AIDS (London, England) · 2026
Contribution of hepatic steatosis to subclinical atherosclerosis progression in people with HIV receiving integrase inhibitors: a 5-year prospective cohort study.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
García-Abellán Javier, García José A, Padilla Sergio, Fernández-González Marta, Bello-Pérez Melissa, Mascarell Paula, Botella Angela, López Leandro, Masiá Mar, Gutiérrez Félix
Аннотация
BACKGROUND AND OBJECTIVES: Cardiovascular disease (CVD) remains elevated among people with HIV (PWH) despite virological suppression. Whether metabolic-hepatic abnormalities contribute to vascular remodeling during contemporary integrase strand transfer inhibitor (INSTI)-based antiretroviral therapy (ART) remains uncertain. We evaluated long-term carotid intima-media thickness (cIMT) trajectories and their metabolic, hepatic, and inflammatory determinants.
METHODS AND DESIGN: We conducted a 5-year prospective cohort study of virologically suppressed adults receiving INSTI-based ART. cIMT was measured at baseline, 48, 96, and 240 weeks. Mixed-effects models assessed longitudinal cIMT, and a complementary increment-based model evaluated predictors of visit-to-visit cIMT change. Measures of insulin resistance (TyG, HOMA-IR), hepatic steatosis (HSI, FLI), and inflammatory biomarkers (D-dimer, sCD14, sCD163, hsCRP, sICAM-1) were evaluated. Mediation through ASCVD risk was explored.
RESULTS: Among 101 participants, cIMT increased significantly over 5 years. In multivariable mixed-effects models, ASCVD risk, HSI, TyG, and D-dimer were independently associated with cIMT. In increment-based analyses (visit-to-visit change in cIMT), hepatic steatosis as assessed by the hepatic steatosis index (HSI) was the only metabolic or inflammatory variable independently associated with short-term cIMT progression [odds ratio (OR) 1.042, 95% confidence interval (CI) 1.008-1.079]. HSI exerted a fully direct effect on cIMT progression ( P < 0.001), without mediation through ASCVD risk, and increased the explained variance by 5.1% beyond ASCVD alone. TyG, D-dimer and sCD163 were associated with cIMT in mixed-effects models, but not with cIMT increments.
CONCLUSIONS: HSI-defined hepatic steatosis contributed independently and incrementally to subclinical atherosclerosis progression in PWH receiving INSTI-based ART, beyond traditional cardiovascular risk estimation. Incorporating simple hepatic-metabolic indices such as HSI may improve cardiovascular risk stratification in this population.
METHODS AND DESIGN: We conducted a 5-year prospective cohort study of virologically suppressed adults receiving INSTI-based ART. cIMT was measured at baseline, 48, 96, and 240 weeks. Mixed-effects models assessed longitudinal cIMT, and a complementary increment-based model evaluated predictors of visit-to-visit cIMT change. Measures of insulin resistance (TyG, HOMA-IR), hepatic steatosis (HSI, FLI), and inflammatory biomarkers (D-dimer, sCD14, sCD163, hsCRP, sICAM-1) were evaluated. Mediation through ASCVD risk was explored.
RESULTS: Among 101 participants, cIMT increased significantly over 5 years. In multivariable mixed-effects models, ASCVD risk, HSI, TyG, and D-dimer were independently associated with cIMT. In increment-based analyses (visit-to-visit change in cIMT), hepatic steatosis as assessed by the hepatic steatosis index (HSI) was the only metabolic or inflammatory variable independently associated with short-term cIMT progression [odds ratio (OR) 1.042, 95% confidence interval (CI) 1.008-1.079]. HSI exerted a fully direct effect on cIMT progression ( P < 0.001), without mediation through ASCVD risk, and increased the explained variance by 5.1% beyond ASCVD alone. TyG, D-dimer and sCD163 were associated with cIMT in mixed-effects models, but not with cIMT increments.
CONCLUSIONS: HSI-defined hepatic steatosis contributed independently and incrementally to subclinical atherosclerosis progression in PWH receiving INSTI-based ART, beyond traditional cardiovascular risk estimation. Incorporating simple hepatic-metabolic indices such as HSI may improve cardiovascular risk stratification in this population.