Factors associated with liver steatosis in people living with HIV on contemporary antiretroviral therapy. Open Forum Infectious Diseases
Riebensahm et al. aimed to describe determinants of liver steatosis among people living with HIV (PLWH) who receive antiretroviral therapy (ART) in the Swiss HIV Cohort Study.
Between November 2019 and August 2021, individuals without HBV or HCV coinfection from the University Hospital of Bern were assessed for liver steatosis using transient elastography. Liver steatosis was defined as controlled attenuation parameter (CAP) ≥248 dB/m (M-probe) or ≥242 dB/m (XL-probe). The authors used multivariable logistic regression to evaluate clinical and treatment-associated predictors of liver steatosis.
The study included 416 individuals (27% female, median age 51 years, 51% with a BMI ≥25 kg/m2). Of those, 16.6% had mild (S1-S2), and 34.4% had severe liver steatosis (S3). Among overweight/obese individuals, the proportion of PLWH with liver steatosis reached 70% compared to 31.4% among those with a normal BMI. Being overweight or obese (BMI ≥25 kg/m2, aOR 5.8, CI 3.6-9.3), older than 50 years (aOR 1.9, 1.1-3.1), and of European origin (aOR 3.2, CI 1.7-5.9) were associated with liver steatosis. Whereas no association was found with the use of integrase inhibitors. Individuals who received tenofovir alafenamide (TAF) at the time of CAP measurement were more likely to have liver steatosis (aOR 1.7, 1.1-2.7) compared to individuals receiving other ART backbones.
In conclusion, 50% of PLWH had evidence of liver steatosis in this study. Risk factors for liver steatosis included older age, overweight/obesity, and ethnicity. In addition, participants currently receiving TAF were twice as likely to have steatosis as those unexposed to this drug. Whether the association with TAF is mediated by weight increases or reflects an independent effect remains to be determined. The high prevalence of liver steatosis even in the absence of obesity highlights the need for further study of the mechanisms driving metabolic comorbidities in PLWH.