Nonalcoholic Fatty Liver Disease Among HIV-Infected Persons

Abstract

Objective To describe the prevalence and factors associated with nonalcoholic fatty liver disease (NAFLD) among HIV-infected persons not infected with hepatitis C virus (HCV). Design A cross-sectional study among HIV-infected patients in a large HIV clinic. Methods NAFLD was defined as steatosis among patients without viral hepatitis (B or C) co-infection or excessive alcohol use. The prevalence of NAFLD was identified by ultrasound examination evaluated by two radiologists blinded to the clinic information; liver biopsies were performed on a subset of the study population. Factors associated with NAFLD evaluated by proportional odds logistic regression models. Results Sixty-seven (31%) of 216 patients had NAFLD based on ultrasound evaluation. Among those with NAFLD, steatosis was graded as mild in 60%, moderate in 28%, and severe/ marked in 12%. Factors associated with the degree of steatosis on ultrasound examination in the multivariate model included increased waist circumference (odds ratio [OR] 2.1 per 10 cm, p<0.001), elevated triglycerides (OR= 1.2 per 100 mg/dl, p=0.03), and lower HDL levels (OR 0.7, p=0.03). African Americans were less likely to have NAFLD compared to Caucasians (14% vs. 35%), although this did not reach statistical significance (OR= 0.4, p=0.08). Similar associations were noted for the subset of patients diagnosed by liver biopsy. CD4 cell count, HIV viral load, duration of HIV infection, and antiretroviral medications were not independent risk factors associated with NAFLD after adjustment for dyslipidemia or waist circumference. Conclusion NAFLD was common among this cohort of HIV-infected, HCV-seronegative patients. NAFLD was associated with a greater waist circumference, low HDL and high triglyceride levels. Antiretroviral medications were not associated with NAFLD; prospective studies are needed to confirm this finding.

Hepatic Steatosis in Patients Coinfected with Human Immunodeficiency Virus/Hepatitis C Virus: A Meta-Analysis of the Risk Factors

“…8 Several studies addressed the topic with a noninvasive approach and the majority did not exclude patients with HCV coinfection. Two well-designed studies, one assessing HS with ultrasonography 10 and the other with computed tomography (CT) scans, 11 found prevalences of 31% and 37%, respectively. Although the main risk factors found in these studies were metabolic, another study compared two groups of patients with HS and different HIV status; the results showed that HIV-infected patients had lower body mass index (BMI) and lower body fat percentage.…”

Liver Test Abnormalities in Patients with HIV Mono-Infection: Assessment with Simple Non-Invasive Fibrosis Markers

“…Guaraldi et al detected steatosis by CT scan in 37% of 225 HIV-monoinfected patients, and found an association with cumulative NRTI exposure (OR 1.12, 95%CI 1.03-1.22; P=<0.001) and obesity (OR 1.07, 95%CI 1.03-1.11; P<0.001) [23]. In contrast, in another study, though steatosis was present on US in 31% and by histology in 33% of 216 HIV-mono-infected patients, there was no association with either duration of HIV infection or ART, as only obesity (OR 2.1, 95%CI 1.6-2.8; P<0.001) and hypertriglyceridemia (OR 1.2, 95%CI 1-1.5; P=0.03) reached statistical significance [24]. Nevertheless, in both studies less than 30% of patients had deranged LFTs; this could possibly explain the lower prevalence of steatosis compared to our findings.…”

Viral mechanisms of adipose dysfunction: lessons from HIV-1 Vpr

“…This is of great interest in view of the high prevalence of non-alcoholic fatty liver disease among HIV patients (currently estimated at 30-35% of monoinfected patients, i.e., those without concomitant hepatitis B or C infection). [38][39][40][41][42][43] Accelerated lipolysis in visceral adipose tissue undoubtedly contributes to the fatty liver phenotype, but we also found evidence pointing to additional mechanisms: diminished oxidative disposal of fatty acids and defective VLDL-triglyceride export. Evidence for the former was found in blunted expression of hepatic genes regulating fat oxidation (Ppara, Cpt1, Lcad, Aox), and for the latter in decreased expression of Mtp1, encoding microsomal triglyceride transfer protein which is critical for hepatic VLDL-TG export.…”