Hui R W H, Seto W-K, Cheung K-S, Mak L-Y, Liu K S H, Fung J, Wong D K-H, Lai C-L, Yuen M-F
Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China.
State Key Laboratory for Liver Research, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China.
J Viral Hepat. 2018 Jan;25(1):97-104. doi: 10.1111/jvh.12766. Epub 2017 Aug 25.
The potential interaction between chronic hepatitis B (CHB) and nonalcoholic fatty liver disease (NAFLD), two of the most prevalent liver diseases worldwide, has not been well defined. We performed liver stiffness (LS) and controlled attenuation parameter (CAP) measurements using transient elastography in 1202 CHB patients. Of these, 601 steatotic patients were matched with nonsteatotic controls in a 1:1 ratio by age, gender, nucleoside analogue treatment status, and treatment duration. Severe fibrosis was defined according to EASL-ALEH criteria, and steatosis was defined as CAP ≥222 dB m . Anthropometric measurements and metabolic-related parameters were recorded. The mean age of the 1202 patients (51.4% male) was 51.8 years. 696 patients (57.9%) were on nucleoside analogues for a median duration of 76.2 months. Among treatment-naïve patients, median serum HBV DNA was lower in steatotic individuals than in controls (3.0 vs 3.4 log IU mL , P < .05), with this inverse relationship remaining significant in multivariate analysis (odds ratio 0.859, 95% CI 0.743-0.994, P < .05). With increased steatosis severity, there was a stepwise decrease in median HBV DNA levels (3.1 and 2.6 log IU mL in no steatosis and severe steatosis, respectively, P = .032). Steatosis was associated with a higher median LS (5.4 kPa vs 5.0 kPa, P < .001). Severe steatosis, when compared to mild/moderate steatosis, was associated with an increased percentage of severe fibrosis (23.2% and 12.6%, respectively, P = .005). We conclude that severe steatosis was associated with increased fibrosis in CHB patients. Increasing steatosis was independently associated with lower serum HBV DNA levels, suggesting its potential negative effects on viral replication.
慢性乙型肝炎（CHB）和非酒精性脂肪性肝病（NAFLD）是全球最常见的两种肝脏疾病，它们之间的潜在相互作用尚未明确界定。我们使用瞬时弹性成像技术对1202例CHB患者进行了肝脏硬度（LS）和受控衰减参数（CAP）测量。其中，601例脂肪变性患者按年龄、性别、核苷类似物治疗状态和治疗时长以1:1的比例与非脂肪变性对照进行匹配。根据欧洲肝脏研究学会-以色列肝脏研究协会（EASL-ALEH）标准定义严重纤维化，脂肪变性定义为CAP≥222 dB m。记录人体测量学指标和代谢相关参数。1202例患者的平均年龄为51.8岁（男性占51.4%）。696例患者（57.9%）接受核苷类似物治疗，中位治疗时长为76.2个月。在未经治疗的患者中，脂肪变性个体的血清HBV DNA中位数低于对照组（3.0对3.4 log IU/mL，P <.05），在多变量分析中这种负相关关系仍然显著（比值比0.859，95%可信区间0.743 - 0.994，P <.05）。随着脂肪变性严重程度增加，HBV DNA中位数水平呈逐步下降趋势（无脂肪变性和严重脂肪变性时分别为3.1和2.6 log IU/mL，P = 0.032）。脂肪变性与更高的LS中位数相关（5.4 kPa对5.0 kPa，P <.001）。与轻度/中度脂肪变性相比，严重脂肪变性与严重纤维化的比例增加相关（分别为23.2%和12.6%，P = 0.005）。我们得出结论，严重脂肪变性与CHB患者纤维化增加相关。脂肪变性增加与血清HBV DNA水平降低独立相关，提示其对病毒复制可能存在负面影响。
