Hepatitis Bs antibody in alcoholic cirrhosis.

Mills, Peter R.; Pennington, T. H.; Kay, Peter; Macsween, R. N. M.; Watkinson, G.

doi:10.1136/jcp.32.8.778

Cited by 51 publications

(6 citation statements)

References 25 publications

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“…This up-regulation may not only promote chronicity with higher, sustained viral loads, but may also trigger antiviral immune responses that are responsible for severe bouts of liver disease. Although the results of this work provide an explanation for the increased frequency of HBV markers among alcoholics, [3][4][5][6][7][8][9][10][11][12] it in no way excludes the possibility that chronic alcoholics are also more susceptible to HBV infection than the general population.…”

Section: Discussionmentioning

confidence: 99%

Chronic ethanol consumption stimulates hepatitis B virus gene expression and replication in transgenic mice

Larkin

2001

Hepatology

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Epidemiologic observations show a higher frequency of hepatitis B virus (HBV) serologic markers in chronic alcoholics compared with the general population. This may be the result of an increased susceptibility of alcoholics to infection and/or to an ethanol-mediated stimulation of HBV gene expression and replication. To test the latter hypothesis, HBV transgenic SCID mice, which support consistent levels of virus replication, were fed with a standard LieberDiCarli or isocaloric diet for 5 weeks. In ethanol-fed mice, the levels of hepatitis B surface antigen (HBsAg) and viral DNA in serum increased by up to 7-fold compared with mice fed the control diet. Ethanol-treated mice also had elevated HBV-RNA levels, and increased expression of surface, core, and X antigens in the liver, especially in the pericentral regions. None of these changes were observed in transgenic mice fed isocaloric diets. Chronic alcoholism and hepatitis B virus (HBV) infection are major public heath problems worldwide. Both of these agents target the liver and may result in hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). 1,2 In many studies, there was a 2-to 4-fold higher frequency of HBV markers in the serum of chronic alcoholics, 3-5 and among patients with alcoholic hepatitis 6,7 and cirrhosis, 8 compared with the general population. While the frequency of hepatitis B surface antigen (HBsAg) is higher than expected among heavy drinkers, 9 there is also a high frequency of hepatitis B surface antibody (anti-HBs) and hepatitis B core antibody (anti-HBc) among HBsAg-negative alcoholics. 10 Some of the latter patients had immune-complexed HBsAg 11 and were also positive for HBV DNA. 12 Combined with the finding that HBVinfected alcoholics develop chronic liver disease (CLD) and HCC at an earlier age than uninfected alcoholics suggests synergy between HBV and alcohol in liver cell damage and disease progression. 13,14 The nature of these ethanol-virus interactions is not clear. The finding that ethanol is mildly immunosuppressive, 15,16 and that HBV gene expression and replication levels are inversely related to the vigor of antiviral immune responses, 17 implies that HBV markers would be detected more often and at high concentrations in alcoholic patients. Alcohol may also directly alter host-cell metabolism and gene expression, 18 resulting in increased virus gene expression and replication. The finding that ethanol treatment of HepG2.2.15 cells, which replicate HBV, resulted in the enhanced expression of HBsAg 19 suggests a direct effect of ethanol on the virus. In contrast, short-term administration of ethanol to HBVinfected chimpanzees 20 or to human carriers 21 did not alter the course of infection. Chronic ethanol feeding of HBsAg transgenic mice inhibited its secretion, which resulted in its accumulation within the liver. 22 These observations may underlie HBV infections with atypical serology among alcoholics. [10][11][12]23 If alcohol causes intrahepatic retention of virus antigens, then it may make hepatocytes more suscept...

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Section: Discussionmentioning

confidence: 99%

Chronic ethanol consumption stimulates hepatitis B virus gene expression and replication in transgenic mice

Larkin

2001

Hepatology

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“…It has been suggested that viral hepatitis is also more commonly present in alcoholics than in corresponding nonalcoholic populations and thereby could contribute to the increased incidence of hepatocellular carcinoma. Indeed an increased prevalence of serologic markers of viral hepatitis was reported in alcoholics (111). This response was felt to be specific for HBV, since these subjects did not demonstrate increased titers against other common infectious agents.…”

