Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic infection by hepatitis B and C viruses is frequently associated to the development of primary liver cancer. Liver cirrhosis, induced by these viral infection, plays an important role in the liver carcinogenesis. In addition, HBV has a direct role in liver cell transformation by a transactivating effect of some viral proteins as well as insertional mutagenesis. The role of hepatitis C virus is not known. The strong association, even in France, of primary liver cancer to these viral infections underline the importance of their prevention by vaccination.
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PMID:[Liver cancer and hepatitis B and C virus]. 133 32

Chronic infection with hepatitis B virus (HBV), the delta agent (HDV) or hepatitis C virus (HCV) carries high risks of chronic liver disease which can result in cirrhosis and hepatocellular carcinoma. Many antiviral agents have been tried to inhibit viral replication and thereby limit infectivity and the risks of eventual serious liver disease. Interferon offers a 30-40% chance of viral clearance to the hepatitis B carrier, offers a good chance of clinical response in parenterally acquired chronic non-A non-B hepatitis and may be of benefit for some patients with chronic delta infection.
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PMID:Therapy of chronic viral hepatitis. 171 77

Chronic infection with hepatitis B viruses (hepadnaviruses) is a major cause of hepatocellular carcinoma (HCC), but the incubation time varies from 1 to 2 years to several decades in different host species infected with indigenous viruses. To discern the influence of viral and host factors on the kinetics of induction of HCC, we exploited the recent observation that ground squirrel hepatitis virus (GSHV) is infectious in woodchucks (C. Seeger, P. L. Marion, D. Ganem, and H. E. Varmus, J. Virol. 61:3241-3247, 1987) to compare the pathogenic potential of GSHV and woodchuck hepatitis virus (WHV) in chronically infected woodchucks. Chronic GSHV infection in woodchucks produces mild to moderate portal hepatitis, similar to that observed in woodchucks chronically infected with WHV. However, HCC developed in GSHV carriers about 18 months later than in WHV carriers. Thus, although both viruses are oncogenic in woodchucks, GSHV and WHV differ in oncogenic determinants that can affect the kinetics of appearance of HCC in chronically infected animals.
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PMID:Woodchuck hepatitis virus is a more efficient oncogenic agent than ground squirrel hepatitis virus in a common host. 200 38

Two major aetiological factors have been definitively incriminated in the pathogenesis of HCC: these are chronic hepatitis and hepatic cirrhosis. Chronic infection with hepatotropic viruses may account for the majority of cases of hepatocellular carcinoma in high incidence areas, and a varying prevalence of human hepatitis B and hepatitis C virus infection appears to determine the differing geographical prevalence of hepatocellular carcinoma in high and low incidence areas of the world. Patients with advanced hepatocellular carcinoma have a grave prognosis. However, at-risk groups have been characterized, and recent advances in hepatic imaging and tumour marker testing have made screening for asymptomatic primary liver cancer feasible. It it not clear, however, whether screening for small hepatocellular carcinoma improves the prognosis. Lipiodol has been shown to serve as a useful vehicle for diagnosis of small, centimetre sized nodules of tumour, and for delivery of cancer chemotherapeutic or radioactive agents to HCC. The combination of early diagnosis, and coupled medical and surgical treatments including targeted lipiodol or monoclonal antibody conjugates and hepatic resection or transplantation may lead to an improved outlook for viral-associated hepatocellular carcinoma.
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PMID:Hepatocellular carcinoma associated with chronic viral hepatitis. Aetiology, diagnosis and treatment. 216 44

Chronic infection with the hepatitis B virus can result in the development of serious liver disease such as chronic active hepatitis, cirrhosis, and hepatocellular carcinoma. Vertical transmission from infected mothers to infants is thought to be partially responsible for the high prevalence of infection in certain high-risk groups. Immunoprophylaxis using hepatitis B vaccine and hepatitis immune globulin has been highly effective in decreasing the probability of chronic hepatitis B virus infection in infants with exposure. Previously, the Centers for Disease Control recommended screening pregnant women considered at high risk of hepatitis B infection to detect newborns who would benefit from postnatal immunizations directed at preventing the HBV carrier state. Because of the poor sensitivity of high-risk criteria in distinguishing pregnant women who harbor the hepatitis B virus, these recommendations have recently been revised to call for the routine screening of all pregnant women in the United States.
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PMID:Hepatitis B in pregnancy. 266 19

Chronic infection with hepatitis B virus (HBV) accounts for 1-10% of hepatocellular carcinoma (HCC) in low-risk countries and for 56-94% in high-risk populations. However, although HBV is perhaps the second most important human carcinogen so far identified, chronic HBV infection is neither a sufficient nor a necessary cause of HCC. Other factors must be causally related to HCC, and some of them have been identified: aflatoxins, tobacco smoking, and use of alcohol and oral contraceptives. The evidence for an association between these factors and HCC is reviewed, as well as their joint effects. Finally, prospects for epidemiological research on HCC, and specifically the assessment of viral and chemical interactions, are discussed.
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PMID:Prospects for epidemiological studies on hepatocellular cancer as a model for assessing viral and chemical interactions. 284 66

