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Hepatitis B and C virus and hepatocellular carcinoma

Hepatitis B and C virus and hepatocellular carcinoma AbstractAntibody to hepatitis C virus (anti-HCV) was detected in 18·7% of patients with hepatocellular carcinoma (HCC) and in 10·9% of controls (P < 0·001). The corresponding prevalences of hepatitis B surface antigen (HBsAg) were 59·3% and 50·0% (P < 0·001). Using patients with non-hepatic disease as controls, stepwise logistic regression analysis indicated that both anti-HCV (odds ratio 6·88%; 95% confidence interval [CI] 1·63–9·77) and HBsAg (odds ratio 6·46; 95% CI 1·68–18·13) were independent risk factors for HCC. Calculation of the incremental odds ratio indicated no interaction between hepatitis B virus (HBV) and HCV. Blood transfusion was a significant risk factor for acquiring HCV infection with odds ratios of 5·48 (95% CI 1·07–29·0) and 2·86 (95% CI 1·31–22·72) for HCC cases and controls, respectively. The mean age of HCC cases with HBsAg and anti-HCV was lower than that of HCC patients with anti-HCV alone (P < 0·01). It is concluded that there is a high rate of HBV infection, and a low rate of HCV infection, among Nigerian patients with HCC. However, HBV and HCV are independent risk factors for the development of HCC, with HBV having an effect more rapidly. Screening of blood products for transfusion might minimize the risk of HCV transmission. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Transactions of The Royal Society of Tropical Medicine and Hygiene Oxford University Press

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References (23)

Publisher
Oxford University Press
Copyright
© Published by Oxford University Press.
ISSN
0035-9203
eISSN
1878-3503
DOI
10.1016/S0035-9203(97)90387-4
Publisher site
See Article on Publisher Site

Abstract

AbstractAntibody to hepatitis C virus (anti-HCV) was detected in 18·7% of patients with hepatocellular carcinoma (HCC) and in 10·9% of controls (P < 0·001). The corresponding prevalences of hepatitis B surface antigen (HBsAg) were 59·3% and 50·0% (P < 0·001). Using patients with non-hepatic disease as controls, stepwise logistic regression analysis indicated that both anti-HCV (odds ratio 6·88%; 95% confidence interval [CI] 1·63–9·77) and HBsAg (odds ratio 6·46; 95% CI 1·68–18·13) were independent risk factors for HCC. Calculation of the incremental odds ratio indicated no interaction between hepatitis B virus (HBV) and HCV. Blood transfusion was a significant risk factor for acquiring HCV infection with odds ratios of 5·48 (95% CI 1·07–29·0) and 2·86 (95% CI 1·31–22·72) for HCC cases and controls, respectively. The mean age of HCC cases with HBsAg and anti-HCV was lower than that of HCC patients with anti-HCV alone (P < 0·01). It is concluded that there is a high rate of HBV infection, and a low rate of HCV infection, among Nigerian patients with HCC. However, HBV and HCV are independent risk factors for the development of HCC, with HBV having an effect more rapidly. Screening of blood products for transfusion might minimize the risk of HCV transmission.

Journal

Transactions of The Royal Society of Tropical Medicine and HygieneOxford University Press

Published: Jan 1, 1997

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