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)

In Black Africa, the role of hepatitis C virus (HCV) in the onset of chronic hepatic disease is unclear. This is particularly true in Senegal where the prevalence of HCV is moderate. To gain insight into this question, a case-control study including 73 patients and 73 controls was carried out at Principal Hospital in Dakar in 1995. The patients included in this study presented chronic hepatitis in 2 cases cirrhosis in 25 and hepatocellular carcinoma in 46. Patients and controls underwent serologic testing for HCV (ELISA screening test followed by 3rd generation ELISA test in case of positive results and confirmation by immunoblot) with determination of HCV serotype using the immunoenzymatic method. Testing also included research for infection by hepatitis B virus and for anti-delta antibodies. Anti-HCV antibodies were detected in two patients (3 p. 100) and serology was suspicious in two others. Serotype 2 was detected in one of these patients. No positive results were recorded in controls. Fifty-four patients (74 p. 100) and 15 controls (21 p. 100) presented the HBs antigen including 13 patients (24 p. 100) and I control (7 p. 100) with anti-delta antibodies. This study shows that HCV currently plays a minor role in the onset of hepatic disease in hospitalized patients in Senegal. It also confirms the predominant role of hepatitis B and complicating effect of the delta hepatitis virus. These findings are compared with reported data for Black African countries. The impact of HCV appears to be lower in Senegal than in central Africa.
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PMID:[Hepatitis C virus and chronic hepatopathies in Dakar: case-control study]. 1098 87

Hepatitis delta virus (HDV) was responsible for a high proportion of cases of acute and chronic liver disease in Southern Europe during the 1970s. Some data suggest that by the 1990s HDV circulation had substantially declined. We have assessed the prevalence of HDV infection and its clinical impact in 834 Italian hepatitis B surface antigen (HBsAg) carriers in 1997. Anti-HDV antibodies were sought in all consecutive chronic HBsAg carriers observed in 14 referral liver units throughout Italy. Risk factors for anti-HDV positivity were evaluated. Anti-HDV antibodies were found in 69 of 834 (8.3%) HBsAg-positive patients. Cohabitation with an anti-HDV-positive subject, intravenous drug addiction, residence in the South of the country, and the presence of cirrhosis were independently associated with the presence of anti-HDV antibodies. The overall prevalence of anti-HDV antibodies was lower than those observed in 2 multicenter surveys performed in 1987 and 1992 (23% and 14%, respectively). By 1997, the percentage of anti-HDV-positive subjects had sharply decreased in the 30 to 50 years age group, whereas it was almost unchanged in subjects over 50 years of age. The highest prevalence of anti-HDV antibodies (11.7%) was found in patients with cirrhosis. This prevalence was as high as 40% in the 1987 study. The circulation of HDV sharply decreased in Italy, by 1.5% per year, from 1987 to 1997. This decrease resulted mainly from the reduction in chronic HDV infections in the young, for whom high morbidity and mortality rates were recorded in the past. The results anticipate the almost complete control of HDV infection in the near future.
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PMID:Chronic hepatitis D: a vanishing Disease? An Italian multicenter study. 1100 29

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

The First International Conference on Therapies for Viral Hepatitis, held in December 1995, brought together researchers, clinicians, and pharmaceutical manufacturers devoted to finding more effective ways to treat several varieties of hepatitis. Hepatitis B (HBV) affects an estimated 300 to 350 million people; up to 25 percent of that number will die of liver cirrhosis or hepatocellular carcinoma. The only currently available treatment is interferon, which is effective in only forty percent of the cases and has dose-limiting side effects. Nucleoside analog drugs have gained increasing attention because of their use in treating opportunistic infections in HIV-positive patients. Hepatitis C (HCV) affects only 75 to 100 million but is potentially more dangerous, since 85 percent of those with the disease will develop persistent and chronic liver infections and 70 percent will develop chronic liver disease. Hepatitis D (HDV) requires HBV for its replication cycle, and appears to respond to treatment for HBV. However, interferon is not effective in cases where the patient has both HBV and HDV. Hepatitis G (HGV) causes transfusion-associated non-ABC hepatitis with mild symptoms, and it is unclear if HGV causes chronic liver disease. Regimens for chronic viral hepatitis are desperately needed.
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PMID:First International Conference on Therapies for Viral Hepatitis. 1136 35

