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

Data on 74 pathologically confirmed cases of liver cancer among blacks and whites living in Los Angeles County, California were compared with 162 matched controls. The study was limited to only people with no hepatitis infection and to non-Asians. The risk of liver cancer for women who have used OCs for 5 years was 5.5 times higher than that for women who had never used OCs. This risk was 3 times higher for women who had ever used OCs. The data for women who were in their reproductive years when OCs 1st entered the market in the 1960s showed that the risk for 5 years of OC use increased to almost 30 times that of women who had never used OCs. Even though estrogens were presumed to be the risk factor since they induce liver cancer in animals, no significant association was found between estrogens used in estrogen replacement therapy and liver cancer. Overall, diabetics were at 3.3 times the risk for liver cancer compared with nondiabetics. People who had diabetes for at least 10 years had 4.3 times the risk and those dependent on insulin injections had 18.5 times the risk. Cigarette smokers had a 2.1 times greater risk of liver cancer than nonsmokers. Most of the women did not drink heavily which showed the independent effect of cigarette smoking. As of December 1991, these data represented the best data on OCs and cigarette smoking to date. The risk for heavy drinkers of alcohol (80g of alcohol/day=9 cans of beer, 9 glasses of wine, or 9 shots of spirits) was 4.7 times the risk of nondrinkers or light drinkers. It is concluded that alcohol and/or cigarettes caused 56% of liver cancer cases in men and that cigarettes and/or OCs caused 54% of liver cancer cases in women.
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PMID:Birth control pills, cigarettes, alcohol linked to liver cancer. 153 35

Persistent infection with hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC) in humans. HCC has also been observed in animals chronically infected with two other hepadnaviruses: ground squirrel hepatitis virus (GSHV) and woodchuck hepatitis virus (WHV). A distinctive feature of WHV is the early onset of woodchuck tumors, which may be correlated with a direct role of the virus as an insertional mutagen of myc genes: c-myc, N-myc, and predominantly the woodchuck N-myc2 retroposon. In the present study, we searched for integrated GSHV DNA and genetic alterations of myc genes in ground squirrel HCCs. Viral integration into host DNA was detected in only 3/14 squirrel tumors and did not result in insertional activation of myc genes, despite the presence of a squirrel locus homologous to the woodchuck N-myc2 gene. This suggests that GSHV may differ from WHV in its reduced ability to induce mutagenic integration events. However, the high frequency of c-myc amplification (6/14) observed in ground squirrel HCCs indicates that myc genes might be preferential effectors in the tumorigenic processes associated with rodent hepadnaviruses, a feature not reported so far in HBV-induced carcinogenesis. Together with previous observations, our results suggest that hepadnaviruses, despite close genetic and biological properties, may use different pathways in the genesis of liver cancer.
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PMID:Frequent amplification of c-myc in ground squirrel liver tumors associated with past or ongoing infection with a hepadnavirus. 157 Mar 7

Researchers from the US National Cancer Institute compared data on 25-49 year old US women who died of primary liver cancer between 1985 and 1986 with data on age matched controls who died of causes other than liver conditions or oral contraceptive (OC) related conditions to determine the association between primary liver cancer and parity. Women who had experienced at least 1 live birth wear 1.9 times more likely to have died of primary liver cancer than were nulliparous women. The association was not significant (p=.22), however. The highest risks were among children with at least 6 children (odds ratio [OR]=2.9) and with 2 children (2.1). Further the risks were greater when the parents or spouse completed the questionnaire and the association almost reached significance (p=.07). This may have been due to parents and spouse providing more complete information than a friend or neighbor. The risks of developing primary liver cancer were higher among women who had never used OCs than they were among those who ever did. For example, the OR for never users past parity 2 was 3.6 compared with 1.3 for ever OC users. There was a higher risk associated with parity among long term OC users (=or 5 years) than with short-term OC users, however. The researchers concluded that since parity was positively associated with increased risk of primary liver cancer in the US (a low risk country), endogenous hormones may contribute to liver cancer development. The following facts add to this plausibility. Estrogen profiles of parous women are different from those of nulliparous women. Estrogen levels rise considerably during pregnancy. Estrogens alter liver metabolism. Pregnancy makes the body more defenseless against hepatitis and its sequelae. In low risk countries, the risk of primary liver cancer rises among women using exogenous hormones.
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PMID:Parity and primary liver cancer among young women. 161 86