Chronic infection with hepatitis B virus (HBV) results in a spectrum of hepatic abnormalities ranging from minimal liver dysfunction to severe liver failure. These patients provide an opportunity to examine the relationship between the evolution of the liver disease and the ability to metabolize drugs. We have examined hepatic drug disposition in patients with chronic persistent hepatitis, chronic active hepatitis, and cirrhosis due to HBV infection. Four model drugs were used: two low-extraction capacity-limited drugs (antipyrine and aminopyrine) and two high-extraction flow-limited drugs (ICG and lidocaine). The disposition of the four drugs tested was comparable to that of healthy controls in patients with chronic persistent hepatitis, chronic active hepatitis, and mild cirrhosis. In patients with severe cirrhosis (as defined by the presence of ascites, encephalopathy, or large esophageal varices), there was a significant impairment in the aminopyrine breath test (-31%) and in the clearance of antipyrine (-53%), lidocaine (-49%), and ICG (-54%). These results indicate that impairment of drug clearance occurs only late in the evolution of HBV-related chronic liver disease. This is in keeping with the known slow and insidious progression of the disease.
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PMID:Drug disposition in patients with HBsAg-positive chronic liver disease. 359 83

Chronic infection with hepatitis B virus (HBV) is closely associated with the etio-pathogenesis of primary hepatocellular carcinoma (PHC). It has been proposed that infection with HBV early in life, frequently transmitted by an HBV-carrier mother, leads to persistent infection with HBV, which in turn is associated with the development of chronic active hepatitis (CAH), post-necrotic cirrhosis and PHC. If this view is correct, then there should be clustering of chronic carriers of HBV in families of patients with chronic liver disease. We tested this hypothesis in Korea by collecting serum from 132 patients with these chronic liver diseases admitted to the Seoul National University Hospital and 664 of their first-degree relatives. Controls (636) were members of two churches in Seoul and a rural village population; 261 of the controls were between the ages of 30 and 59, the age range that included 95% of the cases of chronic liver disease. Sera were assayed for hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs) and antibody to hepatitis B core antigen (anti-HBc). Almost all cases showed evidence of present or past infection with HBV; 80% were HBsAg(+) and 14% were anti-HBs(+); 100% of 47 cases of PHC, 100% of 35 cases of cirrhosis, and 94% of 50 cases of CAH were anti-HBc(+); 6% of males and 4% of females in control population (30-59 years of age) were HBsAg(+), 71% were anti-HBc(+), and 51% were anti-HBs(+). HBsAg(+) patients with chronic liver disease tended to be younger than HBsAg(-) patients with anti-HBs or anti-HBc antibodies. Mothers of patients with more frequently (HBsAg(+) (9 of 33) than age-matched women in the control population (0 of 34) or wives of patients (5 of 68). Five of 23 fathers were also HBsAg(+) compared with 1 of 25 age-matched controls. As first observed in Africa, there was a deficit of anti-HBs in the fathers of cases compared with the controls. Siblings of patients were frequently HBsAg(+) (45% of 154), with the highest prevalence in brothers (53%). Family history shows that five fathers, two mothers and five brothers of cases have died of PHC. These data are compatible with the hypothesis tested and lend further support to the view that prevention of infection with HBV will lead to a marked decrease in the incidence of CAH, cirrhosis and PHC in areas where these diseases are endemic. Members of the families of patients with these diseases are at high risk of developing persistent infection with HBV and chronic liver disease. It would be appropriate to focus preventive strategies on infants and children in such families.
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PMID:Hepatitis B virus and primary hepatocellular carcinoma: family studies in Korea. 628 79

Chronic infection with hepatitis B virus is widespread, and there are other forms of chronic hepatitis in which the host's immune response is pathogenic. A conference study group report assessed faulty immune effector mechanisms. The immune pathways considered were effector cell recruitment and cytolytic mechanisms, including hepatocyte killing by antigen-specific T lymphocytes, non-antigen-specific cells (K and NK cells, macrophages), and antibody plus complement. Also considered were "modulating" effects of surface-located antibody which could result in reduction of killing by T cells of virus-infected hepatocytes which could facilitate chronicity. Evidence for participation of these immune effector processes has not yet been convincing in human chronic hepatitis. Future research must be directed to defining the type and specificity of cytolytic effector systems and circumstances under which host antibody diminishes or augments the activity of such systems, delineating putative auto-antigens, and developing suitable animals models.
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PMID:Issues in immunologically-mediated hepatic injury. 697 96

A retrospective analysis of the first 200 recipients of renal transplants at the Johannesburg Hospital showed that 23 (11,5%) were chronic carriers of the hepatitis B virus (HBV) and a further 10 (5%) had previously been exposed to the virus as evidenced by detectable concentrations of antibody to the hepatitis B surface antigen in their serum. In no patient did graft function appear to suffer as a result of chronic HBV infection. However, 7 of the patients with hepatitis B surface antigenaemia had biochemical evidence of liver dysfunction. In 3 of these patients liver tissue was examined histologically; 2 had a macronodular cirrhosis and 1 chronic persistent hepatitis. One further patient developed acute fulminant B virus hepatitis and was the only one who died of liver failure in either group. Chronic infection with HBV may cause liver disease in renal transplant recipients, and strict techniques to limit the spread of the virus in renal transplant and dialysis units should continue to be enforced.
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PMID:Hepatitis B virus-associated liver disease after renal transplantation. 700 8


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