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药物性肝损伤。第二部分:晚期并发症及肝毒性监测。

Drug-induced liver injury. Part II: Late complications and hepatotoxicity monitoring.

作者信息

Kozielewicz Dorota M, Stalke Piotr

机构信息

Department of Infectious Diseases and Hepatology, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, Poland.

Department of Liver Diseases, Provincial Infectious Disease Hospital of T. Browicz, Bydgoszcz, Poland.

出版信息

Clin Exp Hepatol. 2025 Jun;11(2):89-96. doi: 10.5114/ceh.2025.151868. Epub 2025 Jun 9.

Abstract

The picture of drug-induced liver injury (DILI) is polymorphic, with variable intensity of clinical symptoms and prognosis. Most cases of DILI are acute, although the incidence of chronic hepatopathy has been reported to range from 3.4% to 39.0% in the period 6-12 months after discontinuation of the drug. The long-term chronic consequences of DILI in terms of morbidity and mortality are unclear. The rare obstructive bile duct syndrome is associated with an unfavorable prognosis - a higher risk of chronic liver failure and the need for liver transplantation. Other long-term forms of hepatopathy following DILI include progressive liver fibrosis, autoimmune hepatitis, hepatic steatosis, secondary sclerosing cholangitis, vascular lesions, and liver tumors. Recently, immune checkpoint inhibitors, which can cause an autoimmune-like phenotype, have also been shown to cause sclerosing cholangitis with infiltration of cytotoxic T cells in the biliary tract.

摘要

药物性肝损伤(DILI)的表现具有多态性,临床症状的严重程度和预后各不相同。大多数DILI病例为急性,不过据报道,在停药后6至12个月期间,慢性肝病的发生率在3.4%至39.0%之间。DILI在发病率和死亡率方面的长期慢性后果尚不清楚。罕见的梗阻性胆管综合征预后不良——慢性肝衰竭风险较高且需要进行肝移植。DILI后的其他长期肝病形式包括进行性肝纤维化、自身免疫性肝炎、肝脂肪变性、继发性硬化性胆管炎、血管病变和肝肿瘤。最近,可导致自身免疫样表型的免疫检查点抑制剂也被证明可引起硬化性胆管炎,并伴有细胞毒性T细胞浸润于胆道。

本文引用的文献

2
Checkpoint inhibitor hepatotoxicity: pathogenesis and management.检查点抑制剂肝毒性:发病机制与管理
Hepatology. 2024 Jan 1;79(1):198-212. doi: 10.1097/HEP.0000000000000045. Epub 2023 Jan 13.
9
Drug-Induced Liver Injury - Types and Phenotypes.药物性肝损伤——类型与表型
N Engl J Med. 2019 Jul 18;381(3):264-273. doi: 10.1056/NEJMra1816149.

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