Hye Won Lee1, Terry Cheuk-Fung Yip2, Yee-Kit Tse3, Grace Lai-Hung Wong2, Beom Kyung Kim4, Seung Up Kim4, Jun Yong Park4, Do Young Kim4, Henry Lik-Yuen Chan2, Sang Hoon Ahn5, Vincent Wai-Sun Wong6. 1. Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea; Insitute of Gastroenterology, Yonsei University College of Medicine, Seoul, South Korea; Liver Center, Severance Hospital, Seoul, South Korea. 2. Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China. 3. Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China. 4. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea; Insitute of Gastroenterology, Yonsei University College of Medicine, Seoul, South Korea; Liver Center, Severance Hospital, Seoul, South Korea. 5. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea; Insitute of Gastroenterology, Yonsei University College of Medicine, Seoul, South Korea; Liver Center, Severance Hospital, Seoul, South Korea. Electronic address: ahnsh@yuhs.ac. 6. Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China. Electronic address: wongv@cuhk.edu.hk.
Abstract
OBJECTIVES: It is unclear if anti-hepatitis B virus (HBV) treatment can eliminate incident hepatic decompensation. Here we report the incidence and predictors of hepatic decompensation among cirrhotic patients receiving antiviral therapy for chronic hepatitis B. METHODS: This is a post hoc analysis of two prospective HBV cohorts from Hong Kong and South Korea. Patients with liver stiffness measurement (LSM) ≥10 kPa and compensated liver disease at baseline were included. The primary endpoint was incident hepatic decompensation (jaundice or cirrhotic complications) with competing risk analysis. RESULTS: 818 patients (mean age, 54.9 years; 519 male [63.4%]) were included in the final analysis. During a mean follow-up of 58.1 months, 32 (3.9%) patients developed hepatic decompensation, among whom 34% were secondary to HCC. Three (0.4%) patients experienced variceal bleeding alone, 27 (3.3%) had non-bleeding decompensation and 13 (1.6%) had more than 2 decompensating events Baseline LSM, diabetes, alanine aminotransferase, platelet, total bilirubin, albumin, prothrombin time, and eGFR were independent predictors of hepatic decompensation. 30/506 (5.9%) patients fulfilling the Baveno VI criteria (LSM ≥20 kPa and/or platelet count <150ⅹ109/L) and 2/312 (0.6%) patients not fulfilling the criteria developed hepatic decompensation (P < .001). CONCLUSIONS: Hepatic decompensation is uncommon but not eliminated in patients receiving antiviral therapy for HBV-related cirrhosis, and only a third of decompensating events are secondary to HCC. The Baveno VI criteria, which was originally designed to detect varices needing treatment, can be effectively applied in this population to identify patients at risk of decompensation.
OBJECTIVES: It is unclear if anti-hepatitis B virus (HBV) treatment can eliminate incident hepatic decompensation. Here we report the incidence and predictors of hepatic decompensation among cirrhotic patients receiving antiviral therapy for chronic hepatitis B. METHODS: This is a post hoc analysis of two prospective HBV cohorts from Hong Kong and South Korea. Patients with liver stiffness measurement (LSM) ≥10 kPa and compensated liver disease at baseline were included. The primary endpoint was incident hepatic decompensation (jaundice or cirrhotic complications) with competing risk analysis. RESULTS: 818 patients (mean age, 54.9 years; 519 male [63.4%]) were included in the final analysis. During a mean follow-up of 58.1 months, 32 (3.9%) patients developed hepatic decompensation, among whom 34% were secondary to HCC. Three (0.4%) patients experienced variceal bleeding alone, 27 (3.3%) had non-bleeding decompensation and 13 (1.6%) had more than 2 decompensating events Baseline LSM, diabetes, alanine aminotransferase, platelet, total bilirubin, albumin, prothrombin time, and eGFR were independent predictors of hepatic decompensation. 30/506 (5.9%) patients fulfilling the Baveno VI criteria (LSM ≥20 kPa and/or platelet count <150ⅹ109/L) and 2/312 (0.6%) patients not fulfilling the criteria developed hepatic decompensation (P < .001). CONCLUSIONS: Hepatic decompensation is uncommon but not eliminated in patients receiving antiviral therapy for HBV-related cirrhosis, and only a third of decompensating events are secondary to HCC. The Baveno VI criteria, which was originally designed to detect varices needing treatment, can be effectively applied in this population to identify patients at risk of decompensation.