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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic hepatitis C is now a major cause of chronic liver disease, cirrhosis and hepatocellular carcinoma. In March 1997, the National Institutes of Health sponsored a Consensus Development Conference entitled "Management of Hepatitis C". The final statement from the Consensus Panel set forth clear, evidence-based guidelines and recommendations regarding the diagnosis, evaluation, prevention and therapy of hepatitis C. The conclusions of the Consensus Panel have been widely accepted and have brought some degree of uniformity to the management of hepatitis C. An important issue is how to keep such recommendations current in such a rapidly evolving area of medicine. In the 2 years since the Consensus Conference there have been important advances in the management of chronic hepatitis C. Two recommendations of the Consensus Panel deserve modification: first, on the clinical usefulness of genotyping of hepatitis C virus and second, on the optimal therapeutic regimen. Two large multicenter, prospective controlled trials have shown that the combination of alpha interferon with ribavirin provides higher sustained virologic responses than interferon alone and that optimal therapy is a 24-week course for patients with genotypes 2 and 3 and a 48-week course for patients with genotype 1. Furthermore, therapy can be stopped at 24 weeks if HCV RNA is still present. Many clinical challenges remain. Major current needs are for accurate means of assessing the grade and stage of disease, for the likelihood of disease progression and of response to therapy as well as for viral eradication by treatment. Also important are new therapies for hepatitis C that might be used alone or in combination with interferon and ribavirin; therapies that could be applied to a wide variety of patients, with different stages of disease and with other comorbitities.
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PMID:Management of hepatitis C: current and future perspectives. 1062

Six different hepatitis viruses have now been characterized. Hepatitis B and C are the two hepatitis infections that are of greatest concern for surgeons. Hepatitis B and C share several features that have led to this concern. Both are blood-borne infections. Both are associated with chronic infection ultimately leading to cirrhosis, portal hypertension, and hepatocellular carcinoma, and both can be occupational infections for the surgeon after percutaneous injury associated with infected blood. Chronic hepatitis B infection is seen in 1.25 million people in the U.S. It is associated with a transmission rate to healthcare workers of 25 to 30 per cent following a hollow needle stick injury. Five per cent of acute infections result in chronic disease. It can be effectively prevented as an occupational infection by vaccination with the highly effective hepatitis B vaccine. Chronic hepatitis C infection is present in nearly 4 million people in the U.S. It has a lower rate of transmission than hepatitis B following needle stick injury, but it has a 50 to 80 per cent rate of chronic disease after acute infections. There is no vaccine for hepatitis C, and only prevention of blood exposure will avoid the risks of this occupational infection. Other hepatitis viruses are likely to be identified. Prevention of blood exposure, by the better use of barriers in the operating room and modification of surgical techniques, is recommended to prevent occupational infection from both known and unknown blood-borne viruses from the surgical patient.
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PMID:Hepatitis: risks for the surgeon. 1069 49

Acute hepatitis can be caused by the enterically spread hepatitis A and E viruses and the parenterally spread hepatitis B, C or D viruses. The clinical features of acute viral hepatitis are similar among the five viruses and include non-specific symptoms and icterus. In general, a specific therapy is not necessary, but patients with fulminant hepatitis may require liver transplantation. For acute hepatitis C, the effect of interferon-alpha on the risk of chronicity is evaluated in clinical trials. Chronic hepatitis is defined as inflammatory reaction in the liver that continues without improvement for at least 6 months after infection with hepatitis B, C or D viruses. Hepatitis B resolves in more than 90% of the patients, but chronic infection can lead to liver cirrhosis and hepatocellular carcinoma. Chronic hepatitis C is an insidious disease, because early diagnosis is missed easily due to asymptomatic presentation and about 70% of infected patients develop chronic hepatitis. The benefits of interferon-alpha and/or nucleoside analogues have been proven in recent clinical trials that show sustained responses in more than a third of all patients with chronic viral hepatitis. The future treatment of chronic viral hepatitis will likely include immunomodulation and gene therapy.
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PMID:[Clinical aspects and therapy of viral hepatitis]. 1084 Jun 5

