Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of sorbiperan was assessed during radiological examinations of 15 patients with hypomobility of the gallbladder, associated in some cases with atonic dyspepsia, and 25 cases of spastic colon with constipation and/or diarrhea due to diverticulosis, dolichocolon, sigmoiditis, or parasitosis. Patients with gallbladder dysfunction were examined radiologically before and after oral administration of 20 to 40 ml of sorbiperan, the dose varying as a function of bodyweight. In 3 patients, the hypermobility of the gallbladder provoked by this agent was greater than that observed with all usually employed products, in 11 cases the cholagogue produced an excellent effect, while in one case there was no observed effect. Patients with colitis were administered a barium enemea, and an initial series of films were taken. These were repeated after addition of 80 ml of sorbiperan to the same enema. Total, rapid evacuation of the colon was observed in 8 cases, while in 15 cases it was of excellent quality. No effect was noted in 2 cases. Sorbiperan provokes effective contractions of the gallbladder, favours sphincter of Oddi dynamics, increases motility of all digestive tract segments, and very significantly accelerates gastro-entero-colic peristalsis. Tolerance was excellent.
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PMID:[Cineradiological study of the activity of sorbiperan on the gallbladder and colon (author's transl)]. 626 14

When the endoscopic lesion typical anorectocolonic candidiasis is absent, the author demonstrates that mild cases of colonopathy due to Candida albicans do not always present the commonly described classic symptoms of anomarginal, copperhued, running lesions... The proctosigmoidoscope reveals that in half of the cases with concurrent ordinary digestive troubles and Candida albicans present in the stools, the mucosa is congestive and, very often, the rectal cytology disturbed. A good correlation exists between modifications of the rectosigmoid mucosa and the number of Candida albicans colonies isolated from the feces of these patients. In addition, anal pruritus, a rare clinical event by itself, can be attributed to candidiasis using the proctosigmoidoscope and coproculture. Mild anorectocolonic candidiasis can exist as a secondary infection with chronic inflammatory colitis (ulcerative colitis, etc.) or acute mucous colitis. These infections can also be primary and, in these cases, sometimes appear consequent to recent antibiotic therapy.
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PMID:[Contribution of proctosigmoidoscopy in colonopathies caused by Candida albicans]. 639 5

In two patients, treatment of amebic dysentery was followed (despite the disappearance of the infecting organism) by an illness with the clinical, pathological, and radiological characteristics of nonspecific ulcerative colitis. Their case histories indicate that in addition to persistent or recurrent amebic infection, the irritable colon syndrome, and ulcerative postdysenteric colitis, nonspecific ulcerative colitis should be kept in mind in the evaluation and therapy of continuing symptoms in patients with treated amebic dysentery.
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PMID:Nonspecific ulcerative colitis as a sequel to amebic dysentery. 640 60

Rectal folds are seen best in the lateral view. Normal values for the thickness of the folds have been established by measuring these in patients with a diagnosis of irritable bowel syndrome who had no evidence of rectal disease. In severe ulcerative colitis the valves disappear, but they are present earlier in the disease. The first barium enema examination in patients with ulcerative colitis was assessed. When the valve thickness could be measured in these patients it showed values significantly greater than normal. It is uncommon for this finding to be the sole indicator of disease. Patients with Crohn's disease of the rectum showed no increase in the fold thickness. This observation may be helpful in distinguishing between these two forms of colitis.
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PMID:Rectal fold thickness as an indicator of disease. 687 49

In a 4-year period 45 patients were admitted to our gastroenterological u nit with acute infective colitis. The endemic pathogens responsible for the colitis were Yersinia enterocolitica (46%), Campylobacter fetus jejuni (20%), common Salmonellae (13%), less virulent strains of Shigella (9%), Entamoeba hystolytica (7%) and Cytomegalovirus (4%). These microorganisms caused very severe disease in 18% of the patients, who were mostly predisposed. While Salmonella- and amoebic colitis always mimicked ulcerative colitis by the presence of diffuse lesions, the other pathogens caused focal colitis, thus necessitating differential diagnosis vis a vis Crohn's colitis. Two patients (4%) died of complications, while 93% of the patients were cured by proper antimicrobial therapy. In the same period 12 patients were admitted with an acute attack of inflammatory bowel disease due to an intercurrent infection with the same pathogens. In most of these patients clinical remission of IBD was achieved by treating the intercurrent infection. These data indicate that in the presence of an acute attack of colitis an infective etiologic agent must always be sought, and that an attack of chronic idiopathic inflammatory bowel disease may be caused by an intercurrent infection.
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PMID:Acute infective colitis caused by endemic pathogens in western Europe: endoscopic features. 714 Jun 55

We have described a murine model of IBD that was induced in C.B-17 scid mice by transfer of the CD45RBhi subpopulation of CD4+ T cells from normal BALB/c mice and could be prevented by cotransfer of the CD45RBlo CD4+ T cell subset. Here we have dissected the mechanism of pathogenesis of IBD in this model and used this information for rational immunotherapy of the disease. CD4+ cells from diseased mice displayed a highly polarized Th1 pattern of cytokine synthesis upon polyclonal stimulation in vitro. The administration of anti-IFN gamma MAb to mice soon after T cell transfer prevented development of colitis for up to 12 weeks. Continual neutralization of TNF with anti-TNF MAbs reduced the incidence of severe disease; however, neutralization of TNF during only the first 3-4 weeks had no effect. Severe colitis was completely abrogated in mice treated systemically with rIL-10, but not with rIL-4.
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PMID:Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells. 760 Feb 84

