Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009324 (ulcerative colitis)
 17,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of mycobacterial heat shock proteins (Hsp) of the 65 kilodalton Hsp family as a possible factor governing cell-mediated immune responses, leading to chronic mucosal inflammation, was examined. Purified peripheral blood mononuclear cells (PBMC) from patients with CD and ulcerative colitis (UC), and from healthy and disease controls were stimulated in culture with a highly purified, recombinant 65 kilodalton Hsp (rHsp65) of M. bovis BCG for 5 d. Cultures were then pulsed with 3H-thymidine for 24 h and uptake determined by liquid scintillation. We found that PBMC from patients with active CD exhibited a significant proliferative response to the soluble rHsp65 as compared with normal controls. In contrast, the proliferative responses of PBMC from patients with inactive CD, inactive and active UC, pancreatitis and cecal carcinoma were found to be not different from controls. Purified T cells or non-T cells of PBMC in the absence of antigen-presenting cells from active CD patients exhibited a lack of proliferative responses to the rHsp65 stimulation in culture. The data indicate an aberrant sensitization of T cells to the 65 kilodalton mycobacterial Hsp in a specific type of IBD, and thus may provide an important clue for the etiopathogenesis of Crohn's disease.
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PMID:Evidence for T lymphocyte reactivity to the 65 kilodalton heat shock protein of mycobacterium in active Crohn's disease. 128 31

The expression of the vascular adhesion molecules ELAM-1 (endothelial leukocyte adhesion molecule 1) and VCAM-1 (vascular cell adhesion molecule 1) was evaluated in colonic mucosa of patients with inflammatory bowel disease and normal controls by immunocytochemistry. VCAM-1 was found to be constitutively expressed in lymphoid aggregates in normal colonic mucosa and was not significantly enhanced or altered in distribution in mucosa of patients with inflammatory bowel disease regardless of the activity of the inflammatory process. In contrast, ELAM-1 was not detected by these techniques in normal colonic mucosa (n = 11) or in colonic mucosa of patients with inflammatory bowel disease which was either uninvolved or quiescent (n = 30). However, high levels of ELAM-1 were consistently found on endothelial surfaces in association with active inflammation in affected areas of colonic mucosa in patients with either ulcerative colitis (n = 27) or Crohn's colitis (n = 9). In addition, ELAM-1 appeared to be present within neutrophils which had migrated into crypt abscesses in affected mucosa. Similar analysis was carried out in the cotton-top tamarin (CTT), a primate that experiences an idiopathic chronic diffuse colitis resembling human ulcerative colitis. Although anti-human VCAM-1 antibodies did not react with the CTT, anti-human ELAM-1 stained endothelial surfaces in mucosal biopsies from CTT with active colitis. No ELAM-1 was identified in mucosa of CTT in which colitis activity was quiescent. Thus ELAM-1 is expressed on colonic endothelial surfaces in association with inflammation and may play an important role in facilitating leukocyte migration into sites of active IBD involvement.
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PMID:Expression of vascular adhesion molecules in inflammatory bowel disease. 137 55

Significantly decreased levels of serumcholinesterase (CHE) were found in acute Crohn's disease (= CD) (3.2 +/- 1.0 KU/L) and acute ulcerative colitis (= UC) (3.54 +/- 1.6 KU/L) as compared to patients with mild or quiescient disease (CD: 5.5 +/- 1.1 KU/L; UC: 5.59 +/- 0.94 KU/L) and healthy controls (5.69 +/- 1.3 KU/L). Suppression of CHE was most evident in Crohn's colitis (2.98 +/- 1.0 KU/L) and extensive UC (2.96 +/- 1.28 KU/L). Intraindividual comparison showed an increase of CHE-levels during treatment with steroids and salicylates. There was no significant correlation to the reduced bodyweight-levels in severe IBD. Best correlations were seen between CHE/albumin (CD: r = +0.61; UC: r = +0.73) and CHE/hematocrit (CD: r = +0.50; UC: r = +0.61) in severe inflammatory bowel disease. The results of a discriminant analysis showed that CHE-levels can predict the degree of activity correctly in the majority of patients with CD and UC. It is suggested that the decrease of serumcholinesterase reflects an inhibition of liver synthesis as an acute phase response-induced by endotoxins and cytokines.
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PMID:[Serum cholinesterases as activity parameters in chronic inflammatory bowel diseases]. 138 Jul 51

