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)

Hepatitis B virus (HBV) is a small enveloped virus containing partially double-stranded DNA. The DNA and HBV-specific DNA polymerase are surrounded by the HBV core antigen (HBcAg), which in turn is surrounded by a lipoprotein envelope containing the HBV surface antigen (HBsAg). Serum of HBV-infected patients contains complete virus particles, as well as non-infectious spherical or filamentous HBsAg particles. Acute hepatitis is characterized by the appearance of serum HBV markers, including HBsAg and IgM anti-HBc, which then disappear during convalescence. Persistence of HBsAg for more than 6 months indicates a carrier state. Chronic hepatitis develops in 90% of newborns who become infected, compared with 29-40% of children infected and 5-10% of adults infected. The immune status of the infected person also influences the development of chronic hepatitis. Chronic HBV infection can be diagnosed by serology (identification of HBsAg and HBV DNA), biochemistry (elevated aminotransferase levels) and liver biopsy. The last is important to assess the severity of disease, its stage and prognosis, and to exclude other hepatic diseases. The outcome of chronic HBV infection varies between individuals, with estimated 5-year survivals of 97% for chronic persistent hepatitis, 86% for chronic active hepatitis, and 55% for chronic active hepatitis with cirrhosis. Treatment with interferon alpha is effective in up to 40% of cases, but in view of the very large number of infected people worldwide, vaccination to prevent spread of the disease is a more cost-effective option.
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PMID:Clinical course and consequences of hepatitis B infection. 1068 39

In the management of hepatitis B new therapeutic options have been established in the last years. Patients with fulminant course are rarely observed and should be submitted in a hepatological center. In chronic hepatitis B today we see mainly HBeAg negative/anti-HBe positive patients with replication of HBV-mutants. The tendency is to treat these cases with lamivudine (LAM) for some years. This is also true for HBV-cirrhosis in stage Child A. The progressed cirrhosis (Child B/C) without option for liver transplantation is not an indication for nucleosidanaloga and a contraindication for interferon. However before liver transplantation the viraemia should be diminished lower than 5 pg/ml. That means the HBV-hybridization test should become negative, which can be achieved with LAM in most cases. During and after liver transplantation the HBV-infected patients receive passive immunoprophylaxis with anti-HBs-hyperimmunoglobulin. In the situation of reinfection and hepatitis, nucleosidanaloga are indicated, in the first line LAM. In the case of LAM-resistance, interferon alpha is a further option. Patients after renal transplantation and HBV-infection should also be treated with LAM. In these patients IFN should be avoided, because graft rejection can be induced. Combined infection with HBV plus HDV, HCV or HIV need an individual concept for treatment. Extrahepatic manifestations of HBV-infection with clinical relevance, e.g. panarteriitis or glomerulonephritis are indications for antiviral treatment. If treatment with glucocorticosteroids is necessary in these situations, the steroids should be given only in combination with LAM. In non-cirrhotic patients with normal aminotransferases but quantify-able viraemia the liver histology is helpful for the indication of treatment.
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PMID:[Therapy of problem cases in hepatitis B]. 1089 96

Chronic hepatitis C (CHC) is a major health problem worldwide, with approximately 200 million affected individuals and a significant rate of progression to end-stage cirrhosis and hepatocellular carcinoma (HCC). If hepatitis C virus (HCV) infection is left untreated in the population, then the number of liver-related deaths will soon double and the need for liver transplantation may increase to five times that seen today. Available therapies for CHC are restricted to interferon alpha (IFN alpha) monotherapy and to the combination of IFN alpha and ribavirin. Despite their high cost and side effects, both of these therapies have proved to be cost effective, particularly combination therapy. IFN alpha monotherapy for one year can induce sustained response (SR) rates of approximately 10% in naive patients infected with HCV genotype 1, and above 50% in those infected with other genotypes. Combination therapy can double or even triple the rate of SR in genotype 1 infections and may further increase the SR rate in the other HCV genotypes. Combination therapy has also been proven to be effective in approximately 50% of relapsed responders to IFN alpha monotherapy. In clinical practice, the decision to treat should be individualized and tailored on the basis of several virus- and host-related factors, particularly the grade and stage of liver disease, HCV genotype and levels of viremia. Appropriate monitoring of therapy by careful clinical evaluation, liver biochemistry and serum HCV RNA testing is mandatory. IFN alpha therapy may also prove to be effective in reducing the rate of HCC development in CHC regardless of whether a virological response is achieved, but this remains to be established.
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PMID:Why and how to treat chronic hepatitis C. 1093 5

