Clinical Addiction Research and Education (CARE) Unit, Section of General Internal Medicine, Department of Medicine , Boston Medical Center and Boston University School of Medicine, Boston, Massachusetts.
Alcohol Clin Exp Res. 2013 Sep;37(9):1527-35. doi: 10.1111/acer.12129. Epub 2013 May 3.
The effect of alcohol on liver disease in HIV infection has not been well characterized.
We performed a cross-sectional multivariable analysis of the association between lifetime alcohol use and liver fibrosis in a longitudinal cohort of HIV-infected patients with alcohol problems. Liver fibrosis was estimated with 2 noninvasive indices, "FIB-4," which includes platelets, liver enzymes, and age; and aspartate aminotransferase/platelet ratio index ("APRI"), which includes platelets and liver enzymes. FIB-4 <1.45 and APRI <0.5 defined the absence of liver fibrosis. FIB-4 >3.25 and APRI >1.5 defined advanced liver fibrosis. The main independent variable was lifetime alcohol consumption (<150 kg, 150 to 600 kg, >600 kg).
Subjects (n = 308) were 73% men, mean age 43 years, 49% with hepatitis C virus (HCV) infection, 60% on antiretroviral therapy, 49% with an HIV RNA load <1,000 copies/ml, and 18.7% with a CD4 count <200 cells/mm(3) . Forty-five percent had lifetime alcohol consumption >600 kg, 32.7% 150 to 600 kg, and 22.3% <150 kg; 33% had current heavy alcohol use, and 69% had >9 years of heavy episodic drinking. Sixty-one percent had absence of liver fibrosis and 10% had advanced liver fibrosis based on FIB-4. In logistic regression analyses, controlling for age, gender, HCV infection, and CD4 count, no association was detected between lifetime alcohol consumption and the absence of liver fibrosis (FIB-4 <1.45) (adjusted odds ratio [AOR] = 1.12 [95% CI: 0.25 to 2.52] for 150 to 600 kg vs. <150 kg; AOR = 1.11 [95% CI: 0.52 to 2.36] for >600 kg vs. <150 kg; global p = 0.95). Additionally, no association was detected between lifetime alcohol use and advanced liver fibrosis (FIB-4 >3.25). Results were similar using APRI, and among those with and without HCV infection.
In this cohort of HIV-infected patients with alcohol problems, we found no significant association between lifetime alcohol consumption and the absence of liver fibrosis or the presence of advanced liver fibrosis, suggesting that alcohol may be less important than other known factors that promote liver fibrosis in this population.
酒精对 HIV 感染患者肝脏疾病的影响尚未得到充分描述。
我们对存在酒精问题的 HIV 感染患者进行了一项前瞻性多变量分析，以研究终生饮酒与肝纤维化之间的关系。使用 2 种非侵入性指数（包括血小板、肝酶和年龄的“FIB-4”，以及包括血小板和肝酶的天门冬氨酸氨基转移酶/血小板比值指数[APRI]）来估计肝纤维化。FIB-4<1.45 和 APRI<0.5 定义为无肝纤维化。FIB-4>3.25 和 APRI>1.5 定义为晚期肝纤维化。主要的独立变量是终生饮酒量（<150 kg、150 至 600 kg、>600 kg）。
研究对象（n=308）中，73%为男性，平均年龄 43 岁，49%患有丙型肝炎病毒（HCV）感染，60%接受抗逆转录病毒治疗，49%的 HIV RNA 载量<1,000 拷贝/ml，18.7%的 CD4 计数<200 个/mm3。45%的人终生饮酒量>600 kg，32.7%的人终生饮酒量为 150 至 600 kg，22.3%的人终生饮酒量<150 kg；33%的人目前有大量饮酒，69%的人有>9 年的大量饮酒史。61%的人无肝纤维化，10%的人根据 FIB-4 存在晚期肝纤维化。在 logistic 回归分析中，在控制年龄、性别、HCV 感染和 CD4 计数后，终生饮酒与无肝纤维化（FIB-4<1.45）之间未发现关联（调整后的优势比[OR]：150 至 600 kg 与<150 kg 相比为 1.12[95%CI：0.25 至 2.52]；>600 kg 与<150 kg 相比为 1.11[95%CI：0.52 至 2.36]；总体 p=0.95）。此外，终生饮酒与晚期肝纤维化（FIB-4>3.25）之间也没有关联。使用 APRI 时，结果相似，在感染 HCV 和未感染 HCV 的患者中也是如此。
在本队列中，HIV 感染且存在酒精问题的患者中，我们发现终生饮酒与无肝纤维化或晚期肝纤维化之间无显著关联，这表明与其他已知促进肝纤维化的因素相比，酒精可能在该人群中不那么重要。
