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 B virus (HBV) infection affects over 350 million people worldwide and over 1 million die annually of HBV-related chronic liver disease. Although many individuals eventually achieve a state of nonreplicative infection, the prolonged immunologic response to infection leads to the development of cirrhosis, liver failure, or hepatocellular carcinoma (HCC) in up to 40% of patients. In endemic areas, where carrier rates are >5%, most individuals are infected perinatally, by vertical transmission, or in early childhood. In the United States, where prevalence is low except in particular areas and populations (e.g., Alaskan natives, immigrants from highly endemic areas), transmission is generally horizontal, percutaneous, or via sexual contact in adulthood. A variety of host (age at infection, gender, immune status); viral (viral load, genotype, mutation); and external (concurrent viral infections, alcohol consumption, chemotherapy) factors influence disease progression. Several variables (age at infection, gender, ethnicity, immune status) also influence the risk of chronic infection. Perinatal transmission, the most common mode of infection worldwide, can be reduced by appropriate prophylaxis (vaccination of the infant at birth together with hepatitis B immune globulin); anti-viral therapy in late pregnancy may also be beneficial. Five drugs are now FDA-approved for the treatment of HBV (interferon, lamivudine, adefovir, entecavir, and peginterferon alfa-2a), and suppressive anti-viral therapy improves the natural history of HBV. Patients with decompensated cirrhosis or HCC are highly likely to die unless they successfully undergo liver transplantation. While novel anti-viral drugs have improved the management of cirrhosis, strategies to prevent and treat HCC remain inadequate.
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PMID:Introduction to chronic hepatitis B infection. 1644 46

Chronic hepatitis B infection presents a number of challenges to clinicians. There are additional considerations when defining management strategies for individuals with advanced liver disease, or coinfection, or those at high risk of developing hepatocellular carcinoma (HCC). Treatment of decompensated cirrhosis is particularly important. Evidence suggests that suppression of viral replication through nucleos(t)ide analog therapy leads to longer time to transplantation, improved liver function, and improved survival times. The use of interferon in patients with decompensated hepatitis B is associated with serious complications and is currently contraindicated for these patients by the AASLD Practice Guidelines. Hepatitis B coinfection is often associated with more extensive disease. In patients with HBV/HCV coinfection, one disease is usually dominant and consequently should be the focus of therapy. HIV/HBV coinfection increases the risk of progressive liver disease. Therapeutic agents active against both viruses should be utilized at the correct dose to limit the development of resistance. Agents specific for HBV, e.g., entecavir, enable hepatitis to be treated while avoiding the risk of HIV resistance developing. Dual infection with HBV and HDV is particularly challenging. Nucleos(t)ide analogs are ineffective in treating HDV infection, and there is limited data concerning the efficacy of interferon in this setting. The association between chronic hepatitis B infection and hepatocellular carcinoma (HCC) is well established. In patients at high risk of HCC, screening regimes may be effective. Furthermore, there is an increasing body of evidence indicating that effective suppression of viral replication may be associated with a reduced risk of HCC.
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PMID:Optimizing management strategies in special patient populations. 1644 49

The prevalence of hepatitis B surface antigen (HBsAg) carriage in France is 0.68% and that of HBcAb 8.18%. Chronic hepatitis B is more frequent in subjects of low socioeconomic status and those receiving government health insurance for the needy (CMU). The prevalence of chronic hepatitis B that is HBeAg-positive is now 64.4%. Nearly 60% of these patients were not born in France. Patients with HBeAg-negative chronic hepatitis B are more likely to be older, male, and have cirrhosis; they also have lower levels of serum transaminase activity and HBV DNA than those with HBeAg-positive chronic hepatitis B.
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PMID:[Epidemiology of chronic hepatitis B]. 1649 34

Chronic hepatitis B develops in 3 phases: immune tolerance, where viral replication is strong and there is little or no fibrosis; immune activity phase with low viral replication and rapidly developing fibrosis as well as an elevated risk of cirrhosis; low viral replication and remission, with a risk, nonetheless, of reactivation. Antiviral treatment is indicated in patients with moderate or severe levels of either fibrosis or activity (necrotic and inflammatory lesions). Standard interferon treatment produces a prolonged response rate on the order to 20-40%; side effects are frequent but generally mild and reversible when treatment stops. Pegylated interferon (standard interferon conjugated with polyethylene glycol) has substantially better efficacy and comparable tolerance. Lamivudine (a nucleoside analog) has several advantages over interferon: oral administration, excellent tolerance, and rapid antiviral effect. Its principal disadvantage is the frequency of resistant mutations. Adefovir and entecavir have oral administration, are well tolerated and associated with a low incidence of resistance. They induce a sustained response after withdrawal of therapy in only a minority of patients and therefore the treatment needs to be indefinitely administered in the majority of patients.
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PMID:[Treatment of chronic hepatitis B]. 1649 37

