Abstract
The pathogenesis of hepatocellular carcinoma (HCC) related to habitual betel quid (BQ) chewing is unclear. Risk of HCCis increased with adverse hepatic fibrosis. This study aimed to assess the impact of chronic viral hepatitis on adverse hepatic fibrosis in HCC related to BQ chewing. This hospital-based case-control study enrolled 200 pairs of age- and gender-matched patients with HCC and unrelated healthy controls. Serologic hepatitis B surface antigen (HBsAg), antibodies to hepatitis C virus (anti-HCV), α-fetoprotein (AFP), and surrogate markers for significant hepatic fibrosis were measured. Information on substance-use habits was obtained with a questionnaire. By analysis of surrogate markers for hepatic fibrosis, the prevalence of significant hepatic fibrosis in patients chewing BQ was between 45.8% and 91.7%, whereas that for patients without BQ chewing was between 18.4% and 57.9%. The difference was significant (P <0.05 for each surrogate marker). Multivariate analysis indicated that cirrhosis with Child-Pugh C (odds ratio (OR) = 3.28; 95% confidence interval (CI), 1.29- 8.37), thrombocytopenia (OR = 3.92, 95% CI, 1.77-8.68), AFP >400 mg/L (OR = 2.21, 95% CI, 1.05-4.66) and male gender (OR = 4.06, 95% CI, 1.29-12.77) were independent factors associated with habitual BQ chewing. In conclusion, adverse hepatic fibrosis and severe liver damage play important roles in the pathogenesis of BQ- related HCC, which could be aggravated by chronic hepatitis B and hepatitis C. BQ-cessation programs and prevention of chronic HBV/HCV infection are needed to prevent HCC related to BQ chewing.
Highlights
Hepatocellular carcinoma (HCC) ranks the fifth in frequency among men and the seventh among women worldwide (Jemal et al, 2011)
By a formal epidemiological approach and application of non-invasive surrogate markers for hepatic fibrosis, this study indicated that habitual betel quid (BQ) chewing was correlated with adverse hepatic fibrosis (Table 3 and Table 4) and more severe liver damage (Table 5 and Table 6)
Further analysis indicated that chronic hepatitis B virus (HBV)/hepatitis C virus (HCV) infection aggravated the adverse hepatic fibrosis (Table 4) which may contribute to the pathogenesis of BQ-related hepatocellular carcinoma (HCC) (Table 4, Table 5, and Table 6)
Summary
Hepatocellular carcinoma (HCC) ranks the fifth in frequency among men and the seventh among women worldwide (Jemal et al, 2011). The well-known environmental risk factors for HCC include chronic infection with the hepatitis B virus (HBV) and hepatitis C virus (HCV) (Bouchard and Navas-Martin, 2011; El-Serag, 2012) and habitual betel quid (BQ) chewing (Tsai et al, 2001, 2004; IARC, 2004; Secretan et al, 2009; Hamed and Ali, 2013). The BQ prepared in Taiwan is quite different from that in other parts of the world It consists of 2 halves of a fresh areca nut, sandwiched with a piece of the betel leaf, and red slaked lime paste. There is sufficient evidence that betel quid without added tobacco causes HCC (Tsai et al, 2001, 2004; IARC, 2004)
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