Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 have previously described circulating autoantibodies to a portal tract antigen in patients with primary sclerosing cholangitis. In this study the antigen has been shown by double-labelling studies to be specifically located in the nuclei of tissue neutrophils. Using isolated peripheral blood neutrophils and an immunoperoxidase technique, anti-neutrophil nuclear antibody (ANNA) was found in the serum of 84% of patients with primary sclerosing cholangitis (PSC: n = 32) with a median titre of 1/1000 and a peak titre of 1/500,000. ANNA was also detected in 86% of patients with inflammatory bowel disease alone (IBD: n = 76) with a median titre of 1/10 and a peak titre of 1/10,000. In contrast, only 12% of controls had ANNA, and in none was the titre greater than 1/10. In PSC the ANNA titre correlated with the serum aspartate transaminase concentration, suggesting that it is related to disease activity. In IBD the titre of ANNA was significantly higher in patients with recently active disease. There was no significant difference between the titres seen in ulcerative colitis and Crohn's disease. ANNA was not associated with neutropaenia. The results provide further evidence of involvement of autoimmune mechanisms in inflammatory bowel disease and primary sclerosing cholangitis.
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PMID:Anti-neutrophil nuclear antibody in ulcerative colitis, Crohn's disease and primary sclerosing cholangitis. 278 79

Endoscopy has assumed a preeminent role in the diagnostic approach to IBD. It is more sensitive than radiography in detecting early, subtle changes of IBD, both through endoscopic appearance and histologic sampling of mucosa. Endoscopy also appears to be a safe technique in patients presenting with severe forms of colitis and can play an important role in defining the etiologic basis of disease in this subgroup of patients. In addition to its diagnostic role, endoscopy has proven useful in surveying disease activity, through the development of endoscopic disease activity indices. Endoscopy has also found a prominent role in the diagnostic and therapeutic approach to IBD complications. Endoscopic surveillance of chronic UC patients at risk for colon carcinoma has helped to define a therapeutic approach to this serious complication of UC. Endoscopic therapy has been applied to treat stricture formation associated with long-standing CD. Biliary endoscopy also represents the strategy of choice for diagnosing primary sclerosing cholangitis, an extraintestinal complication occurring in 5% of UC patients. Finally, endoscopy may help facilitate the discovery of disease pathogenesis in IBD, through the use of endoscopically recovered biopsy specimens in the research laboratory. Endoscopy allows for ready access to human tissue that has been the cornerstone of disease-related research over the past two decades.
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PMID:The role of endoscopy in inflammatory bowel disease. 796 13

The role of cholestasis and ileal dysfunction on sterol metabolism was studied in 79 patients with inflammatory bowel diseases (IBDs) and in 23 irritable bowel syndrome (IBS) controls by determining serum sterol/cholesterol proportions. The sterols included cholesterol precursors (delta 8-cholestenol, desmosterol and lathosterol), markers of cholesterol synthesis, cholestanol and plant sterols (campesterol and sitosterol), markers of cholesterol absorption and biliary secretion. The IBD patients were subgrouped into distal ulcerative colitis (dUC, n = 21), pancolitis (pUC, n = 29), ileal Crohn's disease (iCD, n = 20) and colonic Crohn's disease (cCD, n = 9). The cholestanol proportions were increased in the 3 colonic IBD groups, up to two times in cCD patients and seven times in a case with clinically overt primary sclerosing cholangitis, but were within the control IBS levels in the patients with iCD. The sitosterol, but not campesterol, proportion was significantly increased only in the pUC group. In the iCD group only the serum precursor sterol proportions, especially those for delta 8-cholestenol and lathosterol, were elevated probably due to ileal dysfunction induced bile acid malabsorption and compensatorily increased cholesterol synthesis. In conclusion, the findings suggest that the increased cholestanol proportion in colonic IBD is determined mainly by impaired biliary elimination of this sterol, while in ileal affision the dominating change in sterol balance is activated cholesterol synthesis. Thus increased serum cholestanol is a novel finding in colonic IBD, apparently indicating the presence of subclinical cholestasis in a marked number (20-50%) of IBD patients.
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PMID:Serum cholesterol, cholesterol precursors and plant sterols in different inflammatory bowel diseases. 878 5

Anti-neutrophil cytoplasmic antibodies (ANCA) are autoantibodies directed against cytoplasmic constituents of neutrophil granulocytes. Antibodies with specificity for proteinase 3 and myeloperoxidase are seromarkers for systemic vasculitides. ANCA with specificity for lactoferrin were described in patients with several idiopathic inflammatory diseases, such as the inflammatory bowel diseases and rheumatoid arthritis. However, the clinical significance of anti-lactoferrin autoantibodies is still unclear. In this study, we determined the clinical significance of anti-lactoferrin autoantibodies in sera from large groups of patients with ulcerative colitis (UC), Crohn's disease (CD), and primary sclerosing cholangitis (PSC). Antibodies to human lactoferrin were detected by ELISA and by immunoblotting, using an extract of sonicated neutrophils as antigen source. Autoantibodies to lactoferrin were found in 29% of patients with UC, 13% of patients with CD, and 22% of patients with PSC. In inflammatory bowel diseases, the presence of anti-lactoferrin antibodies was not related to treatment, disease activity, duration of disease, or disease extent. In PSC, the presence of autoantibodies to lactoferrin did not correlate with duration of disease or the presence of cirrhosis. However, patients with PSC and coexistent UC had significantly more frequently antibodies to lactoferrin than PSC patients without IBD. In conclusion, autoantibodies to lactoferrin are a common feature of inflammatory bowel diseases and PSC. However, the clinical significance of those autoantibodies is limited as they lack sensitivity and specificity for those disorders. Future research should address the pathophysiological role of anti-lactoferrin ANCA and the influence of anti-lactoferrin ANCA binding on the functional properties of the lactoferrin molecule.
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PMID:Prevalence and clinical significance of anti-lactoferrin autoantibodies in inflammatory bowel diseases and primary sclerosing cholangitis. 978 75

