Journal of acquired immune deficiency syndromes (1999) · 2025
Liver Fibrosis Regression in People Living With HIV After Successful Treatment for Hepatitis C.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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.
Young Jim, Wang Shouao, Sacks-Davis Rachel, Stewart Ashleigh, van Santen Daniela K, van der Valk Marc, Doyle Joseph S, Matthews Gail, Berenguer Juan, Wittkop Linda, Lacombe Karine, Rauch Andri, Stoové Mark, Hellard Margaret, Klein Marina B, InCHEHC Collaboration
Аннотация
BACKGROUND: Successful treatment of hepatitis C virus (HCV) can lead to liver fibrosis regression. It is not known who will experience fibrosis regression or how quickly it will occur.
METHODS: We modeled transient elastography (TE) measurements from 1470 HIV-HCV coinfected participants followed in cohorts contributing data to InCHEHC, an international collaboration. Participants were eligible if they had at least 1 TE measurement in the year before starting a successful direct-acting antiviral treatment for HCV. This measurement was used to classify participants into 1 of 3 fibrosis subgroups. We analyzed measurement sequences in each subgroup using a covariate-adjusted generalized additive mixed model, with an adaptive spline representing changes in the mean measurement before, during, and after treatment.
RESULTS: Each fibrosis subgroup had a distinctly different response. Most participants with cirrhosis (F4, TE ≥14.6 KPa) before HCV treatment did not show meaningful fibrosis regression-approximately 70% were predicted to remain >12 KPa 3 years after treatment ended. Participants with significant fibrosis (F2-F3, TE ≥7.2 and <14.6 KPa) showed appreciable regression in the first 2 years after treatment, falling on average to levels <7.2 KPa. Those without fibrosis before treatment (F0-F1) did not progress.
CONCLUSIONS: Most coinfected people with cirrhosis before HCV cure will remain cirrhotic. For those with significant fibrosis, regression can be expected within 2 years to levels not normally associated with an increased risk of end-stage liver disease. A TE measurement 2 years after cure should give a reliable estimate of residual fibrosis.
METHODS: We modeled transient elastography (TE) measurements from 1470 HIV-HCV coinfected participants followed in cohorts contributing data to InCHEHC, an international collaboration. Participants were eligible if they had at least 1 TE measurement in the year before starting a successful direct-acting antiviral treatment for HCV. This measurement was used to classify participants into 1 of 3 fibrosis subgroups. We analyzed measurement sequences in each subgroup using a covariate-adjusted generalized additive mixed model, with an adaptive spline representing changes in the mean measurement before, during, and after treatment.
RESULTS: Each fibrosis subgroup had a distinctly different response. Most participants with cirrhosis (F4, TE ≥14.6 KPa) before HCV treatment did not show meaningful fibrosis regression-approximately 70% were predicted to remain >12 KPa 3 years after treatment ended. Participants with significant fibrosis (F2-F3, TE ≥7.2 and <14.6 KPa) showed appreciable regression in the first 2 years after treatment, falling on average to levels <7.2 KPa. Those without fibrosis before treatment (F0-F1) did not progress.
CONCLUSIONS: Most coinfected people with cirrhosis before HCV cure will remain cirrhotic. For those with significant fibrosis, regression can be expected within 2 years to levels not normally associated with an increased risk of end-stage liver disease. A TE measurement 2 years after cure should give a reliable estimate of residual fibrosis.