Apart from inflammatory reaction, the death of hepatocytes is also a characteristic of chronic hepatitis. Necroinflammation is followed by compensatory proliferation, which plays a rather important role in maintaining the liver function. Authors studied the DNA content of hepatocytes in patients with chronic hepatitis C, and determined the ratio of hepatocytes in phases G1, S and G2 to determine the hepatocyte proliferation and regeneration capacity of the liver. Liver biopsy samples were taken from 23 patients with chronic hepatitis C and from 16 with chronic hepatitis with non viral origin, from which nuclear suspension counts were done based on the histological slides. A total of 16 normal liver tissue samples served as control. The DNA index, G1, S, G2 and polyploid fraction were determined using the DNACE (Digital Image Analyzer for Nuclear Deoxyribonucleic Acid Content Estimation, KFKI/NIO, Hungary) digital imaging process. The DNA index was found to be significantly higher in the chronic hepatitis C than in the non-C group, with the verification of aneuploidy (DI > 1.10). The chronic non-C hepatitis cases showed lower G1 (88 +/- 6) and higher S (7.8 +/- 6.6) fractions. In comparison to the normal liver tissues, the chronic hepatitis C cases also revealed a significantly (p < 0.05) lower G1 (91 +/- 5) and a higher S (5.4 +/- 3.6) fraction, though staying behind the values found for the non-viral group. The deviation can be explained by the presentation of the HCV proliferation inhibitory effect. The polyploid cell fraction revealed a significantly higher value in the chronic non-viral cases as compared to the C virus group, reflecting on the decreased regeneration capacity of the liver. When comparing the HCV groups, significant differences were found between the mild and moderate cases in respect to the G1 and G2 fractions. At the same time, the moderate and severe cases showed statistical deviation regarding the DNA index. Chronic hepatitis C virus infection reduces the proliferation of hepatocytes and the regeneration capacity of the liver. The aneuploid DNA index reflects on genetic instability, which could be the basis of the malignant transformation of the cells.
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PMID:[Hepatocyte proliferation and DNA content in chronic hepatitis C]. 1095 66

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

Both hepatitis B and hepatitis C are spread parenterally. Chronic hepatitis C is fast becoming the leading indication for liver transplantation. Most infected patients go on to develop chronic hepatitis, with approximately 20% developing liver cirrhosis or hepatocellular carcinoma after 20 years. Standard treatment now is with a combination of alpha-interferon and ribavirin, which is successful in up to 40% of patients. A vaccine is still a remote possibility and prevention remains all-important. Despite having a successful vaccine, chronic hepatitis B remains an important cause of liver cirrhosis and hepatocellular carcinoma. Treatments for active hepatitis include alpha-interferon and the newer nucleoside analogues such as lamivudine and adefovir. In patients undergoing liver transplantation, recurrence of hepatitis B in the graft can be reduced with a combination of hepatitis B immunoglobulin and these nucleoside analogues.
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PMID:Chronic viral hepatitis. 1107 May 70

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

Chronic hepatitis C is a common indication for liver transplantation, accounting for 25% to 50% of all transplantation candidates in most transplant centers. Despite uncertainties regarding rates of disease progression after transplantation, a consensus is emerging that recurrent HCV infection results in liver failure in a significant although currently unmeasured proportion of patients, and that the period over which this progression occurs is shorter than in the immunocompetent population. As the disease process moves into its second decade after transplantation it can be anticipated that future morbidity and liver-related mortality will increase. Whether disease progression is accelerated by definable factors is not yet fully established, but HCV RNA levels before or soon after transplantation and aggressive immunosuppressive measures appear to influence the post-transplantation outcome. Strategies to prevent or to reduce the effect of HCV infection after liver transplantation are therefore essential. The ability to intervene in this disease is currently limited. The main obstacles are the difficulty in predicting the outcome in the individual patient and the lack of effective therapy. In contrast with hepatitis B, in which hepatitis B immune globulin has improved survival, there are no therapeutic strategies to prevent recurrent HCV infection. Neither IFN nor ribavirin, when administered as a single agent, results in sustained viral clearance. However, administration of both drugs in combination, either to prevent disease or to treat recurrence, appears promising. The inability of currently available antiviral therapy to eliminate HCV in the setting of liver transplantation suggests that indefinite treatment designed to suppress viral replication will be necessary. The feasibility of such an approach will depend on the development of drugs that reduce the histologic activity of hepatitis, improve graft and patient survival, and have side effect profiles that are acceptable to patients.
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PMID:Treatment strategies for recurrent hepatitis C after liver transplantation. 1129 Dec 57

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

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


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