Pouchitis is a potential complication after proctocolectomy and restorative ileoanal anastomosis. It is more frequent in UC than in familial polyposis. Little is known about the etiopathology of pouchitis. Risk factors include the presence of extraintestinal manifestations, primary sclerosing cholangitis, cessation of smoking, and previous course of disease. A host of pathophysiological pathways have been identified as potential mechanisms of pouchitis, which include inflammatory mediators, adhesion molecules, oxygen radical species, p-ANCA, and short-chain fatty acids. The microflora in the pouch may also be an important factor in causing inflammation. The risk of developing cancer in cases of pouchitis has not been established as clearly as in those of UC. Particular attention should be paid to patients who have remaining anorectal mucosa after pouch construction. Experience in the treatment of chronic relapsing and chronic refractory pouchitis is limited. The continuation of conventional anti-inflammatory treatment is successful only in a small percentage of patients. New biological response-modifying therapies which target novel immunoregulatory molecules in IBD will also have impact on the systemic and topical treatment of pouchitis.
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PMID:Pouchitis: pathophysiology and treatment. 987 Jan 62

Patients with primary sclerosing cholangitis (PSC) in Japan have two peaks in age distribution, one in their twenties and the other in their fifties and sixties. PSC patients in Japan have different characteristics from those in other countries: there is a higher incidence of eosinophilia (27%) and positivity for anti-nuclear antibody (30%), less frequent complication with inflammatory bowel diseases (IBD; 21%), and more frequent complication with chronic pancreatitis (15%). In younger patients in Japan (those aged less than 40 years), the incidence of positivity for anti-nuclear antibody was lower (20% vs 38% P < 0.05), complication with IBD was more frequent (39% vs 9% P < 0.01), complication with chronic pancreatitis was less frequent (4% vs 22% P < 0.01), and damage to both the intra- and extrahepatic bile ducts was more frequent (89% vs 56% P < 0.01) than in older patients (those aged 40 years or more). These findings suggest that younger PSC patients in Japan have characteristics similar to those of patients in other countries, and that in Japan older PSC patients have a different pathogenesis from that of younger patients.
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PMID:Recent status of primary sclerosing cholangitis in Japan. 1066 80

Primary sclerosing cholangitis is a cholestatic liver disease strongly associated with IBD. Considerable advances in the understanding of its pathogenesis have been made. The idea of autoimmunity affecting genetically susceptible individuals is largely accepted; however, much remains to be explained about the origin of this disease. Despite active investigation of different therapeutic modalities with the goal of modifying disease progression, liver transplantation continues to be the only option to provide survival benefit in these patients.
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PMID:Primary sclerosing cholangitis. 1506 1

Inflammatory bowel disease is associated with extra-intestinal manifestations which occur either at the same time as flares of bowel inflammation (skin and eye disease) or run a course that is independent to inflammation in the bowel (liver and some joint syndromes). It has been suggested that the skin and eye complications occur as a consequence of the recruitment of activated effector cells released from the gut into the circulation to extra-intestinal site where they cause acute damage. However, this does not explain how patients can develop primary sclerosing cholangitis many years after having their colon removed for colitis. We propose that long-lived populations of memory lymphocytes arise as a consequence of bowel inflammation and that these cells express homing receptors that direct their subsequent migration not only to the gut but also to the liver. These long-lived cells may recirculate to the liver for many years and, in the absence of a local activating stimulus, will not cause damage. However, if they are subsequently activated in the liver this will lead to the development of inflammation and tissue damage which promotes the recruitment of more mucosal lymphocytes resulting in persistent inflammation and disease. The recent findings that MAdCAM-1 and CCL25, previously thought to be restricted to the gut, are up-regulated in the liver during inflammatory liver diseases that complicate IBD support the concept that common mechanisms control lymphocyte recruitment to the inflamed liver and gut.
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PMID:Lymphocyte homing in the pathogenesis of extra-intestinal manifestations of inflammatory bowel disease. 1513 41

According to the literature data the modern concepts of the etiological factors, the pathomorphological features, the diagnosis, the clinical features and the treatment of the drug-induced and the idiopathic pancreatitis, accompanying the IBD are reviewed. The results of a retrospective review of the clinical data of 50 patients, operated on--16 with Crohn's disease and 34 with ulcerative colitis, are shown. Postoperative hyperamylasemia was found in 2 patients with Crohn's disease and in 3 patients with ulcerative colitis. One of them also had primary sclerosing cholangitis. All patients were treated with Metronidazole and Cortizone. Nine years after the operation one of the patients with ulcerative colitis had acute pancreatitis, treated conservatively.
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PMID:[Pancreatitis accompanying inflammatory bowel diseases, and our observations]. 1570 45


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