as the major regulator of the hypothalamic-pituitary-adrenal axis. Recently, local production of CRH has been detected in normal human colonic enterochromaffin cells. CRH is locally secreted in granulomatous and arthritic tissues in rats and humans, where it seems to act as a local proinflammatory agent. To find out if CRH is present in colonic tissues of patients with ulcerative colitis, this study examined the expression of this peptide in the large bowel of patients with ulcerative colitis. Colonic tissues of patients with ulcerative colitis obtained by endoscopic biopsy were immunostained with anti-CRH antibody. CRH messenger (m) RNA was also examined in biopsy specimens of ulcerative colitis by the reverse transcribed polymerase chain reaction method and by in situ hybridisation. Considerably enhanced expression of immunoreactive CRH was found in mucosal inflammatory cells. Intense staining with anti-CRH antibody was also shown in mucosal macrophages. CRH mRNA was expressed in mucosal epithelial cells. The expression of immunoreactive CRH in colonic mucosal epithelial cells of ulcerative colitis slightly increased, but not significantly, compared with normal colonic mucosal epithelial cells. These results suggest that CRH may play a part in the modulation of intestinal immune and inflammatory system, and as a modulator in the pathogenesis of ulcerative colitis.
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PMID:Corticotropin releasing hormone in colonic mucosa in patients with ulcerative colitis. 748 43

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


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