Currently seven viruses, A, B, C, D, E, G and transfusion transmitted virus (TTV), are recognised in the hepatitis virus alphabet. Hepatitis G virus and TTV probably do not cause liver disease in humans. Hepatitis A and E usually cause a self-limiting hepatitis followed by complete recovery but occasionally cause fulminant hepatic failure. Hepatitis B and C are major public health problems worldwide due to their sequelae of chronic hepatitis, cirrhosis and primary liver cancer. Chronic hepatitis C is a particular health issue for Western Europe already, accounting for 40% of end-stage cirrhosis and 30% of liver transplants. The contribution of hepatitis C to chronic liver disease is predicted to rise in the future. Vaccines can prevent hepatitis A and B. Interferon alpha is effective treatment in 25-30% of patients with chronic hepatitis B or C. The prospects for treating chronic hepatitis B have been improved by the introduction of reverse transcriptase inhibitors. Lamivudine is the first drug of this class to be licensed. The optimal use of these new drugs is currently being studied. The success rate for treating chronic hepatitis C can be raised to about 40% with combination therapy of interferon alpha and ribavirin. A large research effort to discover new antiviral agents against hepatitis C is already giving the prospect of more effective therapies in the next few years.
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PMID:Virus hepatitis update. 1119 85

So far seven hepatotropic viruses were identified. They are described by letters A,B,C,D,E, G and TTV. The virus of hepatitis F is so far speculative. Virus of hepatitis A and E are transmitted by the orofaecal route and cause only acute hepatitis. The remaining hepatotropic viruses are transmitted by the parenteral route and have a longer incubation period than viruses A and E. The infection with the virus of hepatitis B develops into the chronic stage in about 10% and that of virus C in 50-90%. At least one third of chronic carriers of the virus of hepatitis B or C develop within 10-20 years liver cirrhosis or hepatocellular carcinoma. The objective of therapeutic regimes is eradication of the viruses or at least arrest or retarding of the activity of the disease. Corticoids are not used. The basis of therapeutic regimes is interferon alpha or lamivudine in hepatitis B and interferon alpha with ribavirine in hepatitis C. There is a permanent therapeutic response only in cca 40-50%. Active immunisation is possible against virus of hepatitis A and B. The virus of hepatitis D is a false virus, i.e. a so-called virold, and the cause is a super- or co-infection with the virus of hepatitis B. In this country it is practically not encountered, similarly as the virus of hepatitis E. The assembled findings on virus of hepatitis G are not applied so far very much in practice.
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PMID:[Characteristics of still unknown hepatotropic viruses and a clinical picture of the disease]. 1122 77

Our aim was to evaluate the severity of liver disease resulting from chronic hepatitis C in haemophilia or von Willebrand disease and the efficacy of 6 months treatment with interferon alpha and ribavirin. Fifty-five liver biopsies were performed in 43 patients without any bleeding complications, as seen with ultrasound immediately after the biopsy and 48 h thereafter. Histological changes were mild, with low scores for both inflammation and fibrosis, in spite of long exposure to blood products (mean 27 years). Two patients had compensated cirrhosis. Thirty-five out of 39 included patients completed study treatment. Hepatitis C virus (HCV)-RNA was negative in 77% (30/39) of patients at the end of treatment, and 36% (14/39) achieved a complete sustained response at follow-up 6 months after treatment. Treatment failure was more frequent in patients with virus genotype 1 compared with non-1 (P = 0.0003). The response rate correlated well with that of non-haemophilic patients. In summary: (1) liver biopsy was safe with our regimen; (2) liver disease in our patients was usually mild and had a slow progress; (3) only HCV genotype 1 predicted treatment failure; (4) our treatment results agreed with those from non-haemophilic patients.
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PMID:Clinical spectrum of hepatitis C-related liver disease and response to treatment with interferon and ribavirin in haemophilia or von Willebrand disease. 1132 86

