Hepatitis B virus infection and decreased risk of nonalcoholic fatty liver disease: A cohort study
Hepatitis B virus infection and decreased risk of nonalcoholic fatty liver disease: A cohort study
复制标题
DOI：
10.1002/hep.29252
复制
发表时间：
2017-08
期刊：
影响因子：
13.5
通讯作者：
Chia-Chi Wang;J. Kao
中科院分区：
文献类型：
--
作者：
Chia-Chi Wang;J. Kao
我们怀着极大的兴趣阅读了Joo等人的文章。在这项研究中，83，339名基线时没有非酒精性脂肪肝（NAFLD）的参与者，在中位随访期6.6年期间确定了20，200例NAFLD病例。与HBsAg阴性受试者相比，B型肝炎表面抗原（HBsAg）阳性受试者发生NAFLD的校正风险比为0.83。调整混杂因素后，B型肝炎病毒（HBV）感染与NAFLD发生风险降低之间的相关性仍然存在，表明HBV感染可能对NAFLD的发生具有保护作用。虽然这项大规模的队列研究提高了我们对HBV感染与NAFLD发展之间关系的认识，但仍有一些问题值得讨论和进一步研究。首先，这项研究表明，与HBsAg阴性参与者相比，HBsAg阳性参与者发生NAFLD的风险降低，甚至在基线时具有更大的体重指数和更高的肥胖百分比。此外，HBsAg阳性受试者的有利血脂谱，如较低的甘油三酯、胆固醇和低密度脂蛋白，以及较高的高密度脂蛋白，可能解释了NAFLD发生风险降低的原因。这些结果与我们以前的观察结果一致，表明慢性HBV感染可能由于血脂异常频率较低而防止NAFLD的发展。然而，持续性HBV感染改变脂质代谢的机制仍不清楚，需要进一步研究。其次，NAFLD被认为是代谢综合征的肝脏表现，与胰岛素抵抗相关。虽然慢性丙型肝炎病毒感染与胰岛素抵抗有关，但HBV感染与胰岛素抵抗之间的关系尚未确定。在这项研究中，使用稳态模型评估胰岛素抵抗（HOMA-IR）的基线胰岛素抵抗在HBeAg阳性和HBeAg阴性受试者之间是相当的。为了阐明HBV感染、NAFLD和胰岛素抵抗之间复杂的相互作用，作者可能会在末次访视时比较HBsAg阳性和HBsAg阴性受试者的HOMA-IR，以了解慢性HBV感染是否影响胰岛素抵抗。第三，由于代谢综合征及其组分可以加速慢性HBV感染患者的肝病向肝硬化甚至肝细胞癌的进展，因此必须认识到哪些因素可以预测这些患者的NAFLD发展。作者可能会进行亚组分析，以确定与HBsAg阳性受试者中NAFLD事件相关的风险因素，然后通过改变生活方式或药物进行修改，以减少肝损伤的进展。
We read with great interest the article by Joo et al. In this study involving 83,339 participants without nonalcoholic fatty liver disease (NAFLD) at baseline, 20,200 incident NAFLD cases were identified during a median follow-up period of 6.6 years. The adjusted hazard ratio of hepatitis B surface antigen (HBsAg)positive participants for incident NAFLD was 0.83 compared with HBsAg-negative participants. After adjustment for confounders, the association between hepatitis B virus (HBV) infection and decreased risk of incident NAFLD remained, suggesting HBV infection may have a protective effect on the development of NAFLD. Although this large-scale cohort study improves our understanding about the relationship between HBV infection and the development of NAFLD, several issues deserve discussion and further investigation. First, this study showed a decreased risk of incident NAFLD in HBsAg-positive participants, even having larger body mass index and higher percentage of obesity at baseline compared with HBsAg-negative participants. Furthermore, the favorable lipid profiles in HBsAgpositive subjects such as lower triglyceride, cholesterol, and low-density lipoprotein, as well as higher highdensity lipoprotein, may explain the decreased risk of NAFLD development. These results were consistent with our previous observations, suggesting chronic HBV infection protects against the development of NAFLD possibly due to a lower frequency of dyslipidemia profiles. However, the mechanisms involved in altered lipid metabolism by persistent HBV infection remain largely unclear and require additional study. Second, NAFLD is considered to be the liver manifestation of metabolic syndrome, which is associated with insulin resistance. Although chronic hepatitis C virus infection is known to be associated with insulin resistance, the relationship between HBV infection and insulin resistance has been inconclusive. In this study, baseline insulin resistance using homeostatic model assessmentinsulin resistance (HOMA-IR) was comparable between HBsAg-positive and HBsAg-negative subjects. To clarify the complex interaction between HBV infection, NAFLD, and insulin resistance, the authors may compare HOMA-IR between HBsAg-positive and HBsAgnegative subjects at the last visit to see whether chronic HBV infection affects insulin resistance. Third, because metabolic syndrome and its components can accelerate the progression of liver disease to cirrhosis and even hepatocellular carcinoma in patients with chronic HBV infection, it is imperative to realize which factors could predict the development of NAFLD in these patients. The authors may perform a subgroup analysis to identify the risk factors associated with the incident NAFLD in HBsAg-positive subjects and then modify them with lifestyle modification or medications to reduce the progression of liver damage.