AIDS (London, England) · 2026
Pitavastatin effect on enterocyte injury markers in an antiretroviral therapy-treated HIV population.
СтатьяРандомизированное исследованиеНазвание 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.
Awwad Aya, Das Adhikari Upasana, Burdo Tricia H, Baak Stephen, Dalal Miloni S, Fichtenbaum Carl J, Zanni Markella V, Aberg Judith A, Currier Judith S, Bloomfield Gerald S, Chu Sarah M, Lu Alex B, Douglas Pamela S, Ribaudo Heather J, Kwon Douglas S, Grinspoon Steven K
Аннотация
OBJECTIVE: To determine whether pitavastatin reduces enterocyte injury, assessed by intestinal fatty acid-binding protein (I-FABP), among antiretroviral therapy-treated people with HIV (PWH) enrolled in the REPRIEVE mechanistic substudy.
DESIGN: Randomized, double-blind, placebo-controlled trial.
METHODS: We analyzed fasting plasma I-FABP at entry and month 24 among participants randomized to pitavastatin 4 mg daily or placebo. Baseline characteristics were summarized across I-FABP quartiles. Associations between entry I-FABP and inflammatory and immune activation biomarkers were assessed using Spearman correlations. Longitudinal changes were evaluated using intention-to-treat and per-protocol analyses and generalized estimating equation models.
RESULTS: Among 710 participants with entry I-FABP measurements (median age 50 years; 18.5% women; 98% with undetectable viral load), median I-FABP levels were 2690 (Q1-Q3: 1888-3770) (pg/ml). Entry I-FABP correlated modestly with markers of systemic inflammation and monocyte activation, including GDF-15 and soluble CD14 + . Over 24 months, I-FABP levels declined similarly in the pitavastatin and placebo arms, with no significant differences in absolute or fold change.
CONCLUSION: In this well treated HIV cohort, higher baseline I-FABP levels were associated with increased inflammatory markers at study entry. However, pitavastatin did not reduce I-FABP over follow-up. These findings suggest that the cardiovascular benefit of pitavastatin in REPRIEVE is unlikely to be mediated through reductions in enterocyte injury, although gut-barrier effects of other statins cannot be excluded.
DESIGN: Randomized, double-blind, placebo-controlled trial.
METHODS: We analyzed fasting plasma I-FABP at entry and month 24 among participants randomized to pitavastatin 4 mg daily or placebo. Baseline characteristics were summarized across I-FABP quartiles. Associations between entry I-FABP and inflammatory and immune activation biomarkers were assessed using Spearman correlations. Longitudinal changes were evaluated using intention-to-treat and per-protocol analyses and generalized estimating equation models.
RESULTS: Among 710 participants with entry I-FABP measurements (median age 50 years; 18.5% women; 98% with undetectable viral load), median I-FABP levels were 2690 (Q1-Q3: 1888-3770) (pg/ml). Entry I-FABP correlated modestly with markers of systemic inflammation and monocyte activation, including GDF-15 and soluble CD14 + . Over 24 months, I-FABP levels declined similarly in the pitavastatin and placebo arms, with no significant differences in absolute or fold change.
CONCLUSION: In this well treated HIV cohort, higher baseline I-FABP levels were associated with increased inflammatory markers at study entry. However, pitavastatin did not reduce I-FABP over follow-up. These findings suggest that the cardiovascular benefit of pitavastatin in REPRIEVE is unlikely to be mediated through reductions in enterocyte injury, although gut-barrier effects of other statins cannot be excluded.