抗结核药物肝损伤与熊去氧胆酸

S. Lang, Emad Al-Nemnem, H. Schiffl
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引用次数: 1

摘要

标准抗结核药物(异烟肼、利福平、吡嗪酰胺)引起的肝毒性可导致显著的发病率,很少甚至死亡。抗结核治疗的这一主要副作用对患者的依从性和患者的预后以及结核病控制都有负面影响。早期识别和及时停药是治疗抗结核药物性肝损伤的最关键干预措施。直到最近,还没有药物或草药提取物被证明可以预防或逆转抗结核病药物引起的肝毒性。熊去氧胆酸是美国食品药品监督管理局唯一批准的治疗原发性胆汁性胆管炎的药物,也已成功用于各种胆汁淤积性肝病。尽管仍处于实验阶段,但最近的对照临床研究表明,口服熊去氧胆酸可以预防抗结核药物诱导的肝损伤的发作,并加速肝损伤的恢复。这些临床数据得到了抗结核药物诱导肝毒性实验模型的支持。迫切需要进一步的随机临床试验来证明熊去氧胆酸具有良好的肝保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Anti-Tuberculosis Drug Induced Liver Injury and Ursodeoxycholic Acid
Hepatotoxicity induced by standard anti-tuberculosis drugs (isoniazid, rifampicin, pyrazinamide) can result in significant morbidity and, rarely, even mortality. This major adverse side-effect of anti-tuberculosis treatment has a negative impact on patient adherence and patient outcomes as well as on tuberculosis control. Early recognition and prompt withdrawal of the offending drugs are the most critical interventions in the management of anti-tuberculosis drug-induced liver injury. No drug or herbal extract has been shown until recently to prevent or reverse anti-tuberculosis drug-induced hepatotoxicity. Ursodeoxycholic acid is the only FDA approved drug for the treatment of primary biliary cholangitis and has also been successfully used in various cholestatic liver diseases. Although still experimental, recent controlled clinical studies suggested that oral administration of ursodeoxycholic acid may prevent the onset of anti-tuberculosis drug-induced liver injury and accelerate the recovery of liver injury. These clinical data are supported by experimental models of anti-tuberculosis drug-induced hepatotoxicity. There is an urgent need for further randomized clinical trials to document the promising hepatoprotective properties of ursodeoxycholic acid.
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