Experimental and epidemiological studies of risk factors for hepatocellular carcinoma (HCC): cirrhosis, male sex, oral contraceptives, alcohol, smoking, and aflatoxins, are evaluated, with meta-analysis for oral contraceptives, alcohol, and smoking. It is likely that an initiating event and one or more promoting events interact, probably with prolonged inflammation, necrosis and regeneration, to cause cancer in several types of cirrhosis. Over 90% of HCC patients have cirrhosis, usually from hepatitis B virus. The viral post-necrotic liver is often chronically dysplastic, but other types of cirrhosis are associated with HCC if they endure long enough. The proportion of men with HCC increases as hepatitis progressors to cirrhosis and then to HCC. Meta-analyses of 3 oral contraceptive studies resulted in a risk of 2.8 for 8 years of use, but 9.9 for 8 years. Population studies do not show any concentration of HCC in countries with high pill use, so the rarity of this cancer may have biased the results. Large epidemiologic studies are needed to refine risk estimates for oral contraceptives and HCC. Alcohol abuse of 80 g/day gives a risk of about 1.65 in pooled studies, compared to a risk of 1.1 for 80 g/day. Smoking gives a risk of 1.9, but there is no evidence for a secular trend by country in proportion to dose, as is evident for lung cancer. There is good experimental evidence that aflatoxin acts as an initiator for liver cancer, but there is not practical way to judge exposure for clinical studies.
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PMID:Hepatocellular carcinoma: risk factors other than HBV. 166 Mar 33

Hepatitis viruses may cause liver cancer (HCC) through an indirect mechanism inducing inflammation and cirrhosis. Only hepatitis B virus (HBV) was shown to have a direct oncogenetic potential. Hepatitis D virus (HDV) infection, superimposed on the oncogenetic background provided by chronic HBV infection, appears to provide an additional risk for HCC. Patients with florid infections from both HBV and HDV and active liver inflammation develop HCC at a significantly younger age than those infected by HBV alone or infected by hepatitis C virus (about 10 years earlier). In patients positive for serum HBV-DNA/HDV-RNA and/or IgM anti-HBc/IgM anti-HD it is mandatory to program a more frequent (thrice a year) schedule of screenings (ultrasound scan, alpha-1-phetoprotein, etc.) for prophylaxis of HCC.
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PMID:Pathobiology of chronic hepatitis virus infection and hepatocellular carcinoma (HCC). 166 Nov 97

The incidence and phenotype of preneoplastic and neoplastic liver lesions appearing in LEC rats after recovery from severe hereditary hepatitis were studied in comparison with the liver lesions appearing in chemical liver carcinogenesis. The livers of 168 rats (90 male, 78 female) were stained for seven histochemical markers at different time periods from the 20th week to the 122nd week of life. Glucose-6-phosphatase (G6Pase), adenosine triphosphatase (ATPase) and non-specific esterase (ES) were used as negative markers. Gamma-glutamyltransferase (GGT), glutathione S-transferase placental form (GSTP), esterase isozyme L-1 (L1) and alpha-fetoprotein (AFP) were used as positive markers. The study on the incidence of liver lesions in the LEC rats revealed sequential development of liver foci, nodules and hepatocellular carcinomas (HCCs) similar to those seen in chemically induced liver carcinogenesis. These lesions appeared earlier and more frequently in male LEC rats than in female ones, suggesting the importance of hormonal environment in spontaneous HCC development. The histochemical analysis of spontaneous liver lesions in LEC rats showed that GSTP was the most reliable positive marker as previously reported in chemical liver carcinogenesis. There was no essential difference in the expression of the markers in spontaneous and chemically induced liver lesions except for L1, which is considered to be related to xenobiotic metabolism. The results of this study suggest that both spontaneous and chemically induced liver cancer may develop by passing through phenotypically similar preneoplastic processes. In addition, the LEC rat uniquely showed chronic liver damage (hepatocyte death and regeneration) at the promotion stage of carcinogenesis. Such a natural history of HCC development in LEC rats is similar to that of human HCC which is frequently associated with chronic liver damage. Thus, the LEC rat provides a useful model for studying the process and underlying mechanisms of human liver cancer development.
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PMID:Phenotype of preneoplastic and neoplastic liver lesions during spontaneous liver carcinogenesis of LEC rats. 169 69

