Metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction-associated alcohol-related liver disease in human immunodeficiency virus.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated alcohol-related liver disease (MetALD) have emerged as increasingly important sources of morbidity among people living with human immunodeficiency virus (HIV). Advances in antiretroviral therapy have substantially improved life expectancy in people living with HIV (PLWH), but have also unmasked a growing burden of metabolic comorbidities which contribute to steatotic liver disease. Recent shifts in nomenclature and the introduction of MetALD emphasize metabolic dysfunction and graded alcohol exposure as central drivers of disease and are particularly relevant to PLWH, a population in whom overlapping metabolic and behavioral risk factors are common. Epidemiologic studies demonstrate that MASLD affects approximately one-third to one-half of PLWH worldwide, often occurring at younger ages and lower body mass index thresholds than in HIV-negative individuals. Emerging data further highlight the synergistic contribution of metabolic dysfunction and alcohol use to accelerated fibrosis progression in PLWH. Pathophysiologic mechanisms linking HIV infection to MASLD and MetALD include chronic immune activation and systemic inflammation, antiretroviral therapy-associated metabolic effects, altered adipose tissue distribution, gut-liver axis dysregulation, and alcohol-metabolic synergy. This review synthesizes contemporary evidence on the definitions, epidemiology, pathogenesis, clinical assessment, and management of MASLD and MetALD in PLWH.