Chronic hepatitis B is usually a benign disease in Caucasian children; however, the long-term prognosis remains unsettled. This report describes the results of a 29-year longitudinal study including 99 white children with chronic hepatitis B, mainly acquired horizontally: 91 were hepatitis B e antigen (HBeAg) positive (4 had cirrhosis), and 8 were HBeAg negative at presentation. Of the 91 HBeAg-positive children, 89 underwent HBeAg seroconversion after a mean period of 5.2 +/- 4.0 years and were included in the study. Of the 85 children without cirrhosis, one had HBeAg-negative hepatitis and the other 84 became inactive carriers. During a mean follow-up of 14.5 +/- 6.1 years after HBeAg seroclearance, 4 carriers experienced reactivation, and 3 of them had HBeAg-negative hepatitis at the last follow-up. Of the 8 initially HBeAg-negative children, 2 had HBeAg-negative hepatitis, and 6 were inactive carriers. Of the 4 children with cirrhosis, 2 had hepatocellular carcinoma (HCC) and remained alive and 2 lost the histological features of cirrhosis in adulthood. Two patients with HBeAg-negative hepatitis and 1 with cirrhosis had experienced drug abuse. At the end of follow-up, 15 of the 89 initially HBeAg-positive patients and 2 of 8 initially HBeAg-negative children had cleared hepatitis B surface antigen. In conclusion, the overall prognosis for chronic hepatitis B in horizontally infected Caucasian children is favorable; however, some patients progress to HCC and HBeAg-negative hepatitis. Long-term monitoring is important, as is counseling on cofactors of liver damage, such as alcohol and drug abuse.
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PMID:Chronic hepatitis B in children after e antigen seroclearance: final report of a 29-year longitudinal study. 1649 23

Chronic hepatitis B is the most common cause of hepatocellular carcinoma (HCC) in Asia. Integration of hepatitis B virus (HBV) genome is likely an early event of carcinogenesis. The integrated HBV genome may activate neighboring cellular genes directly to offer a selective growth advantage to the liver cells. Production of hepatitis B X protein can act as a transactivator on various cellular genes for tumor development. Hepatic inflammation and cirrhosis also favors the process of carcinogenesis. Various viral factors associated with hepatocellular carcinoma development include HBV genotype, basal core promoter mutations, and high viral load. Polymorphisms at the androgen receptor-regulating genes and cytokine genes are possible host factors associated with HCC. This review article summarizes the pathogenesis of HBV-related carcinogenesis and the viral and host factors that may increase the risk of HCC development.
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PMID:Hepatocellular carcinoma and hepatitis B virus. 1667 93

Chronic hepatitis B virus (HBV) infection is the most common cause of cirrhosis and liver cancer worldwide. In Asian and western Pacific countries where HBV is endemic, estimated prevalence of chronic HBV infection ranges from 2.4%-16.0%, and liver cancer is a leading cause of mortality. Although population-based prevalence data for Asians/ Pacific Islanders (A/PIs) living in the United States are lacking, they are believed to constitute a sizeable percentage of persons with chronic HBV infection in the United States, a country of low endemicity. To assess the prevalence of chronic HBV infection among A/PI populations living in New York City, the Asian American Hepatitis B Program (AAHBP) conducted a seroprevalence study among persons who participated in an ongoing hepatitis B screening, evaluation, and treatment program. The results indicated that approximately 15% of participants who had not been previously tested had chronic HBV infection; all were born outside the United States. Screening programs are needed in A/PI communities in the United States to identify persons with chronic HBV infection so that they can be referred for appropriate medical management to prevent cirrhosis and liver cancer and so that their susceptible household and sex contacts can receive hepatitis B vaccine.
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PMID:Screening for chronic hepatitis B among Asian/Pacific Islander populations--New York City, 2005. 1669 Nov 80

