Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The history of alcohol consumption has been nearly as long as the history of mankind. Alcohol-related diseases represent a serious problem all over the world and they show a gradually increasing tendency. It can be stated that the frequency of occurrence, severity and mortality of alcohol-related hepatic diseases are in direct correlation with the amount of alcohol consumed. The direct hepatotoxic effect of alcohol and its metabolites has become obvious by now. In addition to this, other mechanisms also play a part in the development of hepatic diseases: their occurrence and severity are significantly influenced by genetic and environmental factors. The rather wide spectrum of alcohol-related hepatic diseases includes steatosis, perivenular fibrosis, alcohol-related hepatitis, occlusive venous lesions, cirrhosis and hepatocellular cancer. All of these disorders are characterized by clearly defined, characteristic but non-specific changes, which need to be supplemented by histological diagnostic criteria. Cirrhosis, which must still be regarded as an irreversibly lethal condition, is thought to develop in two ways. A well-known and widely accepted assumption is that episodes of alcohol-related hepatitis aggravated by progressive fibrosis sooner or later lead to cirrhosis. Another possible explanation is that steatosis facilitating the development and spreading of perivenular fibrosis--even without episodes of hepatitis--may lead to cirrhosis. Thus, alcohol-related hepatic conditions have characteristic pathohistological features, none of which, however, are pathognomonic at the same time. Therefore, the definitive diagnosis of any form of alcohol-related hepatic disorders needs to take evidence of alcohol consumption into account.
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PMID:[Pathology of alcoholic liver disease]. 1070 21

Hepatitis C virus (HCV) related chronic liver disease is now the leading cause for liver transplantation in many centres. Virological recurrence is inevitable following liver transplantation. Excellent patient and graft survival are seen in the short-term, equivalent to that in patients transplanted for other causes of liver disease. However, histological evidence of disease recurrence or hepatitis is present in over half the patients within a year of transplantation, although a small percentage develop progressive cholestatic hepatitis with graft loss within a year. Cirrhosis can develop in the first year after transplantation and 28% of patients have evidence of cirrhosis by 5 years. There is little agreement over the factors that predict the recurrence of disease, development of cirrhosis within the graft and graft or patient survival. Graft loss due to HCV occurs in up to 9% at 5 years and the long-term prognosis may not be comparable to groups transplanted for other diseases. Patients with hepatocellular carcinoma may benefit from liver transplantation if the tumour is small and without vascular invasion. There are, as yet, no clear guidelines regarding the best combination of immunosuppressants in patients with HCV but viral clearance has been achieved with the use of interferon and ribavirin therapy post-operatively.
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PMID:Liver transplantation for hepatitis C virus related cirrhosis. 1089 Mar 24

Cirrhosis due to hepatitis C is now the commonest indication for liver transplantation in Western Europe and in the United States. Graft reinfection is almost universal. The natural history of recurrent hepatitis C ranges from minimal damage to cirrhosis in a few months or years. Different virus and host immune factors are involved in the pathogenesis of hepatitis and are determinants of the outcome. The association between immunosuppression and severity of HCV recurrence is conflicting and remains to be evaluated fully. The treatment of recurrent HCV disease with IFN or ribavirin, as monotherapy, is ineffective. Preliminary results from combination therapy, however, are encouraging. Currently, a reasonable approach would be to treat patients with histological and clinical disease progression. New approaches for the prophylaxis of recurrent hepatitis C are under evaluation but whether this treatment will influence the severity of liver disease or the outcome of recurrence is still unknown.
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PMID:Recurrent hepatitis C after liver transplantation. 1089 62

Cirrhosis due to hepatitis C virus infection is now the most common indication for liver transplantation in Western Europe and the United States. In the absence of effective prophylaxis, recurrent hepatitis C virus infection is almost inevitable. Although the natural history and intermediate-term outcome of recurrent infection with hepatitis C virus are now better documented, factors that may influence the recurrence of hepatitis and consequent progression of graft disease remain unclear. Interferon used as a single agent for the treatment of recurrent infection has proven unsatisfactory. Early intervention for recurrent infection with the combination of interferon and ribavirin appears promising, and this approach may prevent or delay progression of hepatitis C virus-related graft disease after liver transplantation.
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PMID:Treatment of recurrent hepatitis C following liver transplantation. 1098 Sep 21

