University of California, San Francisco, San Francisco, California, USA.
University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania, USA.
Clin Infect Dis. 2022 Jun 10;74(11):1914-1924. doi: 10.1093/cid/ciab764.
Fatty liver disease (FLD) and hepatitis B virus (HBV) infection occur commonly in human immunodeficiency virus (HIV). FLD resolution is associated with improvement in lipoproteins in HIV-uninfected patients. We evaluated changes in FLD in an HBV/HIV-coinfected cohort.
One hundred eight HBV/HIV-coinfected adults with baseline liver biopsies were followed every 24 weeks (median, 166 weeks) and 60 had follow-up biopsies. Baseline FLD categories (none, ≥5% steatosis, steatohepatitis), their change, and relationships with clinical and lipid/lipoprotein parameters were explored using multivariable modeling.
Median age was 50 years, and 93% were male. At baseline 30% had FLD. With control for lipid-lowering medications and body mass index, low-density lipoprotein (LDL) cholesterol (LDL-C), LDL particle concentration (LDL-P), and apolipoprotein B (apoB) decreased and adiponectin increased over time (all P < .05); On follow-up (vs baseline), there was no significant difference in FLD category (P = .85); 60% remained without FLD, 17% had unchanged, 12% worsening, and 12% improved FLD. Baseline low-density lipoproteins (LDL-C, LDL-P, small LDL-P) and apoB appeared highest in those with unchanged FLD status (all P < .05). No associations between changes in FLD across follow-up (worsening/improvement vs unchanged) and lipid/lipoproteins changes were identified.
In this cohort, there was no significant change in FLD prevalence over a relatively short timeframe. Baseline atherogenic lipids appeared highest in those with persistent steatosis or steatohepatitis, suggesting potentially increased cardiovascular risk in this group, but an independent relationship between individual-level change in FLD status and lipid/lipoprotein levels across follow-up was not observed.
脂肪肝疾病（FLD）和乙型肝炎病毒（HBV）感染在人类免疫缺陷病毒（HIV）中很常见。在未感染 HIV 的患者中，FLD 的缓解与脂蛋白的改善有关。我们评估了 HIV 合并 HBV/HCV 感染患者中 FLD 的变化。
108 例 HBV/HIV 合并感染的成人患者基线时进行肝脏活检，每 24 周（中位数 166 周）进行随访，其中 60 例患者有随访活检。使用多变量模型探索基线 FLD 分类（无、≥5%脂肪变性、脂肪性肝炎）及其变化与临床和脂质/脂蛋白参数的关系。
中位年龄为 50 岁，93%为男性。基线时 30%的患者患有 FLD。在控制降脂药物和体重指数的情况下，低密度脂蛋白（LDL）胆固醇（LDL-C）、低密度脂蛋白颗粒浓度（LDL-P）和载脂蛋白 B（apoB）随时间降低，脂联素增加（均 P <.05）；在随访时（与基线相比），FLD 类别无显著差异（P =.85）；60%的患者无 FLD，17%的患者 FLD 无变化，12%的患者 FLD 恶化，12%的患者 FLD 改善。基线低密脂蛋白（LDL-C、LDL-P、小 LDL-P）和 apoB 在 FLD 状态无变化的患者中最高（均 P <.05）。在随访期间（FLD 恶化/改善与无变化相比），FLD 变化与脂质/脂蛋白变化之间没有关联。
在本队列中，在相对较短的时间内，FLD 的患病率没有显著变化。在那些持续存在脂肪变性或脂肪性肝炎的患者中，动脉粥样硬化脂质似乎最高，这表明该组患者的心血管风险可能增加，但在整个随访过程中，FLD 状态的个体水平变化与脂质/脂蛋白水平之间没有观察到独立的关系。
