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)

Chronic hepatitis C is frequently associated with laboratory markers-including LKM1 autoantibodies--of autoimmunity. A 62-yr-old woman with hepatitis C cirrhosis presented autoantibodies against liver and kidney microsomal proteins. By further evaluation of autoantibodies using ELISA and immunoblotting LKM1 and LKM3 autoantibodies could be revealed. The target antigen of LKM3 autoantibodies proved to be UGT-1.1 isoenzyme. In the absence of chronic hepatitis D infection or autoimmune hepatitis type 2, this is the first case that reports the occurrence of LKM3 autoantibodies in HCV-induced chronic liver disease.
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PMID:LKM3 autoantibodies in hepatitis C cirrhosis: a further phenomenon of the HCV-induced autoimmunity. 1128 May 76

Hepatitis C virus infection is a major health burden affecting an estimated 200 million people worldwide. Chronic hepatitis C is one of the leading causes of cirrhosis and end-stage liver cirrhosis; thus effective therapies are required. For many years interferon-alpha has been the treatment of choice for patients with chronic hepatitis C infection. However, in only 10%-15% of patients is interferon-alpha monotherapy successful, leading to sustained virological response. A combination of interferon-alpha and ribavirin significantly enhanced sustained virological response rates to 40%. Strategies to further improve response rates include modification of the interferon dosing schedule with induction dosing and daily interferon, new interferons such as consensus interferon, or interferon with longer half-life and more favorable pharmacokinetics such as pegylated interferons. Recent trials showed that a combination of pegylated interferons and ribavirin leads to sustained response rates of about 50% with an acceptable safety profile. Hopefully, new treatment modalities will be available in the near future. Helicase, protease and the RNA polymerase are potential targets to suppress HCV replication and several immunotherapeutic approaches are explored.
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PMID:Current and future treatment of hepatitis C. 1129 80

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 hepatitis C virus (HCV) infection is a leading cause of liver cirrhosis and hepatocellular carcinoma (HCC) worldwide. The HCV capside core is a multifunctional protein with regulatory functions that affects transcription and cell growth in vitro and in vivo. Here, we show that both HCV genotype 1a and 3 core proteins activate MEK1 and Erk1/2 MAP kinases and that the costitutive expression of the HCV core results in a high basal activity of Raf1 and MAP/kinase/kinase, as determined by endogenous Raf1 in vitro kinase assay and immunodetection of hyperphosphorylated Erk1 and Erk2 even after a serum starvation. Moreover, the activation of both Erk1/2 and the downstream transcription factor Elk-1 in response to the mitogenic stimulus EGF is significantly prolonged. The sustained response to EGF in cells expressing the HCV core occurs despite a normal induction of the MAP phosphatases MKP regulatory feedback and is likely due to the costitutive activation of Raf-1 activity. The ability of HCV core proteins to directly activate the MAP kinase cascade and to prolong its activity in response to mitogenic stimuli may contribute to the neoplastic transformation of HCV infected liver cells.
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PMID:Sustained activation of the Raf/MEK/Erk pathway in response to EGF in stable cell lines expressing the Hepatitis C Virus (HCV) core protein. 1142 Jun 71

Viral hepatitis features with an incidence of 500 Mio infected individuals worldwide. Chronification of the infection as seen in hepatitis C, B, and D may lead to liver cirrhosis and its associated complications in later stages of the disease. Especially the chronification of acute hepatitis C is observed in a majority of cases (50-80%). Chronic Hepatitis C (cHC) should be treated in generally when elevated serum concentrations of liver enzymes are found or symptoms of disease occur. Treatment goals are viral elimination, improve in histology, prevention of HCC, and a better quality of life for the patients. As HCV and HIV share the same transmission routes, a relatively high rate of HCV-HIV co-infection is observed. Co-infection is characterized by a more progressive natural course of HCV-infection, leading to an increased mortality due to liver failure in the afflicted patients. The development of treatment options for anti-HCV-specific therapy in dually infected patients is urgently needed. The European Conference on Infectious Diseases and Tropical Medicine, EuCID 2001, which took place in May 3-6, 2001, in Leipzig covered aspects of viral hepatitis and its treatment in several sessions and gave latest results on treatment with interferon-alfa, lamivudine, and adefovir in hepatitis B as well as interferon-alfa, pegylated interferon-alfa, and ribavirin in hepatitis C and HCV-HIV co-infection respectively.
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PMID:Therapy of chronic hepatitis B and C and treatment options in HCV-HIV co-infection--European Conference on Infectious Diseases and Tropical Medicine, EuCID 2001, 3-6 May 2001, Leipzig. 1143 99