Neonatal cholestasis syndrome (NCS) in India has largely remained ignored. Three questions need to be addressed: (a) What is known about NCS in India (b) Where do we stand and (c) What needs to be done? Current data on etiology of NCS indicates that biliary atresia contributes to about 40% of all NCS cases. There is considerable delay in the referral of patients to appropriate centres for management. A delay of 120.8 +/- 60.5 days in biliary atresia and 65.9 +/- 39.2 days in neonatal hepatitis were documented. Biliary atresia cases need to be diagnosed and operated by eight weeks of age so as to have the best results. Delayed referral after 3 months of age, not only bring down the success rate considerably but also adversely affect the management with regard to surgical procedures, nutritional support, control of ascites and finally the cost. Cirrhosis rapidly develops in children with biliary atresia. At this stage the only option left is liver transplantation. An important obstacle in the care of infants with NCS is the misconception of jaundice in newborns. This needs to be handled at a professional level in the training of undergraduates and postgraduates and the lay public. Public awareness campaigns like "Yellow Alert" may be useful in this direction.
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PMID:Neonatal cholestasis syndrome: Indian scene. 1113 78

Thirty-eight cases of post-transfustion HCV hepatitis have been followed for 5-24 years. Cirrhosis and hepatocellular carcinoma were found in 44.7 per cent and 13.1 per cent respectively. Cirrhosis was recognised by pathological evidence as early as one and a half years after transfusion and the clinical evidences of decompensated cirrhosis were noted in the fifth year post-transfusion onward. Hepatocellular carcinoma was first recognised in year ten and thereafter. Nine patients died of liver failure or hepatocellular carcinoma during years 8-16 of the follow-up. Therefore, it is of utmost importance to screen out the HCV infected blood donors and to treat the HCV patients as early and as effectively as possible.
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PMID:The long term outcome of thirty eight post-transfusion hepatitis C. 1128 89

This study aimed to investigate the ratios of precore stop mutant (codon 28; TGG to TAG) to total viremia in 53 HBeAg-positive patients with chronic hepatitis B by amplification-created restriction site assays along the course of HBeAg-to-anti-HBe seroconversion. At baseline, 11% had exclusive wild-type hepatitis B virus (HBV), 15% had exclusively precore mutant, and 74% had mixed viral strains. Precore mutant ratios correlated little with age, sex, or HBV DNA levels (all P > 0.1), but correlated modestly with alanine aminotransferase (ALT) levels (P = 0.05). The intervals from presentation to anti-HBe seroconversion correlated significantly with ALT and precore mutant ratios in univariate analysis but with only precore mutant ratios in multivariate analysis (P = 0.003). Precore mutant ratios at baseline were significantly higher (P < 0.001) in six patients with persistent high viremia and ALT elevation after anti-HBe seroconversion (group 1) than in 47 with remission (group 2). All group 1 patients had exclusive precore mutant after anti-HBe seroconversion, as did only 14 (30%) of the group 2 patients (P = 0.003). Among group 2 patients, precore mutant ratios at baseline or after anti-HBe seroconversion showed no significant difference between 34 patients with sustained remission and 13 with relapse. Cirrhosis developed in 50% (5 of 10) of patients with precore mutant ratios >50% at baseline but only in 12% (5 of 43) of those with precore mutant ratios of <50% at baseline (P < 0.05). In conclusion, precore mutant of variable ratios was frequently detected in HBeAg-positive patients with chronic hepatitis B. Precore mutant ratios tended to correlate with ALT levels and anti-HBe seroconversion, but high precore mutant ratios were associated with persistent hepatitis after anti-HBe seroconversion and increased risk of cirrhosis.
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PMID:Precore stop mutant in HBeAg-positive patients with chronic hepatitis B: clinical characteristics and correlation with the course of HBeAg-to-anti-HBe seroconversion. 1177 86

