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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis C virus (HCV) is a lipid-enveloped single-stranded RNA virus with an unknown physical structure as only putative HCV particles have been identified by electron microscopy. Although HCV lacks the retroviral properties of being able to integrate into host DNA, it causes chronic infection in a considerable number of infected individuals (40-60%). Chronic infection is associated with a wide spectrum of liver diseases ranging from normal presentation to the different forms of chronic hepatitis, cirrhosis (about 20% of cases) and hepatocellular carcinoma. HCV therefore is not invariably and equally pathogenic, and genetic heterogeneity could be a major cause of such variability. Diagnosis of HCV infection relies on anti-HCV and HCV-RNA detection. Using second-generation assays, diagnostic sensitivity has increased to about 95%, but detection of anti-HCV does distinguish past from present infections. Only rising anti-HCV titres or anti-HCV seroconversion confirm a recent HCV infection. In anti-HCV-negative infections and cases of early acute hepatitis, HCV-RNA detection by RT-PCR represents a valid diagnostic alternative. In patients undergoing interferon therapy, testing for anti-HCV by immunoblotting represents a valid routine tool to monitor response. Anti-C-22 has the highest titre and persists longer while anti-C-100 is the earliest antibody to disappear in responders. The significant association between serum anti-C-100, HCV-RNA and liver disease suggests that anti-C-100 is an indirect marker of hepatitis C, but true markers of HCV-induced liver disease are still lacking.
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PMID:Hepatitis C virus infection and disease. Diagnostic problems. 850 44

Two biotechnology companies have recently announced the discovery of 4 new hepatitis viruses, provisionally named HGV and GBV agents (GBV-A, GBV-B, and GBV-C). Using a molecular biological approach, the genomes of these viruses were identified from non-A-E hepatients patients who had no markers to any previously known hepatitis viruses. The new viruses are members of family Flaviviridae, and are closely related to hepatitis C virus (HCV). Preliminary studies show that the prevalence of GBV agents and HGV are alarmingly high in blood donors in the United States, Europe, Africa and Japan. The viruses are transmitted parenterally, similar to HCV and hepatitis B virus (HBV), Chronic infection is common and can lead to cirrhosis. Some chronic hepatitis cases caused by these viruses respond to interferon treatment. The viruses can coinfect with HCV and/or HBV. A number of questions about these new viruses remain to be answered, including the magnitude of the problems, clinical significance, mode of transmission and populations at risk, as well as the appropriate treatment.
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PMID:The newly discovered non A-E hepatitis viruses. 903 5

Interpretation of descriptive statistics on liver cancer is affected by misclassification problems, evolving diagnostic procedures and changes in international classifications. Chronic infection with virus B and aflatoxin are major determinants for liver cancer in high-risk areas. In low and intermediate risk areas, including Italy, alcohol and cirrhosis are the most important risk factors. Preventive measures are neonatal vaccination against hepatitis B, reduction in aflatoxin contamination of foods, alcohol and tobacco consumption. Screening programs cannot be recommended as a measure of public health, particularly in western countries.
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PMID:[Epidemiology of malignant liver tumors]. 938 28

Chronic infection of woodchucks with woodchuck hepatitis virus (WHV) invariably leads, within 2-4 years, to the appearance of hepatocellular carcinoma (HCC). HCC is preceded by an extended period of chronic liver damage, probably resulting from the immune response to viral antigens. It may be that infection itself also induces changes in the hepatocyte population. To begin to identify some of the changes in the liver prior to the appearance of HCC, monoclonal antibodies (MAbs) were generated from mice immunized with hepatocytes from a woodchuck chronically infected with WHV or with a tumor lysate. Immunofluorescence microscopy was used to select MAbs that reacted with host markers whose patterns of expression would distinguish chronically infected from uninfected liver or from liver tumors. One of these MAbs (2F2) reacted strongly with a subset of hepatocytes in chronically infected liver; a similar staining pattern was not detected in uninfected or transiently infected liver. Evidence is presented that this strong staining reaction reflects the overexpression or accumulation of the hepatocyte-specific intermediate filament protein, cytokeratin K18, a protein previously implicated in cryptogenic cirrhosis of the liver in humans (Ku, N. O. , Wright, T. L., Terrault, N. A., Gish, R., and Omary, M. B. J. Clin. Invest. 99: 19-23, 1997). Double immunofluorescent staining with antibodies to K18 and M-envelope protein of WHV suggested that strong reactivity to K18 was limited to cells expressing high levels of one or both of the large viral-envelope proteins, M and L; however, high expression of these viral proteins was not always associated with a strong K18 staining reaction.
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PMID:Aberrant expression of a cytokeratin in a subset of hepatocytes during chronic WHV infection. 974 Jul 78

