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 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

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) 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

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

Hepatitis C can cause a range of hepatic histopathology. The virus may cause an acute hepatitis indistinguishable from any other acute viral hepatitis, but it is more likely to be associated with steatosis, bile duct injury, and portal lymphoid aggregates. Chronic infection with hepatitis C can range from mild nonspecific changes, presumably representing a hepatitis C carrier state, to end-stage liver disease with cirrhosis and hepatocellular carcinoma. Between these are chronic hepatitis of varying severity. Steatosis, portal lymphoid aggregates, and bile duct injury, while not specific, are very characteristic of chronic hepatitis C. Reputed precursors of hepatocellular carcinoma, including liver cell dysplasia and adenomatous hyperplasia, frequently follow the development of cirrhosis and are presumed to predispose to the development of malignancy. New techniques for localizing the virus in liver tissue will undoubtedly lead to greater understanding of the pathogenesis of hepatitis C-related diseases.
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PMID:Histopathology of hepatitis C virus infection. 759 46

Chronic infection with hepatitis C virus (HCV) is regarded as a risk factor for hepatocellular cancer, mostly in patients with liver cirrhosis. We looked for HCV genomes in the livers of patients with hepatocellular cancer who did not have cirrhosis to see whether HCV was directly oncogenic. Cancerous and non-cancerous liver tissue, and serum samples from 19 patients negative for hepatitis B surface antigen were analysed by polymerase chain reaction for the presence of HCV genome, HCV replication, HCV genotyping, and HBV genome. 13 of 19 patients were HCV RNA-positive in cancerous and non-cancerous liver tissue; 8 of 17 tested were anti-HCV positive. Among the 13 HCV RNA-positive patients, 11 had genotype 1b and 2 had genotype 2a. 7 of 13 serum samples were HCV RNA positive. 7 of 19 patients were HBV DNA positive in cancerous and non-cancerous liver tissue, 5 of them anti-HBc positive. 4 patients were both HCV RNA and HBV DNA positive and 3 were both HCV RNA and HBV DNA negative. Our results provide evidence for the association of HCV, mostly genotype 1b, with hepatocellular cancer without the intermediate step of cirrhosis.
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PMID:HCV-associated liver cancer without cirrhosis. 772 33

The main etiological cause of liver cirrhosis that account for approximately 80% of liver cirrhosis in Japan in hepatitis virus, and HBV and HCV account for 38% and 59% of this hepatitis virus-induced liver cirrhosis, respectively. Liver cirrhosis develops in patients with persistent infection of HBV or HCV. A diminution in HBV replication can occur due to the immune response in cases with chronic hepatitis. In such cases, the liver disease may become almost normal or inactive after conversion to the nonreplicative phase. To the contrary, in some cases with HBV infection, such conversion does not occur leading finally to liver cirrhosis. Chronic infection takes place in 65% of the patients exposed to HCV, which results in the development of chronic hepatitis, and only quite rarely resolves. About 40% of these patients with chronic HCV infection will develop liver cirrhosis in 10 to 20 years.
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PMID:[Liver cirrhosis and hepatitis viruses]. 811 6


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