Maung Soe T, Decharatanachart Pakanat, Treeprasertsuk Sombat, Chaiteerakij Roongruedee
Division of Gastroenterology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Ma Har Myaing Hospital, Yangon, Myanmar.
J Clin Exp Hepatol. 2024 Jul-Aug;14(4):101388. doi: 10.1016/j.jceh.2024.101388. Epub 2024 Feb 27.
Chronic viral hepatitis B (CHB)-infected patients occasionally develop cirrhosis despite having persistent viral suppression with antiviral therapy. We aimed to identify risk factors for developing cirrhosis in hepatitis B virus (HBV)-suppressed patients.
We conducted a case-control study involving 120 noncirrhotic CHB-infected patients achieving viral suppression with antiviral treatment, with 40 cases developing cirrhosis and 80 age-, sex-, and Fibrosis-4 (FIB-4)-matched controls. Clinical and laboratory data at viral suppression, including body mass index (BMI), comorbidities, pretreatment HBV viral load, HBe antigen status, hepatitis C virus (HCV) and HIV coinfections, liver chemistries, and AST to Platelets Ratio Index (APRI) values, were retrospectively abstracted. Risk factors for cirrhosis post-HBV suppression were identified using Cox proportional hazard analysis.
Case and control groups had similar ages (51.4 ± 9.9 vs. 51.4 ± 10.2 years), proportions of males (80% vs. 80%), and FIB-4 values (1.32 vs. 1.31). The cirrhosis group showed significantly higher BMI (25.1 vs. 22.7, = 0.01) and more diabetes prevalence (50.0% vs. 26.3%, = 0.01), while other comorbidities and laboratory parameters were comparable ( > 0.05). By univariate analysis, BMI >23 kg/m2, diabetes, and APRI >0.7 were significantly associated with cirrhosis, with hazard ratios (HRs) (95%CI) of 2.99 (1.46-6.13), 2.31 (1.23-4.36), and 2.71 (1.05-6.99), = 0.003, 0.010, and 0.039, respectively. In multivariate analyses adjusted for APRI, BMI>23 kg/m remained significantly associated with cirrhosis (aHR: 2.76, = 0.006), while diabetes showed borderline significance (aHR: 1.99, = 0.072).
In HBV-infected patients achieving viral suppression with therapy, a BMI >23 kg/m increases the risk of cirrhosis. Therefore, a comprehensive approach addressing metabolic factors is imperative for preventing disease progression in HBV-infected patients.
慢性乙型肝炎（CHB）感染患者尽管通过抗病毒治疗实现了病毒持续抑制，但仍偶尔会发展为肝硬化。我们旨在确定乙肝病毒（HBV）抑制患者发生肝硬化的危险因素。
我们进行了一项病例对照研究，纳入120例通过抗病毒治疗实现病毒抑制的非肝硬化CHB感染患者，其中40例发展为肝硬化，80例为年龄、性别和纤维化-4（FIB-4）匹配的对照。回顾性提取病毒抑制时的临床和实验室数据，包括体重指数（BMI）、合并症、治疗前HBV病毒载量、HBe抗原状态、丙型肝炎病毒（HCV）和HIV合并感染、肝功能以及AST与血小板比值指数（APRI）值。使用Cox比例风险分析确定HBV抑制后肝硬化的危险因素。
病例组和对照组年龄相似（51.4±9.9岁 vs. 51.4±10.2岁），男性比例相同（80% vs. 80%），FIB-4值相近（1.32 vs. 1.31）。肝硬化组的BMI显著更高（25.1 vs. 22.7，P = 0.01），糖尿病患病率更高（50.0% vs. 26.3%，P = 0.01），而其他合并症和实验室参数相当（P>0.05）。单因素分析显示，BMI>23 kg/m²、糖尿病和APRI>0.7与肝硬化显著相关，风险比（HRs）（95%CI）分别为2.99（1.46 - 6.13）、2.31（1.23 - 4.36）和2.71（1.05 - 6.99），P分别为0.003、0.010和0.039。在根据APRI进行调整的多因素分析中，BMI>23 kg/m²仍与肝硬化显著相关（调整后HR：2.76，P = 0.006），而糖尿病显示出临界显著性（调整后HR：1.99，P = 0.072）。
在通过治疗实现病毒抑制的HBV感染患者中，BMI>23 kg/m²会增加肝硬化风险。因此，应对代谢因素采取综合方法对于预防HBV感染患者的疾病进展至关重要。
