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Statin didn’t slow hepatic steatosis in HIV patients

 

Key clinical point: HIV patients on statin therapy showed increased risk of contracting fatty liver disease, compared with controls.

Major finding: Progression from nonsteatosis at baseline to steatosis over 96 weeks was greater in patients given rosuvastatin than in those given placebo (odds ratio, 4.3; P = .03).

Data source: A randomized, placebo-controlled study of 147 patients with HIV on stable ART.

Disclosures: The National Institutes of Health funded the study. Dr. El Kamari had no disclosures.


 

AT IDWEEK 2017

– Statin therapy wasn’t effective against a rising rate of hepatic steatosis in HIV patients, and may increase nonalcoholic fatty liver disease (NAFLD) risk, according to a small study.

The findings are contrary to the limited data currently available, which suggest statins can have a beneficial effect on hepatic steatosis, according to the study’s investigators.

NAFLD is one of the leading causes of mortality and morbidity in people living with HIV, said Vanessa El Kamari, MD, of Case Western Reserve University, Cleveland, and rates are continuing to increase. With a lack of therapeutic interventions for NAFLD in patients with HIV, finding effective treatments is a major concern for providers.

Dr. El Kamari and her colleagues conducted a secondary analysis of the SATURN-HIV trial, a randomized, placebo-controlled trial of 147 patients with HIV who were on stable antiretroviral therapy (ART) with LDL cholesterol levels at or below 130 mg/dL. Patients were either treated with 10 mg rosuvastatin or placebo.

Patients in the treatment and placebo arms were an average age of 45 years, most patients were male (81% and 76%, respectively), and a majority was African American (69% and 67%, respectively). The two groups reported average CD4+ counts of 644 and 636, respectively.

Investigators used validated scores to determine hepatic steatosis in patients, although researchers acknowledged that liver biopsy is the gold standard for hepatic steatosis measurement.

“We understand liver fat score has its limitation,” said Dr. El Kamari in a question and answer session following the presentation at an annual scientific meeting on infectious diseases. “Further studies are needed in this area in order to detect, in noninvasive ways, hepatic steatosis.”

Liver fat scores (LFS) were measured on entry, at week 48, and week 96.

After 96 weeks, investigators saw significant increases in LFS in both the placebo and rosuvastatin groups (P = .01 and P less than .01, respectively). Progression from nonsteatosis at baseline to steatosis over 96 weeks was greater in patients given rosuvastatin than in those given placebo (odds ratio, 4.3; P = .03).

Studying predictors for LFS changes, a trend toward insignificance among the randomization group led investigators to the conclusion that statin may have negatively affected the liver fat score of patients over the 96-week time period.

The study researchers identified 92 patients who did not have hepatic steatosis at baseline to study how statins influenced the development of hepatic steatosis.

Of the 13 patients who developed steatosis during the trial period, 10 were part of the rosuvastatin group, while only 3 were from the placebo group.

Increases in LFS were associated with increases in insulin resistance, detected presence of HIV-1 RNA, and higher interferon-inducible proteins, according to Dr. El Kamari.

While increased homeostatic assessment of insulin resistance was associated with increased hepatic homeostasis, Dr. El Kamari was not able to determine if statins that are not associated with insulin resistance will have different outcomes.

The investigators cautioned that the findings may not be generalizable to the entire HIV population due to the overwhelming majority of African American patients with increased inflammation, as well as the study patients’ LDL cholesterol levels of less than or equal to 130 mg/dL.

The National Institutes of Health funded the study. Dr. El Kamari had no disclosures.

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