Ratio of von Willebrand factor to ADAMTS13 is a useful predictor of esophagogastric varices progression after sustained virologic response in patients with hepatitis C virus‐related liver cirrhosis

Abstract Aim Esophagogastric varices (EGV) are a serious complication of hepatitis C virus (HCV)‐related liver cirrhosis (HCV‐LC). In most cases, portal hypertension improves after a sustained virologic response (SVR) is achieved with direct‐acting antiviral (DAA) treatment; however, in some cases, EGV exacerbation occurs after HCV elimination. We investigated whether von Willebrand factor (VWF) and a disintegrin‐like metalloproteinase with thrombospondin type‐1 motif 13 (ADAMTS13) can predict EGV progression with HCV‐LC after SVR achievement. Methods This retrospective study enrolled 47 patients with HCV‐LC who achieved an SVR after DAA treatment. Eighteen patients experienced EGV progression after the SVR was achieved (EGV progression group). Twenty‐nine patients did not experience EGV progression after the SVR was achieved (non‐EGV progression group). Plasma VWF antigen levels and ADAMTS13 activity were measured the day before DAA treatment. Results The EGV progression group had significantly higher plasma VWF antigen levels ( p = 0.00331) and VWF‐to‐ADAMTS13 ratios ( p = 0.000249) than the non‐EGV progression group. Multivariate logistic regression models found that a VWF‐to‐ADAMTS13 ratio >2.3 was the only risk factor for EGV progression after the SVR was achieved (hazard ratio [HR], 18.4; 95% confidence interval [CI], 3.08–109; p = 0.00138). During the observation period, patients with a VWF‐to‐ADAMTS13 ratio >2.3 had a significantly higher cumulative incidence of EGV progression after SVR achievement than patients with a VWF‐to‐ADAMTS13 ratio ≤2.3 (HR, 6.4; 95% CI, 1.78–22.96; p = 0.0044). Conclusions The VWF‐to‐ADAMTS13 ratio before DAA treatment for HCV could predict EGV progression after SVR achievement.