Statin Therapy Does Not Reduce Liver Fat Scores in Patients Receiving Antiretroviral Therapy for HIV Infection.

BACKGROUND & AIMS: Therapies are needed to limit progression of fatty liver diseases in patients with HIV infection. We analyzed data from a prospective study of the effects of rosuvastatin (a statin) on hepatic steatosis in HIV-positive adults.

METHODS: We performed secondary analysis of data from a double-blind trial of adult patients with HIV infection (78% male; 68% African American; mean age, 46 years; body mass index, 29 kg/m2 ; HIV1 RNA<1000 copies/mL; LDL-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.

RESULTS: The placebo and rosuvastatin groups each had significant increases in LFS, compared to 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 (CXCL10) (P=.04) and soluble CD163 molecule (P=.01). After we adjusted for baseline characteristics, an increase in LFS over time was significantly associated with blood level of CXCL10 (P=.04), insulin resistance (P<.01), and viral load (P=.02), but not rosuvastatin use (P=.06).

CONCLUSION: 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 hepatic steatosis over 96 weeks. Despite their ability to reduce risk of cardiovascular disease, statins do not appear to reduce hepatic steatosis. Clinicaltrials.gov no: NCT01218802.