Case Western Reserve University School of Medicine, Cleveland, Ohio.
Case Western Reserve University School of Medicine, Cleveland, Ohio; MetroHealth Medical Center, Cleveland, Ohio.
Clin Gastroenterol Hepatol. 2019 Feb;17(3):536-542.e1. doi: 10.1016/j.cgh.2018.05.058. Epub 2018 Jun 14.
BACKGROUND & AIMS: Therapies are needed to limit progression of fatty liver diseases in patients with human immunodeficiency virus (HIV) infection. We analyzed data from a prospective study of the effects of rosuvastatin (a statin) on hepatic steatosis in HIV-positive adults.
We performed a secondary analysis of data from a double-blind trial of adult patients with HIV infection (78% male; 68% African American; mean age, 46 y; body mass index, 29 kg/m; HIV1 RNA < 1000 copies/mL; low-density lipoprotein cholesterol, <130 mg/dL) receiving antiretroviral therapy. The patients were randomly assigned to groups given 10 mg daily rosuvastatin (n = 72) or placebo (n = 75). Demographic and clinical data were collected, and blood samples were analyzed. Changes in liver fat score (LFS, a composite score calculated from metabolic and liver function parameters) and markers of systemic inflammation and immune activation were assessed through 96 weeks of drug or placebo administration. We performed multivariable linear and logistic regressions to study relationships among variables.
The placebo and rosuvastatin groups each had significant increases in LFS, compared with baseline, at 96 weeks (P = .01 and P < .01; P = .49 for difference increase between groups). Baseline LFS was independently associated with blood level of C-X-C motif chemokine ligand 10 (P = .04) and the soluble CD163 molecule (P = .01). After we adjusted for baseline characteristics, an increase in LFS over time was significantly associated with the blood level of C-X-C motif chemokine ligand 10 (P = .04), insulin resistance (P < .01), and viral load (P = .02), but not rosuvastatin use (P = .06).
In a secondary analysis of data from a trial of patients receiving treatment for HIV infection, hepatic steatosis increased over time, regardless of statin treatment, and was independently associated with markers of immune activation. Patients who received rosuvastatin appeared to have a nonsignificant increase in hepatic steatosis over 96 weeks. Despite their ability to reduce the risk of cardiovascular disease, statins do not appear to reduce hepatic steatosis. Clinicaltrials.gov no: NCT01218802.
需要有治疗方法来限制人类免疫缺陷病毒（HIV）感染患者的脂肪肝疾病进展。我们分析了一项前瞻性研究中关于瑞舒伐他汀（一种他汀类药物）对 HIV 阳性成年人肝脂肪变性影响的数据。
我们对接受抗逆转录病毒治疗的 HIV 感染成年患者（78%为男性；68%为非裔美国人；平均年龄 46 岁；体重指数 29 kg/m；HIV1 RNA < 1000 拷贝/ml；低密度脂蛋白胆固醇 < 130 mg/dL）的双盲试验数据进行了二次分析。患者被随机分为每天接受 10 mg 瑞舒伐他汀（n = 72）或安慰剂（n = 75）组。收集人口统计学和临床数据，并分析血液样本。通过 96 周的药物或安慰剂给药，评估肝脂肪评分（LFS，通过代谢和肝功能参数计算的综合评分）以及全身炎症和免疫激活标志物的变化。我们进行了多变量线性和逻辑回归分析，以研究变量之间的关系。
与基线相比，安慰剂组和瑞舒伐他汀组在 96 周时的 LFS 均显著增加（P =.01 和 P <.01；组间差异增加 P =.49）。基线 LFS 与血液中 C-X-C 基序趋化因子配体 10（P =.04）和可溶性 CD163 分子（P =.01）水平独立相关。在调整了基线特征后，随着时间的推移 LFS 的增加与血液中 C-X-C 基序趋化因子配体 10（P =.04）、胰岛素抵抗（P <.01）和病毒载量（P =.02）呈显著相关，但与瑞舒伐他汀的使用无关（P =.06）。
在一项接受 HIV 感染治疗患者的试验数据的二次分析中，肝脂肪变性随着时间的推移而增加，与他汀类药物治疗无关，并且与免疫激活标志物独立相关。接受瑞舒伐他汀治疗的患者在 96 周内肝脂肪变性似乎有非显著增加。尽管他汀类药物能够降低心血管疾病的风险，但它们似乎并不能降低肝脂肪变性。Clinicaltrials.gov 编号：NCT01218802。
