Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inflammation of the bile ducts was studied in liver biopsies from patients with chronic hepatitis C to determine whether the frequency of inflamed bile ducts changes with therapy and correlates with other histological variables and expression of class I and II MHC antigens on ductal epithelium. Twenty patients treated at UMMC between 1991 and 1994 underwent needle biopsies of the liver before and after therapy with interferon alpha 2B (IFN). A complete response to therapy was defined as a return to normal serum alanine aminotransferase levels occurring and persisting during therapy. The number of inflamed bile ducts/total ducts (%IBDs), presence of piecemeal necrosis and lymphoid aggregates, and grade of inflammation were assessed in each high-power field in all areas with bile ducts. The frequencies of these variables were compared in cirrhotics and non-cirrhotics and in patients with complete or incomplete responses to IFN. Frozen sections of biopsies from 5 patients were immunostained using antibodies to HLA-DR and B-2 microglobulin, and positive staining was noted on bile ducts. Before therapy, the %IBD was slightly greater in patients with cirrhosis. After IFN, both %IBD and serum alkaline phosphatase levels decreased in non-cirrhotics who responded to IFN. The change in frequency of IBD with IFN paralleled the changes in the other histological features. No correlation was noted between bile duct inflammation and expression of class I and II antigens. The conclusion is that inflammation of the bile ducts occurs frequently in chronic hepatitis C, correlates with other features of inflammation in the triads, and decreases in response to IFN therapy.
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PMID:Effect of interferon therapy on bile duct inflammation in hepatitis C. 876 34

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

PSC is the most common of the clinically significant hepatobiliary diseases seen in association with IBD, with an incidence that varies from 2.5% to 7.5%. Conversely, 50% to 75% of patients with PSC have IBD. This high degree of association suggests a common pathogenetic mechanism; however, no causal relationship has been established. The etiopathogenesis of PSC remains poorly understood, despite a large number of studies looking at differing hypotheses. The diagnosis is usually established by cholangiography. Liver biopsy can sometimes be helpful in diagnosing pericholangitis. There is a significant overlap of the histology with chronic hepatitis. Serum markers have been studied for diagnosing PSC, particularly for early diagnosis of cholangiocarcinoma, but none have shown the high sensitivity and specificity needed to use them clinically. PSC usually progresses insidiously and eventually leads to cirrhosis. Despite progress in early recognition, optimal management of patients with PSC remains a challenge requiring a multidisciplinary approach among hepatologists, endoscopists, surgeons, and interventional radiologists. Colectomy for ulcerative colitis does not alter the natural history of PSC. There is a high (10% to 15%) incidence of cholangiocarcinoma in patients with PSC. This incidence along with the risk of colon cancer in patients with ulcerative colitis makes it necessary to follow these patients closely. A number of pharmacologic therapies have been evaluated, but none has proven successful in slowing the progression of PSC or prolonging survival. Endoscopic therapy has a proven utility in treating complications of recurrent cholangitis or worsening jaundice in the setting of a dominant stricture, but endoscopy has not been shown to improve survival or decrease the need for liver transplantation. Liver transplantation is life-saving for patients with advanced PSC. Pericholangitis, gallstones, and chronic hepatitis are additional disorders noted in association with IBD, but they are much less common and easier to manage than PSC.
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PMID:Hepatobiliary manifestations of inflammatory bowel disease. 1037 79