Hepatitis B virus (HBV) and hepatitis C virus (HCV) are major causes of acute and chronic liver disease worldwide. Chronic infection with these viruses often leads to chronic liver disease, including cirrhosis or primary hepatocellular carcinoma. Both HBV and HCV are bloodborne viruses; however, HBV is transmitted efficiently by both percutaneous and mucosal exposures, and HCV is transmitted predominantly by percutaneous exposures. Because the relative importance of various modes of transmission of these viruses differs by country, the choice of specific prevention and control strategies depends primarily on the epidemiology of infection in a particular country. Comprehensive hepatitis B prevention strategies should include (1) prevention of perinatal HBV transmission, (2) hepatitis B vaccination at critical ages to interrupt transmission and (3) prevention of nosocomial HBV transmission. The prevention of hepatitis C is problematic because a vaccine to prevent HCV infection is not expected to be developed in the foreseeable future. From a global perspective, the greatest impact on the disease burden associated with HCV infection will most likely be achieved by focusing efforts on primary prevention strategies to reduce or eliminate the risk for transmission from nosocomial exposures (e.g. blood transfusion, unsafe injection practices) and high-risk practices (e.g. injecting drug use).
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PMID:Strategies to prevent and control hepatitis B and C virus infections: a global perspective. 1019 30

Chronic infection with hepatitis B virus (HBV) is a common cause of advanced liver disease, including end-stage liver disease. Liver transplantation is generally regarded as the treatment of choice for decompensated cirrhosis. Although long-term prophylaxis with hepatitis B immune globulin (HBIg) has improved significantly the outcome after transplantation, about 20-36% of transplant recipients still develop recurrent hepatitis B and have reduced survival. Moreover, HBIg prophylaxis has a number of disadvantages, including high cost, difficulty in administration and tolerability problems. Lamivudine, an oral nucleoside analogue, is a potent inhibitor of HBV replication and has been investigated in end-stage liver disease and liver transplantation. Treatment with lamivudine results in suppression of viral replication, and clinical improvement and stabilisation of some patients with end-stage liver disease, leading to increased pre-transplant survival as well as a reduced need for transplantation. Prophylaxis with lamivudine is also effective in preventing recurrent HBV infection and graft reinfection after transplantation, although a combination of lamivudine plus HBIg is preferable to prevent the emergence of YMDD variant HBV (tyrosine-methionine-aspartate-aspartate amino acid motif of HBV polymerase). Lamivudine is also effective for the treatment of recurrent hepatitis B after transplantation, based on improvement in virological parameters of infection as well as clinical and histological manifestations of disease. In all of these clinical settings, lamivudine is well tolerated and dose reduction is not required. In conclusion, lamivudine has a potential role for the treatment of patients with hepatitis B-related end-stage liver disease, for prophylaxis in patients undergoing liver transplantation, and in the treatment of recurrent or de novo HBV infection after transplantation.
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PMID:End-stage liver disease and liver transplantation: role of lamivudine therapy in patients with chronic hepatitis B. 1086 54

Chronic infection with hepatitis C virus (HCV) is estimated to affect almost 170 million individuals worldwide. 20-30% of these individuals develop cirrhosis and its sequelae. Only 15-20% of patients with chronic hepatitis C achieve a sustained virological response to interferon monotherapy. The prevalence of anti-HCV antibodies in dialysis patients varies between 1% and 29% in Western Europe. In patients with ESRD on maintenance HD therapy, in whom a blunted immune response per se is observed, the usefulness of IFN-alpha therapy is usually discussed in the context of subsequent transplantation associated with intensive immunosuppressive treatment regimens. A recent study has shown that in this patient group renal transplantation is associated with a fivefold increase in posttransplantation liver disease as well as a relative risk of death of 3.3 compared to HCV-negative patients. Thus, eradication of HCV infection in patients with ESRD may substantially reduce morbidity and mortality in renal allograft recipients. The imbalance of T-helper (Th) lymphocyte cytokine production may play an important role in the immunopathogenesis of chronic HCV infection. Little is known about the effects of IFN-alpha therapy on Th1/Th2 activity in HD patients. The type of immune response against infectious agents is determined in part by the pattern of cytokines secreted by T lymphocytes. Th1 cells promote cellular immunity against infectious agents, while Th2 cells induce humoral immune response and immune tolerance activity. The measurement of Th1/Th2 profile should increase our understanding of the immune status of patients with HCV infection. Therefore, the recently presented studies were undertaken to evaluate the influence of IFN-a therapy on Th1/Th2 balance in HD patients with chronic HCV infection.
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PMID:[Hepatitis C virus infection in renal diseases: state of knowledge, therapeutic problems and perspectives]. 1089 63