Epidemiology of hepatitis C virus(HCV) infection and clinical prognosis of chronic hepatitis C were presented here to reveal the object of treatment of Chronic Hepatitis C. Hepatitis C Virus is transmitted by blood and blood products. After acute HCV infection, about 70% developed persistent HCV infection, and the diagnosis is by finding viral RNA in the serum of patients with anti-HCV antibody. Persistent HCV infection causes chronic hepatitis, in which the natural clearance of HCV is almost impossible and there is almost no natural cure for chronic hepatitis caused by HCV. Chronic hepatitis C tends to develop gradually and to progress to liver cirrhosis, and is involved in the pathogenesis of hepatocellular carcinoma. In Japanese patients with chronic hepatitis C, 45% developed liver cirrhosis pass through a phase of chronic active hepatitis over a 15-year course after initial HCV infection, and 25% developed hepatocellular carcinoma over a 20-year course after the initial HCV infection. In addition the remaining patients may start to develop rapidly to chronic active hepatitis and to liver cirrhosis after 20 to 30 years duration of inactive phase. Thus, this type of chronic hepatitis reveals a poor long-term prognosis. For etiological treatment of chronic hepatitis C, eradication of persistent HCV infection is needed. If this is impossible, then preventing the development of liver cirrhosis and hepatocellular carcinoma is important.
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PMID:[Prognosis of chronic hepatitis C with regard to the aim of treatment]. 1157 82

Chronic hepatitis C virus (HCV) infection is frequently associated with a variety of autoimmune phenomenons. Mixed cryoglobulinemia (MC) appears in up to 50% of chronic HCV-infected patients. Cryoglobulins consist of immunoglobulin complexes precipitating in vitro when cooled below body temperature. In most cases IgM with rheumatoid factor activity is found in cryoprecipitates which could lead to vasculitis induced by the deposition of immnuocomplexes in small vessels. This vasculitis is thought to cause clinical symptoms called Meltzer's triad. This triad is represented by purpura, arthralgia and weakness. One third of patients suffering from HCV-associated mixed cryoglobulinemia are developing typical symptoms during their course of disease. The striking association between HCV infection and MC has conduced to the hypothesis that HCV is of major importance in the production of MC with followed vasculitis. Both hepatrophism and lymphotrophism have been reported for the hepatitis C virus. Infection of B-cells by HCV could probably lead to a bcl-2 translocation and immunoglobulin gene rearrangement which results in clonal lymphoproliferation and in synthesis of monoclonal IgM with rheumatoid factor activity. These IgM form immunocomplexes with IgG in the cold, which are finally responsible for the described vasculitis. Histopathological changes of the liver are dominated by chronic HCV infection. The majority of times mild activity of hepatitis or mild fibrosis could be found. Nevertheless, cirrhosis is more often found in HCV-infected patients suffering from MC compared to patients without MC. Conventional treatment of MC is aimed to reduce circulating immune complexes by immunosupression and plasmapheresis. With the emerging concept of a viral pathogenesis the therapeutic approach has changed during the last decade. Interferon treatment of MC, particularly of HCV-associated MC is well established nowadays.
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PMID:Hepatitis C virus-associated mixed cryoglobulinemia. Clinical manifestations, histopathological changes, mechanisms of cryoprecipitation and options of treatment. 1164 46

Chronic hepatitis C is a leading cause of liver cirrhosis and hepatocellular carcinoma worldwide. Current treatment options are limited, but recent progress in the understanding of the molecular virology of hepatitis C has led to the identification of novel targets for antiviral intervention. In addition, gene and immunotherapeutic strategies to inhibit hepatitis C virus (HCV) replication or gene expression and to enhance the cellular immune response against HCV are being explored. These and other novel antiviral strategies may eventually complement existing therapeutic modalities. Here, we briefly review current concepts of the epidemiology, molecular virology, pathogenesis, natural history, diagnosis, therapy, and prevention of hepatitis C.
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PMID:Hepatitis C: a concise review. 1167 77

Chronic hepatitis C virus (HCV) infection affects over 170 million people worldwide and is a common cause for liver transplantation in Canada. The prevalence of HCV infection in the dialysis population is estimated to be 20% to 50%. Today, intravenous drug use remains the most common route of transmission. The risk of acquiring HCV infection in patients on long-term hemodialysis is expected to decrease because of the screening of blood products for HCV. The diagnostic tests for hepatitis C include anti-HCV, HCV RNA, serum ALT levels, and liver biopsy. Liver biopsy is the definitive diagnostic procedure. Of patients acutely infected with the virus 50% to 85% will become carriers. HCV infection progresses slowly and the minority of patients develop cirrhosis over 20 years. The risk of hepatocellular carcinoma is increased once cirrhosis is present. The current standard of treatment that employs interferon and ribavirin has its limitations and is not indicated for many patients groups, such as patients on long-term hemodialysis. Interferon monotherapy is possible but is poorly tolerated by patients on dialysis. Patient and family education, as well as counselling, are important in that patients infected with HCV should be partners with health care providers in the management of their disease.
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PMID:Understanding hepatitis C. 1178 89


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