Pattern recognition of the long-term disease course before, during, and after pregnancy can provide us with data about the influence of pregnancy on IBD, and vice versa. Determinants that predict an indolent versus an aggressive disease course are currently being sought. Our intention is to analyze the disease course during pregnancy in an EU-IBD inception cohort of 1200 patients diagnosed from 1991 to 1993 and followed up for 10 years. We also attempt to evaluate such factors as smoking and medication and to predict pregnancy course and fertility in IBD as well as in a cross-sectional study of members of the patient organization EFCCA. One of the questions that arose was: what factor is responsible for the observation that pregnancy decreases the incidence of relapses and the development of fibrostenotic lesions? Relaxin and the glycoprotein YKL-40 are validated in the cohort. The protein relaxin, produced by the corpus luteum during pregnancy, increases the laxity of fibrous tissue. Collagen fibers are dissolved and disorganized. As maternal rejection of the fetus does not occur, a protein from the fetal lymphocytes most likely decreases the maternal lymphocyte response. Multiparity may lead to subtle, acquired immune deficits. Glycoprotein YKL-40, which causes fibrosis in RA and cirrhosis, is speculated to be lower in multiparous women than in nonpregnant women due to the fetal lymphocytes that secrete a protein that is a potential immune modulator. Knowledge gained from future EC-IBD studies may result in new legislation (e.g. regarding adoption) that can benefit IBD patients throughout Europe.
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PMID:Pregnancy, fertility, and disease course in patients with Crohn's disease and ulcerative colitis. 1096 10

Although the word synbiotics was coined to describe the combined action of pre- and probiotics, the ability to, like antibiotics, control infection, the term is now increasingly used in a wider sense, as a name for all the substances released by microbial fermentation in the lower gut. One obvious reason is that most of the substances released seem to influence the immune defense, increase resistance to disease, and, most important, prevent complications to surgery such as infections and thrombosis. Protection layer of lactobacillus does not exist only on the GI tract mucosa, it is important at all exterior body surfaces including those of the eye, the nose, the mouth, the respiratory tract, the vagina, not to forget the skin. It is clearly reduced at all sites when the patient is in the settings of ICU. Each human being has his/her own unique microbial collection, especially of strains of Bifidobacterium and Lactobacillus, and it should be possible to identify an individual on the basis of his/her personal intestinal microflora. The flora seems always to be significantly reduced in the sick, especially in connection with severe disease, care in ICU, and in patients with little food intake or on parenteral nutrition. Supply of both pre- and probiotics can modify functions such as appetite, sleep, mood and circadian rhythm, and this most likely through metabolites produced by microbial fermentation in the gut. Supply of lactic acid bacteria (LAB) can also significantly reduce serum levels of a variety of toxins such as endotoxin. An umbrella of supplemented probiotics could provide to the patients with liver cirrhosis a tool to reduce septic manifestations and the incidence of bleeding. LAB are effective in controlling diarrhea of both bacterial and viral origin. A series of experimental studies and several uncontrolled clinical studies support the idea of using probiotics in patients with IBD. Ecoimmunonutrition with pre- pro- and synbiotics offer to be suitable tools in the new millennium.
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PMID:Use of pro-, pre- and synbiotics in the ICU--future options. 1184 May 88

The authors present the results of a long-term monitoring of patients who presented with clinical signs of bleeding from the upper gastrointestinal tract (GIT) but totally negative endoscopy results on admission. Retrospective-prospective analysis of acute endoscopies in patients with clinical signs of bleeding from the upper gastrointestinal tract performed in the Endoscopy Centre of the OstravaTeaching Hospital from 2002 to 2005, long term monitoring of the sample with negative results on admission. A total of 133 patients, i.e. 16.3 % of all acute procedures, with no source of bleeding detected in the first endoscopy. 26.4% of wrong indications. In the rest of the sample, a source of bleeding was detected by endoscopy in 17 patients (15 in an early examination and 2 within one month from the event), i.e. 17.3%. The rate of bleeding recurrence was 15%. The risk of recurrence was higher in patients with haematemesis and a decrease in the blood count (BC) at the time of the first event. In 19 patients, i.e. 14.3%, the source was not detected. In the remaining 33 patients, the findings were as follows: 1) in 4 patients, the source of bleeding was detected in the small intestine (push enteroscopy or enteroclysis); 2) in 3 patients, the source of bleeding was detected in the colon; 3) in 6 patients, IBD was detected; 4) in 5 patients, cirrhosis of the liver was diagnosed within months or years from the event.
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PMID:[Long-term monitoring of patients with clinical symptoms of upper gastrointestinal tract bleeding with a negative endoscopy result]. 1801 62