Many recent and significant advances in the field of chronic viral hepatitis, including therapy, suggest that an update on chronic hepatitis is timely. Chronic hepatitis B virus infection remains a significant worldwide cause of liver cirrhosis and hepatocellular carcinoma, despite the wide availability of a long established and effective vaccine. Transmission occurs via perinatal, sexual, and parenteral routes (particularly intravenous drug abuse and although blood products still carry a risk, this is now extremely low in Western countries). Only a minority of infected adult cases develop chronic hepatitis but in children under 1 year, 90% develop chronic hepatitis. The clinical spectrum of chronic liver injury ranges from mild inflammation to end stage liver cirrhosis. Interferon alfa has been the mainstay of treatment for patients with active disease but nucleoside analogues (lamivudine and adefovir) are now available with similar efficacy. Patients with end stage liver disease and hepatocellular carcinoma can be offered transplantation but infection in the graft is commonplace. The combination of hepatitis B immunoglobulin and newer antiviral drugs reduce the incidence and severity of graft infection significantly. The hepatitis C virus epidemic of the latter half of the 20th century now affects more than 1% of populations worldwide. This RNA virus is spread parenterally and is becoming the leading indication for liver transplantation. The majority of patients develop chronic hepatitis, which may be progressive, evolving to significant liver disease (cirrhosis or hepatocellular carcinoma) in about 20% cases after decades. Treatment with the combination of interferon alfa and ribavirin is successful in up to 40% cases. Liver transplantation is a therapeutic option for some but graft infection is universal and often complicated by progressive liver fibrosis. A vaccine remains a remote prospect so that prevention is crucial. Hepatitis D virus infection occurs on a background of hepatitis B virus infection and can also cause liver damage. The response to antiviral therapy is poor. The newer "hepatitis" viruses G and TT do not cause significant liver injury.
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PMID:Update on chronic viral hepatitis. 1147 Sep 28

To this day, viral hepatitis remains a major public health problem in Thailand. Chronic infection with hepatitis B and C viruses are the leading causes of chronic liver diseases, including cirrhosis and hepatocellular carcinoma (HCC). Outbreaks of hepatitis A virus continue to occur in Thailand, even after several years of consistently declining prevalence rates. Also, the reduction in prevalence of hepatitis D virus infection has been observed among intravenous drug users over the past decade. Hepatitis E virus constitutes a rather unusual cause of sporadic acute hepatitis in Thailand. Highly effective vaccines are currently available for prevention of hepatitis A and B, however, as yet no effective vaccine for hepatitis C is imminent. Following rapid progress in the development of molecular techniques, several new hepatitis viruses have been identified. Among these, Hepatitis G, TT and SEN viruses have recently been described but their significance as to causation of human liver disease has yet to be established. This article reviews the current epidemiology, molecular biology, and strategies aimed at prevention and control of hepatitis virus infection in Thailand emphasizing new developments and recent data obtained from our research studies.
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PMID:Problems and prevention of viral hepatitis in Thailand. 1152 32

All patients who test positive for hepatitis B virus (HBV) surface antigen (HBsAg) should be evaluated to determine the activity and severity of the infection. Assessment includes tests of disease activity (aspartate transaminase, alanine aminotransferase), tests of liver function (bilirubin, albumin, prothrombin time), and tests of replication status (hepatitis B early antigen, antibody to HBe, HBV DNA titer, and hepatitis D virus antibody). An ultrasound is recommended to assess for signs of cirrhosis and to exclude focal lesions in the liver. In patients with abnormal liver enzyme levels (aspartate aminotransferase, alanine aminotransferase), a liver biopsy is recommended to assess the stage of disease (amount of fibrosis) and to determine the urgency and need for antiviral therapy. Interferon alfa and lamivudine are the two antiviral therapies currently available. There are pros and cons associated with the use of either drug. Individualization of therapy, based upon factors such as patient comorbidities, response to prior therapies, and stage of disease, is recommended. Patients with abnormal liver enzyme levels, indices of active viral replication (positive HBV DNA, with or without positive HBeAg), and compensated liver disease are candidates for treatment with interferon or lamivudine. For patients with abnormal liver enzyme levels, indices of active viral replication (positive HBV DNA, with or without positive HBeAg), and decompensated liver disease, the treatment of choice is lamivudine. Concurrently, these patients should be considered for liver transplantation referral. There are a number of new antiviral agents currently under evaluation in clinical trials. Combination therapy for chronic HBV infection is anticipated. The use of two or more anti-HBV drugs can be expected to enhance efficacy and reduce the likelihood of drug resistance.
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PMID:Chronic Hepatitis B. 1169 75

