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Aspartate aminotransferase to platelet ratio index as a prospective predictor of hepatocellular carcinoma risk in patients with chronic hepatitis B virus infection
Author(s) -
Hann HieWon,
Wan Shaogui,
Lai Yinzhi,
Hann Richard S,
Myers Ronald E,
Patel Fenil,
Zhang Kejin,
Ye Zhong,
Wang Chun,
Yang Hushan
Publication year - 2015
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12664
Subject(s) - medicine , hepatocellular carcinoma , cirrhosis , gastroenterology , prospective cohort study , univariate analysis , hepatitis b virus , quartile , hepatitis c virus , multivariate analysis , immunology , confidence interval , virus
Background and Aim APRI (aspartate aminotransferase [ AST ] to platelet ratio index) is widely used to assess fibrosis and cirrhosis risk, especially in hepatitis C virus ( HCV )‐infected patients. Few studies have evaluated APRI and hepatitis B virus ( HBV )‐related hepatocellular carcinoma ( HCC ) risk. Prospective evidence is needed to assess whether APRI predicts HCC risk in HBV patients. Method In a prospectively enrolled clinical cohort of 855 HBV patients with a 1‐year exclusion window (followed for > 1 year and did not develop HCC within 1 year), the predictive value of APRI in HCC risk was evaluated by C ox proportional hazards model using univariate and multivariate analyses and longitudinal analysis. Results Higher APRI prospectively conferred a significantly increased risk of HCC in univariate analysis (quartile analysis, P trend = 2.9 × 10 −7 ). This effect remained highly significant after adjusting for common host characteristics but not cirrhosis ( P trend = 7.1 × 10 −5 ), and attenuated when cirrhosis is adjusted ( P trend = 0.021). The effect remained prominent when the analysis was restricted to patients with a more stringent 2‐year exclusion window ( P trend = 0.008 in quartile analysis adjusting all characteristics including cirrhosis), indicating that the association was unlikely due to including undetected HCC patients in the cohort, thus minimizing the reverse‐causation limitation in most retrospective studies. Longitudinal comparison demonstrated a persistently higher APRI value in HBV patients who developed HCC during follow‐up than those remaining cancer free. Conclusion APRI might be a marker of HCC risk in HBV patients in cirrhosis‐dependent and ‐independent manners. Further studies are warranted to validate this finding and test its clinical applicability in HCC prevention.