Serum inducible protein 10 kDa/C‐X‐C motif chemokine 10 levels predict regression of M2BPGi‐based liver fibrosis after hepatitis C virus eradication by direct‐acting antiviral agents.

Aim: It is desirable to identify predictors of regression of liver fibrosis after achieving sustained virological response by anti‐hepatitis C virus (anti‐HCV) therapy. We retrospectively investigated the serum interferon‐γ inducible protein 10 kDa (IP‐10) level as a predictive indicator of regression of liver fibrosis after successful hepatitis C virus eradication by direct‐acting antiviral agents (DAAs) therapy. Methods: The study participants were recruited from a historical cohort of 116 chronically hepatitis C virus‐infected patients who had achieved sustained virological response by DAAs therapy and whose serum Mac‐2 binding protein glycosylation isomer (M2BPGi) levels at baseline (before DAAs therapy) were ≥2.0 cut‐off index. We defined patients with M2BPGi levels <1.76 and ≥1.76 cut‐off index at 2 years after the end of treatment (EOT) as the regression (n = 71) and non‐regression (n = 45) groups, respectively. Results: Multivariate analyses revealed that the albumin‐bilirubin score at baseline, and albumin‐bilirubin score, Fibrosis‐4 index at 24 weeks after the EOT, and serum IP‐10 change from baseline to 24 weeks after the EOT (IP‐10 change) were significantly associated with regression of M2BPGi‐based liver fibrosis. In addition, IP‐10 change was significantly associated with regression of M2BPGi‐based liver fibrosis by a multivariate analysis, even when the serum M2BPGi levels were aligned by propensity score matching and in patients with advanced M2BPGi‐based liver fibrosis: M2BPGi levels ≥3.3 cut‐off index at baseline. Conclusions: Serum IP‐10 change from baseline to 24 weeks after the EOT is a feasible predictor of regression of M2BPGi‐based liver fibrosis after achieving sustained virological response with DAA therapy. [ABSTRACT FROM AUTHOR]

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