Plasma adipokines and risk of hepatocellular carcinoma in chronic hepatitis B virus infected carriers: a prospective study in Taiwan
Menée à Taïwan et couplée à une cohorte de 561 participants, cette étude cas-témoins évalue l'association entre le niveau plasmatique d'adipokines et le risque de carcinome hépatocellulaire chez des individus infectés par le virus de l'hépatite B
Background:Obesity is considered a risk factor for hepatocellular carcinoma (HCC); The relationship between adipocytokine and HCC in hepatitis B virus (HBV) carriers remains unclear. We prospectively investigated the association of adiponectin, leptin and visfatin levels with HCC. Methods: We conducted a nested case-control study in a community-based cohort with 187 incident HCC and 374 HCC-free HBV carriers. Unconditional logistic regression was conducted to estimate the odds ratios and 95 percent confidence intervals. Results:Adiponectin, but not leptin and visfatin, levels were associated with an increased risk of HCC after adjustment for other metabolic factors and HBV related factors. The risk was increased (OR=0.51, 95% CI=0.12 - 2.11;OR=4.88 (1.46 - 16.3); OR=3.79 (1.10 - 13.0); OR=4.13 (1.13 - 15.1) with each additional quintiles, respectively) with a significant dose-response trend (ptrend =0.003). HCC risk associated with higher adiponectin level was higher in HBV carriers with ultrasonographic fatty liver, with genotype C infection, with higher viral load and with elevated alanine aminotransferase. Longitudinally, participants with higher adiponectin were less likely to achieve HBsAg seroclearance and more likely to have persistently higher HBV DNA. Eventually, they were more likely to develop liver cirrhosis (OR=1.65 (0.62 - 4.39); OR=3.85 (1.47 - 10.1); OR=2.56 (0.96 - 6.84); OR=3.76 (1.33 - 10.7) for the 2nd, 3rd, 4th and 5th quintiles, respectively; ptrend= 0.017) before HCC. Conclusions:Elevated adiponectin levels were independently associated with an increased risk of HCC. Impact: Adiponectin may play different role in the virus-induced and metabolic related liver diseases, but the underline mechanism remains unknown.