As part of The Gambia Hepatitis Intervention Study (designed to protect children from hepatitis and therefore liver cancer when adults), researchers took blood samples from at least 291 families of 293 index children from Brikama in the western region and 2 neighboring health centers in the Upper River Division (URD) in the eastern area of The Gambia who had received the hepatitis B virus (HBV) vaccine to examine vaccine response in infants in relation to the pattern of HBV infection in their families. 1 family member tested positive for hepatitis B surface antigen (HBsAg) in at least 30% of the children. The researchers did not find a correlation between the level of antibody in the index children and the HBsAg status of the family. 23% of families in Brikama had at least 1 HBsAg positive member compared to 37% in URD (p=.01). Even though no association existed between child's response to the vaccine and type of dwelling, an association did exist between HBsAg positive family members and type of dwelling. 35% of families who lived in a house constructed of mud or grass had at least 1 HbsAG positive family member whereas only 19.7% who lived in a concrete house had at least 1 HBsAg positive family member (p.02). Further, 40.8% of families who lived under a thatched roof had at least 1 HbsAg positive family member compared to 24.8% who had a corrugated roof (p.02). The researchers suggested that houses constructed of mud or grass or with a thatched roof may harbor more insects which transmit HBV. The socioeconomic factors of sanitation and water supply did not contribute to HBV infection. They concluded that the HBV status of a child's family did not affect his/her response to the vaccine. Therefore the vaccine protects children at high risk of becoming HBV carriers.
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PMID:Response to hepatitis B vaccine in relation to the hepatitis B status of family members. 183 53

Anti-hepatitis-C-virus (anti-HCV) antibody was tested for in sera from 410 adults living in Tunisia, Senegal, Burundi and Madagascar, and in 209 Tunisian and Senegalese patients suffering from liver diseases. Anti-HCV antibodies were detected in 4.2% of the adult population from Africa, in 51% of patients suffering from liver cirrhosis and in 37% of patients suffering from primary liver cancer. However, higher proportions of anti-HCV antibodies were detected in HBsAg+ patients than in HBsAg- patients. To assess the role of HCV in the development of both cirrhosis and primary liver cancer, a confirmation test is needed.
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PMID:Prevalence of hepatitis C virus infection in Africa: anti-HCV antibodies in the general population and in patients suffering from cirrhosis or primary liver cancer. 196 39

To provide clues to the causes of liver cancer in China, we studied the correlation of certain dietary and biochemical markers with liver cancer mortality across 65 Chinese counties. Mortality rates were significantly linked to the county-wide prevalence of hepatitis-B surface antigen positivity. Rates were also higher in counties with high plasma levels of total cholesterol and high consumption of liquor, rapeseed oil, and mouldy corn, while inverse associations were observed for wheat consumption. All of the observed associations, except those with cholesterol and rapeseed oil, were more pronounced in men than in women. No significant correlations with liver cancer mortality were found for consumption of several other foods; plasma levels of retinol, beta-carotene, alpha-tocopherol, selenium, zinc and ferritin; or urine levels of aflatoxin B1. Although causal inferences cannot be derived, this ecological study suggests that chronic infection with hepatitis-B virus contributes to the substantial variation in liver cancer mortality in China, and provides leads for further studies into the role of dietary and nutritional determinants.
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PMID:Correlates of liver cancer mortality in China. 206 44

The study of two major risk factors in the development of hepatocellular carcinoma, namely persistent hepatitis virus infection and exposure to dietary aflatoxins, has been hampered by lack of an experimental system. To this end we have used a Pekin duck model to examine the effect of congenital duck hepatitis B virus (DHBV) infection and aflatoxin B1 (AFB1) exposure in the induction and development of liver cancer. AFB1 was administered to DHBV infected or noninfected ducks at two doses (0.08 and 0.02 mg/kg) by i.p. injection once a week from the third month posthatch until they were sacrificed (2.3 years later). Two control groups of ducks not treated with AFB1 (one of which was infected with DHBV) were observed for the same period. Each experimental group included 13-16 ducks. Higher mortality was observed in ducks infected with DHBV and treated with AFB1 compared to noninfected ducks treated with AFB1 and other control ducks. In the groups of noninfected ducks treated with high and low doses of AFB1, liver tumors developed in 3 of 10 and 2 of 10 ducks; in infected ducks treated with the high dose 3 of 6 liver tumors were observed and none in the low dose of AFB1. No liver tumors were observed in the two control groups. Ducks infected with DHBV and treated with AFB1 showed more pronounced periportal inflammatory changes, fibrosis, and focal necrosis compared to other groups. All DHBV carrier ducks showed persistent viremia throughout the observation period. An increase of viral DNA titers in livers and sera of AFB1 treated animals compared to infected controls was frequently observed. No DHBV DNA integration into the host genome was observed, although in one hepatocellular carcinoma from an AFB1 treated duck, an accumulation of viral multimer DNA forms was detected. The metabolism of AFB1 in infected and noninfected duck liver was also examined. The study on the role of DHBV infection and AFB1 in the etiopathogenesis of liver tumors may help to clarify some of the basic mechanisms of carcinogenesis.
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PMID:Contribution of aflatoxin B1 and hepatitis B virus infection in the induction of liver tumors in ducks. 210 70


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