The article analyzes the prevalence of anemia among 18 800 patients treated at the CSRI of Gastroenterology in 2-year observation. Set the frequency of anemia, which was 8.63%, clarified the influence of gender and age on the frequency of anemia. Characteristics of anemia severity, morphological changes of erythrocytes. Highlights the major disease entities: cirrhosis, PBC, IBD, celiac disease tumors in the organs of the gastrointestinal tract, threatening the development of anemia.
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PMID:[The frequency of anemia among patients of gastroenterological hospital]. 2262 92

Primary biliary diseases have been associated in several studies with various malignancies. Understanding the risk and optimizing surveillance strategy of these malignancies in this specific subset of patients are an important facet of clinical care. For instance, primary sclerosing cholangitis is associated with an increased risk for cholangiocarcinoma (which is very challenging to diagnose) and when IBD is present for colorectal cancer. On the other hand, primary biliary cirrhosis patients with cirrhosis or not responding to 12 months of ursodeoxycholic acid therapy are at increased risk of hepatocellular carcinoma. In this review we will discuss in detail the risks and optimal surveillance strategies for patients with primary biliary diseases.
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PMID:Risk and Surveillance of Cancers in Primary Biliary Tract Disease. 2741 66

Sclerosing cholangitides represent a group of chronic biliary obstructive diseases which include primary sclerosing cholangitis (PSC), IgG4 associated sclerosing cholangitis (IgG4-SC) and secondary sclerosing cholangitis (SSC). The manifestations of the diseases are similar, but their asymptomatic course is also frequent. IgG4-SC belongs to the group of IgG4 associated diseases and it is the most frequently related to type 1 autoimmune pancreatitis. Diagnosing of IgG4-SC is based on typical histopathological images, shape changes revealed by diagnostic imaging, serological tests, concurrent impairment of other organs and response to therapy, where IgG4-SC responds well to treatment with corticoids, whereas the only possibility for the remaining units is endoscopic intervention or liver transplantation. Secondary sclerosing cholangitis may develop as a result of many different insults affecting the biliary tree. Among them, the most frequently described include long-lasting biliary obstruction, surgical injury of the biliary tree, and ischemic cholangitis in liver allotransplants or recurrent pancreatitis. We use serological and imaging examination in PSC diagnostics, sometimes we have to resort to liver biopsy. PSC is to a significant degree accompanied by the presence of idiopathic bowel disease, typically ulcerative colitis. As a result, PSC may lead to cirrhosis of the liver and it is a precancerous condition of several malignancies. With regard to variable locations of the biliary tree injuries concerning the aforementioned units, also certain malignancies in subhepatic landscape need to be considered in the differential diagnosis: pancreatic cancer and cholangiogenous carcinoma.Key words: genetic factors - IBD - IgG4 cholangitis - liver transplantation - bile duct cancer - ursodeoxycholic acid - primary sclerosing cholangitis - secondary cholangitis - sclerosing cholangitis.
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PMID:[A contribution to the differential diagnostics of sclerosing cholangitides]. 2822 91

Primary sclerosing cholangitis (PSC) is a chronic disease leading to fibrotic scarring of the intrahepatic and extrahepatic bile ducts, causing considerable morbidity and mortality via the development of cholestatic liver cirrhosis, concurrent IBD and a high risk of bile duct cancer. Expectations have been high that genetic studies would determine key factors in PSC pathogenesis to support the development of effective medical therapies. Through the application of genome-wide association studies, a large number of disease susceptibility genes have been identified. The overall genetic architecture of PSC shares features with both autoimmune diseases and IBD. Strong human leukocyte antigen gene associations, along with several susceptibility genes that are critically involved in T-cell function, support the involvement of adaptive immune responses in disease pathogenesis, and position PSC as an autoimmune disease. In this Review, we survey the developments that have led to these gene discoveries. We also elaborate relevant interpretations of individual gene findings in the context of established disease models in PSC, and propose relevant translational research efforts to pursue novel insights.
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PMID:Genetics of primary sclerosing cholangitis and pathophysiological implications. 2829 27


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