School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong SAR, Hong Kong.
J Hepatol. 2011 Apr;54(4):666-73. doi: 10.1016/j.jhep.2010.07.031. Epub 2010 Sep 22.
BACKGROUND & AIMS: One major cause of hepatic sinusoidal obstruction syndrome (HSOS) is the intake of pyrrolizidine alkaloid (PA)-containing products. Over 8000 PA-induced HSOS cases have been reported worldwide and at least 51 among them were suspected to be attributed to exposure to the Chinese medicine 'Tusanqi'. PA-induced hepatotoxicity involves cytochrome P450-mediated metabolic activation of PAs to electrophilic pyrrolic metabolites which react with macromolecules, such as proteins. However, no studies have found such protein adduction in HSOS patients. We report one HSOS case confirmed by liver biopsy, where the patient claimed taking 'Tusanqi' as self-medication.
The herb was analyzed by HPLC-MS, and its induced hepatotoxicity in rats was assessed by monitoring the alteration of serum ALT level and liver morphology. Blood pyrrole-protein adducts were determined by UPLC-MS.
The herb the patient consumed was identified as Gynura segetum, an erroneous substitute of non-PA-containing Sedum aizoon, called 'Tusanqi'. Hepatotoxic PAs senecionine and seneciphylline were detected in G. segetum. In the PA-exposed patient, serum pyrrole-protein adducts were detected by a newly developed analytical approach. The animal study showed a good correlation of liver injury with the ingestion of G. segetum.
For the first time, serum pyrrole-protein adducts were unequivocally detected in a PA-induced HSOS patient, and such adducts show a potential to be developed as a biomarker for the assessment of PA-induced HSOS. Similar to the well-known case of aristolochic acid-poisoning, the observed HSOS was confirmed to arise from the consumption of PA-containing G. segetum, an erroneous substitute of non-PA-containing S. aizoon.
肝窦阻塞综合征(HSOS)的一个主要原因是摄入含有吡咯里西啶生物碱(PA)的产品。全世界已报告了超过 8000 例 PA 诱导的 HSOS 病例,其中至少有 51 例疑似与中药“土三七”暴露有关。PA 诱导的肝毒性涉及细胞色素 P450 介导的 PA 代谢活化为亲电吡咯代谢物,然后与大分子(如蛋白质)反应。然而,在 HSOS 患者中尚未发现这种蛋白质加合物。我们报告了一例经肝活检证实的 HSOS 病例,该患者声称自行服用“土三七”。
通过 HPLC-MS 分析该草药,通过监测血清 ALT 水平和肝脏形态的变化来评估其在大鼠中的肝毒性。通过 UPLC-MS 测定血液吡咯蛋白加合物。
患者服用的草药被鉴定为菊三七,一种不含 PA 的千里光 Sedum aizoon 的错误替代品,称为“土三七”。在 G. segetum 中检测到肝毒性 PA 千里光宁和千里光菲林。在 PA 暴露的患者中,通过新开发的分析方法检测到血清吡咯蛋白加合物。动物研究表明,肝脏损伤与 G. segetum 的摄入有很好的相关性。
首次在 PA 诱导的 HSOS 患者中明确检测到血清吡咯蛋白加合物,并且此类加合物有望作为评估 PA 诱导的 HSOS 的生物标志物。与众所周知的马兜铃酸中毒病例类似,观察到的 HSOS 被证实是由含有 PA 的菊三七引起的,菊三七是不含 PA 的千里光 Sedum aizoon 的错误替代品。