Serum IP‐10/CXCL10 levels predict regression of M2BPGi‐based liver fibrosis after hepatitis C virus eradication by direct‐acting antiviral agents
Yoshihito Nagura, Takanori Suzuki, Kentaro Matsuura, Shintaro Ogawa, Hayato Kawamura, Kayoko Kuno, Kei Fujiwara, Shunsuke Nojiri, Katsuya Nagaoka, Etsuko Iio, Takehisa Watanabe, Hiromi Kataoka, Yasuhito TanakaInfectious Diseases
It is desirable to identify predictors of regression of liver fibrosis after achieving sustained virological response (SVR) 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 HCV eradication by direct‐acting antiviral agents (DAAs) therapy
The study subjects were recruited from a historical cohort of 116 chronically HCV‐infected patients who had achieved SVR 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 (C.O.I.). We defined patients with M2BPGi levels <1.76 and ≥1.76 C.O.I. at two years after the end of treatment (EOT) as the regression (R, n = 71) and non‐regression (NR, n = 45) groups, respectively.
Multivariate analyses revealed that the albumin‐bilirubin (ALBI) score at baseline, and ALBI score, FIB‐4 index at 24 weeks after the EOT, 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 C.O.I at baseline.
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 SVR with DAA therapy.
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