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Epidemiologic assessment of interactions of hepatitis‐C virus with seromarkers of hepatitis‐B and ‐D viruses, cirrhosis and tobacco smoking in hepatocellular carcinoma
Author(s) -
Tzonou Anastasia,
Trichopoulos Dimitrios,
Kaklamani Evangelia,
Zavitsanos Xenophon,
Koumantaki Yvonni,
Hsieh ChungCheng
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910490311
Subject(s) - hepatocellular carcinoma , medicine , cirrhosis , hbsag , hepatitis c virus , hepatitis b virus , hbeag , gastroenterology , serology , hepatitis b , antibody , hepatitis , immunology , virus , virology
Abstract A recently introduced enzyme immunoassay procedure for antibodies against the hepatitis‐C virus (HCV) was used to test samples from 185 cases with hepatocellular carcinoma (HCC) and 432 hospital controls. The anti‐HCV results were examined in conjunction with previously reported data from this study concerning hepatitis‐B virus (HBV) serology, hepatitis‐D virus (HDV) antibodies, presence of cirrhosis and tobacco smoking. There was evidence for interaction between HBV and HCV in the causation of HCC: as previously reported, the rate ratio (RR) linking the presence of anti‐HCV to HCC among subjects positive for hepatitis‐B surface antigen (HBsAg) was substantially higher than the corresponding RR among those negative for this marker; furthermore, among HCC patients positive for HBsAg, a high proportion (33/61) of those who were positive for hepatitis‐Be antigen (HBeAg) or its antibody were positive for anti‐HCV, whereas among HBsAg‐positive controls who were also positive for HBeAg or its antibody, none was positive for anti‐HCV (0/18; p < 10 −4 . The anti‐HCV‐related RR for HCC was also higher among HCC patients with cirrhosis than among those without evidence of co‐existing cirrhosis (RR 11.4 vs. 4.4; p = 0.06). In addition, there was some evidence of interaction between tobacco smoking and HCV in the origin of HCC; after controlling for age, sex and HBsAg status, the RR for subjects positive for anti‐HCV was 6.8 among smokers but only 3.2 among non‐smokers ( p = 0.26). By contrast, there was no suggestion of an interaction between anti‐HCV and anti‐HDV, in agreement with the presumed minimal role, if any, of HDV in HCC etiology. These results support the notion that HCV is involved in the etiology of HCC by advancing, through a chronic liver disease process, carcinogenesis initiated by other factors.