The survival of a recent series of 823 cirrhosis patients who were followed up for a mean of 48 months was analyzed. Cirrhosis was ascribed to alcohol (26%), hepatitis virus B (58%), hepatitis virus C (11%) or both (2%), or was cryptogenic (3%). Features of decompensation were observed in 51% of the patients at entry, and newly developed in 44% of compensated patients within 5 yr. The 5-yr survival after decompensation was 25%. The leading causes of death were liver failure (53%), hepatocellular carcinoma (HCC, 23%), and variceal bleeding (10%). Early detection of HCC significantly improved the survival of cirrhosis patients. Biannual ultrasonography increased the detection rate of small HCC. Mortality of variceal hemorrhage was much lower in patients with Child-Pugh scores from 5 to 8 than in those with scores above 8 (5% vs. 52%). Endoscopic prophylaxis significantly decreased the incidence of first variceal hemorrhage, but the effect was insufficient to improve the rate of survival. Mortality of first spontaneous bacterial peritonitis was 18%. These data suggest that the mortality of major complications of liver cirrhosis has considerably decreased during the last two decades, while there was no remarkable improvement in long-term survival. More efficient management of etiologic factors would be required.
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PMID:The prognosis of liver cirrhosis in recent years in Korea. 1467 40

Cirrhosis is the end stage of many forms of liver pathologies including hepatitis. The liver is known for its vital role in the processing of xenobiotics, including drugs and toxic compounds. Cirrhosis causes changes in the architecture of the liver leading to changes in blood flow, protein binding, and drug metabolizing enzymes. Drug metabolizing enzymes are primarily decreased due to loss of liver tissue. However, not all enzyme activities are reduced and some are only altered in specific cases. There is a great deal of discrepancy between various reports on cytochrome p450 alterations in liver cirrhosis, likely due to differences in disease severity and other underlying conditions. In general, however, CYP1A and CYP3A levels and related enzyme activities are usually reduced and CYP2C, CYP2A, and CYP2B are mostly unaltered. Both alcohol dehyrogenases and aldehyde dehydrogenases are altered in liver cirrhosis, although the etiology of the disease may determine the expression of alcohol dehydrogenases. Glucuronidation is mainly preserved, but there are a number of factors that determine whether glucuronidation is affected in patients with liver cirrhosis. Low sulphation rates are usually found in patients with liver disease but a decrease in sulfatase activity compensates for the decrease in sulphation rates. In all cases, a reduction in drug metabolizing enzyme activities in liver cirrhosis contributes to decreased clearance of drugs seen in patients with liver abnormalities. The reduction in drug metabolizing enzyme activity must be taken into consideration when adjusting doses, especially in patients with severe liver disease.
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PMID:The effect of liver cirrhosis on the regulation and expression of drug metabolizing enzymes. 1507 93

Primary biliary cirrhosis (PBC), autoimmune cholangitis (AIC = AMA-negative PBC) and primary sclerosing cholangitis (PSC) are autoimmune cholestatic liver diseases. Overlap syndromes combine characteristics of cholestatic liver diseases and autoimmune hepatitis. In PBC, alkaline phosphatase and gamma-glutamyl transferase are elevated, to a lesser degree aminotransferases. Histology shows bile duct lesions. Anti-mitochondrial antibodies are typical. Ursodeoxycholic acid (UDC) is established therapy that slows or even stops the disease progression, at least in early stages of the disease. In non-responders immunosuppression is recommended. PSC is mostly associated with chronic inflammatory bowel diseases. P-ANCA are frequent. Bile duct lesions revealed by retrograde cholangiography are characteristic. UDC is given as therapy. Bile duct strictures or bacterial cholangitis may be late sequelae and should be treated by antibiotics or bile-duct dilatation. Cirrhosis may ultimately develop in PBC and PCS. In progressed PBC or PSC liver transplantation is indicated.
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PMID:[Cholestatic liver diseases]. 1545 69


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