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. 2018 May:94:37-46.
doi: 10.1016/j.ejca.2018.02.010. Epub 2018 Mar 20.

Aflatoxin B1 exposure increases the risk of hepatocellular carcinoma associated with hepatitis C virus infection or alcohol consumption

Yu-Ju Chu  1 , Hwai-I Yang  2 , Hui-Chen Wu  3 , Mei-Hsuan Lee  4 , Jessica Liu  5 , Li-Yu Wang  6 , Sheng-Nan Lu  7 , Chin-Lan Jen  8 , San-Lin You  9 , Regina M Santella  10 , Chien-Jen Chen  11
Affiliations

Aflatoxin B1 exposure increases the risk of hepatocellular carcinoma associated with hepatitis C virus infection or alcohol consumption

Yu-Ju Chu et al. Eur J Cancer. 2018 May.

Abstract

Background: Hepatocarcinogenicity of aflatoxin B1 (AFB1) has rarely been studied in populations with hepatitis C virus (HCV) infection and those without hepatitis B virus (HBV) and HCV infection (non-B-non-C). This case-control study nested in a community-based cohort aimed to investigate the HCC risk associated with AFB1 in HCV-infected and non-B-non-C participants.

Methods: Baseline serum AFB1-albumin adduct levels were measured in 100 HCC cases and 1767 controls seronegative for anti-HCV and HBsAg (non-B-non-C), and another 103 HCC cases and 176 controls who were anti-HCV-seropositive and HBsAg-seronegative. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression.

Results: In 20 years of follow-up, the follow-up time to newly developed HCC was significantly shorter in participants with higher serum AFB1-albumin adduct levels in non-B-non-C (p = 0.0162) and HCV-infected participants (p < 0.0001). Within 8 years of follow-up, HCV infection and AFB1 exposure were independent risk factors for HCC. Elevated serum AFB1-albumin adduct levels were significantly associated with an increased risk of HCC newly developed within 8 years of follow-up in non-B-non-C participants with habitual alcohol consumption [crude OR (95% CI) for high vs. low/undetectable levels, 4.22 (1.16-15.37)] and HCV-infected participants [3.39 (1.31-8.77)], but not in non-B-non-C participants without alcohol drinking habit. AFB1 exposure remained an independent risk predictor for HCV-related HCC after adjustment for other HCC predictors (multivariate-adjusted OR [95% CI], 3.65 [1.32-10.10]).

Conclusions: AFB1 exposure contributes to the development of HCC in participants with significant risk factors for cirrhosis including alcohol and HCV infection.

Keywords: Aflatoxin B(1); Albumin adducts; HCC; HCV infection; Habitual alcohol drinking.

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Conflict of interest statement

Conflict of interest statement

No potential conflicts of interest were disclosed.

Figures

Figure 1
Figure 1. Frequency distribution and box plot of follow-up time from study entry to diagnosis of newly-developed HCC in HCV-infected and non-B-non-C participants by baseline serum AFB1-albumin adduct levels
(A) Distribution of the follow-up time to HCC in non-B-non-C participants (n=100) (low/undetectable vs. high, p=0.05 for testing equality of distribution). (B) Distribution of the follow-up time to HCC in HCV-infected participants (n=103) (low/undetectable vs. high, p=0.003 for testing equality of distribution). (C) Box plot of follow-up year to HCC diagnosis in non-B-non-C participants (means ± standrad devition of 11.6±4.6 years vs. 8.6±6.0 years for low/undetectable vs. high serum levels of AFB1-albumin adducts. p=0.0162). (D) Box plot of follow-up year to HCC diagnosis in HCV-infected participants (means ± standard deviation of 12.9 ± 3.8 years vs. 8.0 ± 4.9 years for low/undetectable vs. high levels of AFB1-albumin adduct. p<0.0001). In the box plot, the filled circles indicate the outliers lying outside the 10th and 90th percentiles
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