World journal of hepatology · 2025
Hepatitis E virus infection-triggered intrahepatic cholestasis: A case report.
Клинический случайСтатьяНазвание 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.
Drexler Stephan, Haedge Frederic, Weber Susanne N, Krawczyk Marcin, Matter Matthias S, Geppert Carol I, Weber Achim, Stieger Bruno, Trautwein Christian, Kremer Andreas E
Аннотация
BACKGROUND: Genetic disorders affecting hepatobiliary transporters can be triggered by various factors, resulting in marked cholestasis.
CASE SUMMARY: We report two patients who experienced a severe episode of intrahepatic cholestasis triggered by an acute hepatitis E virus infection. Following an extensive clinical examination that ruled out common causes of cholestatic liver damage, we conducted next-generation sequencing to determine the genetic profiles of the patients. The analysis revealed several known and unknown variants in genes associated with hepatobiliary transporters and bile salt regulation, including ATP8B1, ABCB11, ABCB4, MYO5B, and FXR. For a comprehensive understanding of the pathophysiology, we performed ClinVar analysis and utilized PolyPhen for bioinformatic prediction of functional impact. Both patients exhibited rapid symptom improvement and a decrease in hyperbilirubinemia when treated with either rifampicin or bezafibrate.
CONCLUSION: Our findings introduce hepatitis E viral infection as a novel trigger for intrahepatic cholestasis, and we categorize the significance of the various genetic variants based on the current state of research.
CASE SUMMARY: We report two patients who experienced a severe episode of intrahepatic cholestasis triggered by an acute hepatitis E virus infection. Following an extensive clinical examination that ruled out common causes of cholestatic liver damage, we conducted next-generation sequencing to determine the genetic profiles of the patients. The analysis revealed several known and unknown variants in genes associated with hepatobiliary transporters and bile salt regulation, including ATP8B1, ABCB11, ABCB4, MYO5B, and FXR. For a comprehensive understanding of the pathophysiology, we performed ClinVar analysis and utilized PolyPhen for bioinformatic prediction of functional impact. Both patients exhibited rapid symptom improvement and a decrease in hyperbilirubinemia when treated with either rifampicin or bezafibrate.
CONCLUSION: Our findings introduce hepatitis E viral infection as a novel trigger for intrahepatic cholestasis, and we categorize the significance of the various genetic variants based on the current state of research.