Section: Role Of Hepatitis B Virus (Hbv) and Cirrhosismentioning

confidence: 95%

Alcohol and cancer

et al. 1986

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In recent years, evidence has accumulated of an increased incidence of hepatocellular carcinoma and other cancers of the alimentary tract in the alcoholic (1-3). The thrust of this paper will be to review only briefly the well-known epidemiologic evidence and to discuss in more depth possible mechanisms whereby alcohol abuse may promote the development of cancer.Clinically, an association between heavy drinking and certain types of cancer has been observed for many years. In 1964, the World Health Organization surveyed the research on alcoholism and cancer and concluded that an association existed between excessive drinking of alcoholic beverages and cancer of the mouth, the larynx and the esophagus (4). In a series of studies (5-7), heavy drinkers were found to have roughly a 10-fold increased risk of developing cancer of the mouth and larynx. Subjects who drink excessively often are also heavy smokers and, in this regard, it appears that alcohol plays a more important role than smoking with respect to cancer of the esophagus (8), whereas smoking seems to be more strongly associated with cancer of the mouth and pharynx (9). Additional sites of cancer associated with alcohol abuse include the pancreas (10, ll), the cardia of the stomach (12, 13), the colon (14-18) and the liver (2, 13, 19-22). Over the last 20 years, a number of animal studies have been conducted in which ethanol, either applied topically or administered as part of the diet, was shown to have a syncarcinogenic or cocarcinogenic effect. Examples of these experiments include: the enhanced carcinogenesis of 7,12-dimethylbenzanthracene applied to the cheek epithelium of young hamsters (23, 24) or the skin of mice (25), the induction of esophageal tumors in rats by diethylnitrosamine (DEN) (26), the induction of liver tumors by vinyl chloride (27), the induction of nitrosopyrrolidine-initiated nasopharyngeal cancers in pair-fed hamsters (28) and dimethylhydrazine-initiated rectal cancer in rats (29). However, it also should be noted that the simultaneous addition of DEN and ethanol in drinking water (25%) did not enhance DEN induction of hepatocarcinogenesis (30) nor did consumption of diets containing ethanol (35% total calories) change the induction of the number of liver tumors by dimethylnitrosamine (DMN) (31) or modify the development of preneoplastic hepatic foci by aflatoxin B, in rats (32). Similar results were obtained by Schwarz et al. Address reprint requests to: Charles S. Lieber, M.D., Alcohol Research and Treatment Center, Veterans Administration Medical Cent,er, 130 West Kingsbridge Road, Bronx, New York 10468.(33) using DEN or N-nitrosomorpholin as carcinogens and 10% ethanol in drinking water. In any event, while there is no evidence from animal feeding studies that ethanol per se is carcinogenic (28, 341, it nevertheless may increase the susceptibility of various tissues to chemical carcinogens by a variety of mechanisms such as activation of chemical carcinogens, altering the metabolism and/or distribution of carcinogens, interferen...

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“…First, recent studies show high proportions of morbidity and mortality from acute liver diseases -fatty liver and alcoholic hepatitis -among non-whites [5, 61. The excess in fatty liver and hepatitis occurs primarily in young adtilt males. Alcohol consumption is specified as the primary actiological agent for acute liver disease in these studies although it is conceivable that other factors such as the high rate of hepatitis B virus among non-whites could increase disease susceptibility [7,8,9].…”

Section: Introductionmentioning

confidence: 99%

Migration, Cultural Transformation and the Rise of Black Liver Cirrhosis Mortality

Herd¹

1985

British Journal of Addiction

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Throughout the 19th and most ofthe 20th century, liver cirrohsis mortality rates among U.S. blacks were usually similar to or slightly below rates in the white population. After 1955 this pattem rapidly changed and black Americans experienced an epidemic of cirrhosis which greatly exceeded the moderate increases in the white population. Increases in cirrhosis mortality were highly specific to geographical region. Rates among blacks increased as much as four limes in urbanised coastal and northern regions and remained low in the southem rural areas of the U.S. Among whites this pattem was reversed and tnortality rates increased more in the south than in northem industrial areas.This paper analyses these epidemiological trends vnth a focus on cohort differences and migration patterns in the U.S. black population. The contemporary distribution of Hack cirrhosis rates appears to refiect in part, shifts in the political climate of the 19th century temperance movement and the mass migration of blacks from the rural south to the urban north in the early decades ofthe century. The early 19th century temperance movement was highly favourable to black political liberty thus creating marty black allies for temperance; by the tum of the century the political base of the temperance movement became associated with strategies for black political disfranchisement and racial segregation, thus alienating many blacks. These changes in the movement and the simultaneous mass migration of blacks to 'wef urban areas seemed to stimulate a rapid alcoholisation of some parts ofthe black population beginning in the 1920s and 1930s.

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Hepatitis Bs antibody in alcoholic cirrhosis.

Cited by 51 publications

References 25 publications

Chronic ethanol consumption stimulates hepatitis B virus gene expression and replication in transgenic mice

Chronic ethanol consumption stimulates hepatitis B virus gene expression and replication in transgenic mice

Alcohol and cancer

Migration, Cultural Transformation and the Rise of Black Liver Cirrhosis Mortality

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