The history and etiology of inflammatory bowel disease which is characterized by two major disease processes: ulcerative colitis and Crohn's disease, remain unknown. Research is focussing on seven major areas of genetic, environmental and physiologic factors that apparently relate to this disease. Based on this background, a population based Inflammatory Bowel Disease Registry was established in 1987 in the Lehigh Valley area of southeastern Pennsylvania. Consent forms, patient data forms and protocols for operation and implementation were developed, and databases were designed to accommodate demographic, basic history, follow-up and relative history data. The databases were correlated with an IBD registry ID number which both enabled relational analyses and ensured confidentiality of data information. The registry continues to grow, providing feedback for both continued medical research and supportive information for IBD patients and their physicians.
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PMID:Data management of an inflammatory bowel disease registry. 140 37

Oxygen-derived free radicals and other reactive oxygen metabolites have emerged as a common pathway of tissue injury in a wide variety of otherwise disparate disease processes. This has given rise to the hope that efforts directed towards the pharmacologic control of free radical-mediated tissue injury (Reilly, P.M., Schiller, H. J. and Bulkley, G. B. (1991) Pharmacologic approach to tissue injury mediated by free radicals and other reactive oxygen metabolites. Am. J. Surg. 161: 488-503) may have particular application to patients suffering from Crohn's disease and/or ulcerative colitis. However, because tissue injury by any mechanism, even direct mechanical trauma, can elicit an inflammatory response which entails the secondary generation of toxic oxidants by neutrophils and tissue macrophages, it is important that the evidence for this association be examined critically, so as to discriminate the possibility of an etiologic role for these toxic compounds from their presence as a reflection of injury caused primarily by other agents. Similarly, in considering the therapeutic potential of free radical ablation for the treatment of patients with IBD it is important to distinguish between interventions that might specifically block the fundamental injury mechanism from those which would act in a more nonspecific, anti-inflammatory role.
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PMID:Free radicals and other reactive oxygen metabolites in inflammatory bowel disease: cause, consequence or epiphenomenon? 140 52

The clinical and laboratory findings of 37 patients with primary sclerosing cholangitis (PSC) were reviewed. Mean age was 43.8 years, sex ratio between males and females was 3:1; IBD was present in 91% of patients with 51% having ulcerative colitis, 23% unclassified colitis and 17% Crohn's disease. Twenty-seven patients (73%) were symptomatic presenting most commonly with fatigue, pruritus and hepato-splenomegaly. Cholangiography revealed abnormalities affecting both extrahepatic and intrahepatic biliary ductal systems in 51.8% of cases, and only the intrahepatic or extrahepatic biliary tree, respectively in 11.1% and in 37% of cases. The last prevalence was very high compared with that previously known. Clinical and biochemical data, when compared between asymptomatics and symptomatics, demonstrated a significant difference only for alkaline phosphatase which increased in the symptomatic group and for prothrombin activity which decreased among symptomatic patients. Nevertheless, predictive value of sALP for the presence of PSC was high when pts were pooled together with a randomly selected group of 36 non-affected persons that underwent ERCP for suspected primary sclerosing cholangitis: sensitivity was 94% and specificity 78%.
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PMID:Primary sclerosing cholangitis: an analysis of 37 retrospective cases. 148 78

We randomly surveyed 997 members of the Crohn's and Colitis Foundation of America with inflammatory bowel disease (320 ulcerative colitis and 671 Crohn's disease) in order to: (1) assess their health status, (2) compare members with ulcerative colitis and Crohn's disease, and (3) determine the correlates of health care use. Data collection included variables relating to physical and psychological symptoms, medication use, daily functional status, perceptions of health, and coping styles. The findings indicate that: (1) despite a number of symptoms and complications related to inflammatory bowel disease, the health status of this population is generally good and may be a result of effective coping styles; (2) those with Crohn's disease have more psychosocial difficulties, which appear related to greater symptom severity; (3) both psychosocial and physical health variables are related to number of physician visits, while primarily physical health variables are related to number of hospitalizations and surgeries. Further studies are needed to determine the representativeness of this self-selected sample with others having IBD. In this study, we have provided the basis for developing a more sensitive measure of health status than currently exists, and one which may have implications for future clinical studies.
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PMID:Health status and health care use in persons with inflammatory bowel disease. A national sample. 174 45