Altered peripheral neutrophil function is a feature of IBD that may contribute to the chronicity and extragastrointestinal manifestations of this disease, but clinical evidence for such alterations is confounded by variations in patient characteristics, disease onset, and use of therapeutics that can influence neutrophil function. The use of a rat model of colitis has permitted us to characterize, in a controlled manner, the causal relationship between colitis and altered peripheral neutrophil function. At various times after induction of colitis with trinitrobenzene sulfonic acid (TNBS), peripheral neutrophils were isolated and assays of phagocytosis, chemotaxis, leukotriene B4 (LTB4) synthesis, and superoxide production were performed using a variety of stimuli. Circulating neutrophil numbers increased about fourfold within 12 hr of TNBS administration and returned to normal levels over the following two weeks. LTB4 synthesis in response to calcium ionophore decreased at 12 hr after induction of colitis, then returned to control levels. The chemotactic responses of peripheral neutrophils to LTB4 and FMLP in vitro and to LTB4 and IL-8 in vivo were profoundly suppressed through the two-week study period. Phagocytosis of nitroblue tetrazolium was significantly enhanced (ca. threefold) at 12 hr after induction of colitis and remained elevated throughout the study period. Superoxide production was also significantly elevated in the early phase of colitis (by ca. fourfold), but was not different from control levels at seven and 14 days. These results demonstrate that colonic inflammation profoundly influences peripheral blood neutrophil function, although the direction and magnitude of the alteration varied among the various functions assessed. The prolonged depression of chemotactic activity may represent a physiological reaction to limit the inflammatory response.
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PMID:Alterations in rat peripheral blood neutrophil function as a consequence of colitis. 782 Nov 10

1. Tumour necrosis factor is a proinflammatory macrophage-derived polypeptide cytokine. Its participation in disease processes has been usually inferred from data obtained from experiments in vitro or from measurements of its plasma circulating levels. To investigate its role in chronic ulcerative colitis, we have quantified in vivo the steady-state release of tumour necrosis factor into the colonic lumen. 2. We studied 19 patients with untreated active ulcerative colitis and seven patients with irritable bowel syndrome as controls. A group of seven patients with active ulcerative colitis were studied before and after 4 weeks on treatment with oral 5-aminosalicylic acid. By means of an intracolonic double-lumen perfusion tube, an isotonic solution was continuously infused 50 cm from the anal verge at a rate of 5 ml/min, and was recovered 30 cm distally by siphonage. Effluents were assayed for tumour necrosis factor by a specific e.l.i.s.a. and for prostaglandin E2 and leukotriene B4 by specific r.i.a.s. 3. The intracolonic release of tumour necrosis factor was undetectable in patients with irritable bowel syndrome, whereas measurable release occurred in 15 out of 19 patients with active ulcerative colitis (P < 0.01). Prostaglandin E2 and leukotriene B4 release were also increased in active ulcerative colitis by comparison with irritable bowel syndrome (P < 0.01). Five out of seven patients with colitis improved with 5-aminosalicylic acid treatment, and tumour necrosis factor release became undetectable or decreased markedly (P < 0.05 compared with before treatment). However, tumour necrosis factor release remained high in the non-responder patients. 4. These findings indicate that intracolonic immunoreactive tumour necrosis factor release is enhanced in active chronic ulcerative colitis, becoming undetectable when mucosal lesions are healed. These results suggest that the luminal release of tumour necrosis factor may serve as an objective index of inflammatory activity in patients with chronic ulcerative colitis.
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PMID:Intraluminal colonic release of immunoreactive tumour necrosis factor in chronic ulcerative colitis. 783 99

Collagenous colitis should be added to the differential diagnosis of chronic, watery, nonbloody diarrhea with normal endoscopic findings. Patients with collagenous colitis are often middle-aged women previously diagnosed as having irritable bowel syndrome. The diagnosis of collagenous colitis is based on histologic evaluation of a rectal biopsy specimen. Biopsy shows a thickened, subepithelial, acellular, eosinophilic collagen band. Symptoms often resolve after treatment with oral sulfasalazine.
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PMID:Collagenous colitis: a cause of chronic diarrhea. 790 84

Atypical forms of IBD include the microscopic colitides, collagenous and lymphocytic colitis, and two macroscopic colitides, SRUS and diversion colitis. Clinical presentations include chronic, watery diarrhea and intermittant rectal bleeding. Constitutional symptoms are typically absent; laboratory data are often nonspecific. Colonoscopic evaluation and mucosal biopsy are essential in establishing these diagnoses and excluding more classic forms of IBD (i.e., Crohn's disease or idiopathic ulcerative colitis). Prognosis and response to treatment are variable; potential therapeutic options include dietary manipulations, topical or systemic anti-inflammatory agents, and, in refractory cases, surgical intervention.
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PMID:Atypical forms of inflammatory bowel disease. 796 8


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