The incidence of hepatitis B virus (HBV) and hepatitis D virus (HDV) infection is in rapid decline in Southern Europe, due to the improvement in hygiene and economic conditions and the vaccination campaigns against hepatitis B. These changes have led to a shift from the classic form of chronic hepatitis B due to the wild-type virus, expressing hepatitis B e antigen (HBeAg) to a liver disease due to a mutated virus which does not express the HBeAg (e-minus mutant). Very interestingly, HBV-DNA has been detected in the liver tissue and in the serum of some subjects who lack hepatitis B surface antigen (HBsAg) in serum. This "occult" infection may be responsible for the residual cases of acute hepatitis B and might influence the course of chronic liver diseases of different aetiologies. A further consequence of the control of HBV infection is a spectacular decline in HDV circulation. At present only 8% of the HBsAg carriers in Italy have anti-HDV antibodies, vs 23% in 1987. Most of the patients with HDV infection are over 40 and present a mild liver disease or a slowly progressive cirrhosis. These epidemiological data support the concept that the epidemiological changes influence the clinical pattern of chronic hepatitis.
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PMID:Type B and D viral hepatitis: epidemiological changes in Southern Europe. 1194 58

The hepatitis D virus (HDV), also called delta virus, is a small circular RNA virus. The HDV is dependent on the hepatitis B virus (HBV) and can cause infection in normal individuals with hepatitis B or yet, superinfect chronic HBV carriers. Three genotypes have already been cloned and sequenced. Infection with HDV has a worldwide distribution and a high HDV endemicity has been documented in the western Amazon region, in Brazil. It has been estimated that 18 million people are infected with this virus amongst the 350 million carriers of the HBV around the world. The HDV transmission and risk factors for infection are similar to those for HBV infection. The diagnosis is based on the immunohistological identification of HDAg in the liver and detection of IgM and IgG anti-HD in serum using RIA or EIA. The clinical course of hepatitis D is variable. Fulminant disease occurs more commonly in hepatitis B and D than in other forms of acute viral hepatitis. Chronic HDV infection is usually associated with severe histological changes in the liver and with a rapidly progressive course, that can lead to cirrhosis, liver failure and death. Treatment of chronic hepatitis D is currently unsatisfactory and interferon alpha is the only agent found to have some effect on the course of chronic hepatitis. Orthotopic liver transplantation is indicated for terminal cases of cirrhosis. Prophylaxis for HDV infection is possible by vaccination against the hepatitis B virus.
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PMID:[Hepatitis D]. 1201 28

Liver transplantation in patients with hepatitis B has been under discussion for 20 years because of inferior results without reinfection prophylaxis; therefore, we analyzed our overall experience with liver transplantation in hepatitis B patients with immunoprophylaxis, particularly the influence of the available antiviral treatment in different periods. From 1988 to 2000, 228 liver transplants in 206 hepatitis B patients were performed. Indications were acute liver failure (10%), hepatitis B virus (HBV) cirrhosis alone (67%) or with hepatitis D virus (HDV) (13%), or hepatitis C virus (HCV) coinfection (7%). All patients received long-term immunoprophylaxis (anti-HBs > 100 U/L). HBV DNA-positive patients were treated before and after surgery with famciclovir or lamivudine since 1993 and 1996, respectively. Since 1993, antivirals also were used for HBV reinfection. The 1-, 5-, and 10-year patient survival rates were 91%, 81%, and 73%. In patients with hepatocellular carcinoma (HCC) (60% 5-year survival, P <.01) or HBV reinfection (69% 5-year survival, P <.01) survival was significantly impaired. Those with HDV or HCV coinfection had a slightly better survival than with HBV monoinfection (P >.05, not significant). Preoperative positive HBV DNA (hybridization-assay) test results were associated with a slightly impaired patient survival (78% 5-year survival, P >.05, not significant versus DNA-negative). Preoperative positive hepatitis B e antigen (HBeAg) predicted significantly worse survival (P <.05 versus negative HBeAg). Graft loss caused by reinfection was most frequent before the availability of antiviral drugs. Two-year patient survival increased from 85% in era I (1988-1993) to 94% in era III (1997-2000, P <.05). The 2-year recurrence rates in these 2 periods were 42% and 8% (P <.05). In conclusion, excellent long-term results can be achieved in hepatitis B patients after liver transplantation with modern strategies, and survival rates are similar to other indications. Based on our experience, hepatitis B patients, including those with active viral replication, should not be excluded from liver transplantation.
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PMID:Increasing applicability of liver transplantation for patients with hepatitis B-related liver disease. 1202 40


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