Chronic hepatitis B viral (HBV) infection greatly increases the risk for cirrhosis and hepatocellular carcinoma. HBV serologic testing is important for the identification of chronically infected individuals, who may benefit from antiviral treatment and regular monitoring for disease sequelae. Elevated rates of cirrhosis and hepatocellular carcinoma among Vietnamese American men can largely be attributed to high rates of chronic HBV infection. We surveyed 509 Vietnamese men aged 18-64 years in Seattle, Washington and examined sociodemographic and health care access factors associated with HBV serology testing. Nearly two-thirds (65%) reported past testing. The following were among those factors associated with HBV testing in bivariate comparisons: older age; short proportion of life in the US; low English fluency; private health insurance; identifying a regular source of medical care; reporting no long waits for medical appointments; and having access to interpreter services. The following were independently associated with HBV testing in multiple logistic regression analysis: older age; college education; low English fluency; private health insurance; having a regular medical provider; and reporting no long waits for medical appointments. Younger and less educated men, and those with difficulty accessing medical care may be at particular risk for never having had HBV testing. Programs to reduce HBV transmission and sequelae should make special effort to target these vulnerable Vietnamese Americans.
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PMID:Health care access and sociodemographic factors associated with hepatitis B testing in Vietnamese American men. 1679 29

Chronic hepatitis B (CHB) is an important public health problem worldwide and in the United States, with approximately 25% of patients infected as neonates dying prematurely from cirrhosis or liver cancer. A treatment algorithm for CHB previously developed and published by a panel of United States hepatologists was revised based on new developments in the understanding of CHB, the availability of more sensitive molecular diagnostic testing, the addition of new treatments, and better understanding of the advantages and disadvantages of approved therapies. This updated algorithm is based on available evidence using a systematic review of the scientific literature. Where data are lacking, the panel relied on clinical experience and consensus expert opinion. Serum HBV DNA can be detected at levels as low as 10 IU/mL using molecular assays and should be determined to establish a baseline level before treatment, monitor response to antiviral therapy, and survey for the development of drug resistance. The primary aim of antiviral therapy is durable suppression of serum HBV DNA to the lowest levels possible. The threshold level of HBV DNA for determination of candidacy for therapy is 20,000 IU/mL or more for patients with hepatitis B e antigen-positive CHB. A lower serum HBV DNA threshold of 2000 IU/mL or more is recommended for patients with hepatitis B e antigen-negative CHB, and 200 IU/mL or more for those with decompensated cirrhosis. Interferon alfa-2b, lamivudine, adefovir, entecavir, and peginterferon alfa-2a all are approved as initial therapy for CHB and have certain advantages and disadvantages. Issues for consideration include efficacy, safety, incidence of resistance, method of administration, and cost.
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PMID:A treatment algorithm for the management of chronic hepatitis B virus infection in the United States: an update. 1684 25

Chronic hepatitis B is a common disease and approximately 20% of infected patients with compensated cirrhosis will decompensate over 5 years. If untreated, the survival of decompensated cirrhosis is poor (15% at 5 years). The extent of hepatitis B virus (HBV) replication, as assessed by serum HBV-DNA level, is a strong predictor of the risk of disease progression and hepatocellular carcinoma. This provides a rationale for antiviral therapy to arrest progression of liver disease. Lamivudine is a pyrimidine analogue that inhibits HBV-DNA reverse transcriptase. It decreases HBV replication, normalises alanine aminotransferase levels and reduces hepatic inflammation and fibrosis in patients with chronic hepatitis B. This article will focus on the use of lamivudine in patients with HBV-cirrhosis. In patients with compensated HBV-cirrhosis, a randomised, placebo-controlled trial has shown that lamivudine significantly reduced the rate of disease progression and hepatocellular carcinoma development over a 3-year period. In patients with decompensated cirrhosis, treatment with lamivudine can produce spectacular improvements of liver function, but the improvement is slow and a clinical benefit is usually not observed until after at least 3-6 months of treatment. A major drawback of lamivudine treatment is the development of resistance, observed in 15-20% of patients after 1 year and up to 70% after 5 years of continued treatment. Thus, patients with HBV-cirrhosis treated with lamivudine should have regular monitoring of serum HBV-DNA levels and prompt institution of additional antiviral therapy if viral breakthrough is observed. Adefovir, tenofovir and entecavir have demonstrated efficacy in patients with lamivudine resistance. In patients with decompensated cirrhosis, in whom the development of resistance can be fatal, combination therapy (such as lamivudine plus adefovir) may prove more effective than monotherapy and this issue needs further study.
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PMID:Lamivudine treatment in patients with chronic hepatitis B and cirrhosis. 1692 9


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