在患者中,单碳代谢与酸诱导的肝功能障碍之间的关联
Jingwei Zhu1, Zhe Wang1, Xiaotong Sun1
1Department of Clinical Laboratory, Qingdao University Medical College Affiliated Yantai Yuhuangding Hospital, Yantai, China.
Frontiers in pharmacology
|March 11, 2024
概括
基因变异的MTHFR (甲基基酸减少酶) 和高水平的同类氨酸 (Hcy) 与酸 (VPA) 诱导的儿科患者的肝损伤有关. 这些因素可能表明个体对VPA肝毒性的敏感性.
科学领域:
- 药物遗传学 药物遗传学
- 肝毒性机制 肝毒性机制
- 治疗的方法 治疗
背景情况:
- 酸 (VPA) 是一种常见的抗药物.
- 长期使用VPA可能会导致肝毒性,但机制尚不清楚.
- 个人对VPA诱导的肝功能障碍的敏感性需要调查.
研究的目的:
- 在儿科患者中调查MTHFR基因多态和VPA诱导的肝功能障碍之间的关联.
- 探索MTHFR变异,同型半氨酸 (Hcy) 水平和肝功能之间的关系.
- 为了确定VPA诱导的肝毒性风险因素.
主要方法:
- 招募了157名儿科患者,分为正常肝功能 (NLF) 和异常肝功能 (ABLF) 组.
- 基因型为MTHFR A1298C和C677T变种.
- 测量了血清Hcy,叶酸 (FA),谷氨 (GSH) 和硫酸酸反应物质 (TBARS) 的水平.
主要成果:
- MTHFR A1298C和C677T变异与VPA诱导的肝功能障碍显著相关 (p=0.001;p=0.023).
- MTHFR A1298C多态性与较高的Hcy (p=0.001) 和较低的FA (p=0.001) 水平相关.
- 升高的Hcy水平与GSH (r=-0.6065) 和TBARS (r=0.6564) 度有很强的相关性.
结论:
- MTHFR A1298C/C677T多态性和Hcy度的增加是VPA引起的肝功能障碍的潜在危险因素.
- 个人对VPA肝毒性的敏感性可能会受到MTHFR基因型和Hcy水平的影响.
- 这些发现可能有助于预防和管理VPA诱导的肝功能障碍.
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