Zhou Enhao, Yang Chun, Gao Yuwen
Department of Infectious Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Department of Infectious Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Email:
Ann Palliat Med. 2021 Jan;10(1):415-424. doi: 10.21037/apm-20-2353.
Hepatitis B virus (HBV) and alcohol are primary causes of cirrhosis. Alcohol can result in replication of HBV, an increase in oxidative stress, a compromised immune response to the virus and an increase in liver inflammation, all of which can result in progression of cirrhosis. The aim was to explore the interaction of alcohol with HBV and to show the effect of different levels of alcohol intake on liver fibrosis and cirrhosis.
We selected 90 patients with hepatitis B cirrhosis and divided them into three groups: non-drinking, moderate drinking and excessive drinking. Indicators of fibrosis (type III procollagen, type IV collagen, laminin, hyaluronic acid), HBV-DNA load, transaminases, quantitative detection of hepatitis B surface antigen (HBsAg), Child-Pugh scoring system rating and the number of complications were tested at three time points: 0, 3 and 6 months after quitting drinking and after medical treatment.
We found that all indicators of fibrosis, HBV-DNA load, alanine (ALT) and aspartate (AST) transaminases in the excessive drinking group were highest among the three groups at any time. There were almost no differences between the moderate drinking and non-drinking groups at 0, 3 and 6 months after quitting drinking and treatment. We also found no difference among the three groups in quantitative detection of HBsAg at any time. It was observed that there are more patients with excessive drinking were in Child-Pugh C class and had more complications compared with the other two groups.
Patients with chronic HBV infection and an excessive drinking habit activate HBV-DNA which increases liver inflammation, thus accelerating the progress of liver cirrhosis. Moderate drinking had no significant effect on the progress of liver cirrhosis. Hepatitis B cirrhosis patients with excessive drinking had more complications and were more likely to be in Child-Pugh C class compared with the other groups.
乙型肝炎病毒（HBV）和酒精是肝硬化的主要病因。酒精可导致HBV复制、氧化应激增加、对病毒的免疫反应受损以及肝脏炎症加剧，所有这些都可导致肝硬化进展。目的是探讨酒精与HBV的相互作用，并显示不同饮酒水平对肝纤维化和肝硬化的影响。
我们选取了90例乙型肝炎肝硬化患者，将他们分为三组：不饮酒组、适度饮酒组和过度饮酒组。在戒酒及治疗后的0、3和6个月这三个时间点，检测纤维化指标（III型前胶原、IV型胶原、层粘连蛋白、透明质酸）、HBV-DNA载量、转氨酶、乙型肝炎表面抗原（HBsAg）定量检测、Child-Pugh评分系统评级以及并发症数量。
我们发现，过度饮酒组的所有纤维化指标、HBV-DNA载量、丙氨酸（ALT）和天冬氨酸（AST）转氨酶在任何时候都是三组中最高的。在戒酒及治疗后的0、3和6个月，适度饮酒组和不饮酒组之间几乎没有差异。我们还发现三组在任何时候的HBsAg定量检测中均无差异。观察到与其他两组相比，过度饮酒组有更多患者处于Child-Pugh C级且并发症更多。
慢性HBV感染且有过度饮酒习惯的患者会激活HBV-DNA，从而加剧肝脏炎症，加速肝硬化进程。适度饮酒对肝硬化进程无显著影响。与其他组相比，过度饮酒的乙型肝炎肝硬化患者并发症更多，更有可能处于Child-Pugh C级。