Chronic infection with the hepatitis C virus (HCV) is a major public health threat in the United States and worldwide. By sharing some routes of transmission, persons infected with the human immunodeficiency virus (HIV) are at risk for coinfection with HCV As a result, hepatic cirrhosis, end-stage liver disease, and hepatocellular carcinoma due to chronic infection with HCV are important causes of both morbidity and mortality in coinfected patients. The advent of highly active antiretroviral therapy improved the management of patients with HIV, leading to decreased morbidity and better survival. As patients infected with HIV live longer, their risk of long-term sequelae from chronic HCV increases. Coinfection with HIV may be associated with rapid progression of chronic HCV. In contrast, the effect of HCV on the natural history of HIV is less clear. Data regarding treatment of HCV in HIV-coinfected patients are limited.
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PMID:Coinfection with HIV and HCV: more questions than answers? 1113 Feb 22

There are a large number of viruses, such as cytomegalovirus, Epstein-Barr, Herpes simplex, mumps, varicella, yellow fever, etc., known to cause inflammatory disease of the liver, but the term viral hepatitis generally refers to the five well described hepatotropic viruses which are divided into enteral and parenteral groups based on their mode of transmission. Hepatitis A and E viruses are enterically transmitted by the faecal-oral route and do not exist in a chronic carrier state. Hepatitis B, C and D viruses are parenterally transmitted, occur both in the acute and chronic forms, and, when they persist in a chronic carrier state, they serve as a reservoir for infection and give rise to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Hepatitis G virus has recently been described but its significance in the causation of human liver disease is yet to be established. Also, the most recently described TT virus in patients with post-transfusion hepatitis awaits further studies. Acute sporadic and epidemic viral hepatitis are common world-wide, mostly in the developing countries, including Ethiopia, and account for high morbidity and mortality, especially among pregnant women. Chronic infection with hepatitis B virus is a significant problem on a global scale, affecting over 300 million people. Hepatitis C virus infection is probably the most common cause of chronic viral hepatitis, end-stage liver disease and hepatocellular carcinoma in the world, especially in sub-Saharan Africa, including Ethiopia. Therefore, this article will review and highlight the relevant epidemiological, preventive and therapeutic aspects of viral hepatitis with emphasis on new developments and recent data obtained from Ethiopian studies.
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PMID:Epidemiology, prevention and treatment of viral hepatitis with emphasis on new developments. 1114 85

Chronic infection with hepatitis C virus (HCV) may result in cirrhosis, liver failure, and hepatocellular carcinoma. A minority of patients have a sustained response to antiviral therapy, and nonresponders remain at risk of developing progressive liver disease. We conducted a randomized, controlled trial of therapy with the combination of interferon (IFN) and ribavirin in patients with chronic hepatitis C who had not responded to an initial course of therapy with IFN alone. A total of 124 patients were randomized to receive the combination of IFN and ribavirin for either 24 or 48 weeks and followed for an additional 24 weeks after stopping therapy. Thirty-eight treated patients (30.6%) achieved a sustained virologic response (undetectable HCV RNA at the 24-week follow-up point). This was associated with significant improvement in necroinflammatory activity noted on liver biopsy. Interestingly, there was not a statistically significant difference in response rates based on the duration of treatment; HCV genotype was the strongest predictor of a sustained response. Sustained responses were noted even in patients with poor predictive factors, including those with advanced hepatic fibrosis or cirrhosis, high levels of HCV RNA in serum, and those infected with HCV genotype 1. The study included 24 patients with normal serum alanine transaminase (ALT) values before therapy who had similar responses to those with initially elevated transaminase values. This study suggests that the combination of IFN and ribavirin is a useful modality of therapy in patients with chronic hepatitis C who did not respond to IFN alone.
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PMID:Combination of interferon and ribavirin in chronic hepatitis C: re-treatment of nonresponders to interferon. 1123 Jul 51


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