A co-infection with HCV and HIV promotes the development of liver cirrhosis. The avoidance of this hepatic death-trap is therefore the primary aim of treatment for hepatitis C. Up until the end of the year 2000, the standard therapy for hepatitis C in HIV-negative patients was the combination of interferon alpha and ribaverin. The pegylated interferons that became available last year appear to offer advantages. For patients co-infected with HIV, however, no studies have so far been carried out. Combination "partners" of interferon capable of replacing or supplementing ribaveron are presently in the clinical development stage.
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PMID:[Chronic hepatitis C and HIV. Current therapeutic options]. 1137 79

The hepatitis C virus (HCV) causes an acute but very often chronic liver disease. An estimated 3% of the world population is chronically infected with HCV. Chronic hepatitis C is the major cause of cirrhosis and hepatocellular carcinoma (HCC), which most often lead to liver transplantation. HCV is a single-stranded enveloped RNA virus; it belongs to the flaviviridae family. The virus has been classified into six genotypes, some of which are distributed worldwide, others of which are confined to more restricted areas. The genotype is an independent predictor of response to antiviral treatment. Blood transfusion was a major risk factor for acquiring HCV infection before donor screening for surrogate marker testing for non-A, non-B (NANB) hepatitis began in the mid-1980s, followed by screening for antibody to HCV in 1990. Today, intravenous drug use and high-risk sexual activity are the most frequently identified risk factors associated with HCV infection. The prevalence of people with unknown HCV infection worldwide is high, so it is necessary to screen people with risk factors. The treatment of patients with chronic HCV infection who have not been treated previously should consist of interferon alpha (IFN-alpha) and ribavirin.
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PMID:Hepatitis C virus infection: 10 years after the discovery of the virus. 1139 24

Hepatitis C virus (HCV) infection often progresses to chronic hepatitis, cirrhosis, and possibly hepatocellular carcinoma. Chronic hepatitis C infection is a leading cause of chronic liver disease and the most common indication for liver transplantation. Combination therapy of interferon alpha and ribavirin is currently the standard regimen for chronic hepatitis C. This combination can achieve viral clearance in approximately 40% of patients, and improve histology and prognosis. The most cost-effective approach to guide duration of combination therapy is HCV genotyping. Cost effectiveness cannot be improved further by taking other well-defined predictive factors for sustained virological response into account. Recent insights into HCV kinetics and the correlation between initial viral decline and sustained virological response will allow us to optimize and individually tailor antiviral treatment Individualized treatment according to the initial viral decline, together with further improvements in drugs (e.g. by long-acting pegylated interferons), will have new impact on antiviral efficacy and cost effectiveness.
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PMID:What is (cost) effective in patients with chronic hepatitis C virus infection? 1139 25

Chronic infection with the hepatitis B virus (HBV) affects 350 million people worldwide, or approximately 5% of the global population, and commonly results in cirrhosis and hepatocellular carcinoma. Until recently, the only available treatment was injectable interferon alpha and response rates were suboptimal. Moreover, this expensive and toxic therapy had little applicability in the endemic regions of the world, i.e., Asia and Africa. The realisation that orally available nucleoside and nucleotide agents may effectively control this infection opened a new era in the management of chronic hepatitis B. Oral lamivudine recently became approved for treatment of hepatitis B worldwide. It is free of significant toxicity, improves liver histology and rapidly diminishes HBV DNA levels; lamivudine is expected to become the first-line therapy of choice. Nevertheless, the consistent emergence of lamivudine-resistant variants mandates the need to develop additional therapeutic agents. Adefovir dipivoxil, a nucleotide, and entecavir, a nucleoside agent, are promising new drugs that might eventually be used in combination with lamivudine and therefore reduce the incidence of drug resistance. There is a critical need to advance the research of hepatitis B antiviral agents so that effective combination therapies can become widely available.
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PMID:Current pharmacotherapy for hepatitis B infection. 1158 97


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