The aim of this study was to determine serum retinol levels in patients with inflammatory bowel disease and to attempt to elucidate the mechanism of changes in vitamin A metabolism in these disorders. It was found that in 15 patients with active ulcerative colitis, 14 patients with active Crohn's disease and in 3 operated patients with recurrent Crohn's disease serum retinol levels and retinol-binding protein were significantly lower than in controls. Concentrations of vitamin A did not depend on the localization of inflammatory bowel disease, previous ileal resections, duration of the disease or age and sex of the patients. During successful treatment of active ulcerative colitis normalization of serum retinol levels without substitution of vitamin A was observed. Repeated determinations in patients with Crohn's disease who had low serum retinol levels in an active phase of disease revealed normal vitamin A levels in an inactive phase. The absorption of vitamins A and E in patients with inflammatory bowel disease was normal. The normal serum retinol concentrations in patients with diarrhea due to irritable bowel syndrome, and in those with anorexia nervosa exclude the influence of diarrhea and body weight itself on vitamin A levels. The results of this study indicate that serum retinol levels in patients with active inflammatory bowel disease are secondary to the decreased serum retinol-binding protein concentrations, and probably depend on the increased protein catabolism in these disorders.
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PMID:Metabolism of vitamin A in inflammatory bowel disease. 176 54

The immunoglobulins level, were estimated in the sera of 51 patients with different colonic disorders and 12 controls. In 27 of them, tissue immunoglobulin level were estimated. In bilharzial patients there was significant increase in the serum level of IgG, IgM and IgE. IgA and IgD showed no change. IgA containing cells were (87.5%), IgG (50%) and IgM (16.7%). In patients with amoebic colitis, there was significant increase in serum IgG and IgE. IgA and IgD showed significant decrease while IgM was within normal limits. Tissue IgA and IgG were detected in all acses. IgM containing cells were detected in 2 cases. In patients with irritable bowel syndrome (I.B.S.), there was significant high levels of IgM and IgE. IgG showed significant low level, while IgG and IgA showed no change. Tissue IgA were detected in (70%), IgG in (10%) and IgM in (20%). In patients with ulcerative colitis (U.C.), there was significant high levels of IgM and IgE. IgD showed significant low level, while IgG and IgA showed no change. Tissue IgA, IgG and IgM were detected in all cases. In patients with Crohn's disease, the 3 immunoglobulins were detected.
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PMID:Estimation of serum and tissue immunoglobulins level in some colonic disorders. 190 1

By using two-color immunofluorescence with fluorescein isothiocyanate (FITC) and phycoerythrin (PE)-labelled monoclonal antibodies and multiparameter flow cytometry, we investigated lamina propria lymphocyte subsets of patients with ulcerative colitis (UC) and Crohn's disease (CD). Leu-3/Leu-2 (CD4/CD8) ratio of lamina propria lymphocytes (LPL) of CD (mean +/- SD: 1.9 +/- 0.8, P less than 0.01) was significantly decreased compared with controls (3.3 +/- 1.1), because of an increased number of CD8+ lymphocytes. The majority of lamina propria CD4+ cells were CD4+, Leu-8- and CD4+, CD45R- both in controls and IBD tissue. Many lamina propria T lymphocytes were activated, expressing HLA-DR antigen not only in IBD but also in controls. NK cells defined by CD16 and CD 56 (3.0 +/- 1.4%, P less than 0.01) were significantly decreased in patients with UC compared with controls (6.5 +/- 3.0%). A low proportion of B cells in the intestinal mucosa expressed Leu-8 antigen and CD23 antigen. The proportion of activated B cells of LPL was high in IBD mucosa as well as normal mucosa. These findings suggest that local activation of B cells leads to the loss of the expression of Leu-8 antigen and CD23.
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PMID:Two-color immunofluorescence and flow cytometric analysis of lamina propria lymphocyte subsets in ulcerative colitis and Crohn's disease. 191 70


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