在中国一家三级医院的阿扎西奥普林治疗儿科炎性肠病中的主动药物基因组学
1Department of Gastroenterology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, China.
Frontiers in pharmacology
|April 10, 2025
概括
药物基因组学,特别是NUDT15变体,对中国儿童炎症性肠病 (IBD) 的阿扎西奥普林安全性产生重大影响. 建议使用较低的阿扎西奥普林剂量,即使是那些具有正常遗传特征的人,以防止骨髓抑制.
科学领域:
- 药物基因组学 药物基因组学
- 胃肠病学 胃肠病学
- 儿科医学 儿科医学
背景情况:
- 阿扎西奥普林仍然是儿科炎性肠病 (IBD) 的关键治疗方法.
- 骨髓抑制是阿扎西奥普林治疗的重要副作用.
- 药物遗传学研究对于优化儿科IBD中阿扎西奥普林的使用至关重要.
研究的目的:
- 评估中国儿科IBD患者的药物基因组概况,这些患者接受了阿扎西奥普林治疗.
- 确定遗传变异与阿扎西奥普林诱导的骨髓抑制之间的关联.
- 在这个人群中为阿扎西奥普林提供个性化剂量策略的信息.
主要方法:
- 对227名中国儿科IBD患者进行药物遗传学测试的回顾性分析.
- 对 thiopurine S-methyltransferase (TPMT) 和 Nudix hydrolase 15 (NUDT15) 基因型的评估.
- 遗传发现与阿扎西奥普林诱导的骨髓抑制发生率的相关性.
主要成果:
- 在227名患者中,66名患者中发现了异常基因型 (TPMT或NUDT15).
- NUDT15变异比TPMT变异 (7名患者) 更为普遍 (59名患者).
- 在58名阿扎西奥普林治疗患者中,有23名患者经历了骨髓抑制,在NUDT15突变携带者中发现了白血病. 在患有骨髓抑制 (p < 0.05) 的患者中观察到较低的阿扎西奥普林剂量.
结论:
- NUDT15 C415T变种在中国儿科IBD患者中很常见,并增加了阿扎西奥普林诱导的骨髓抑制的风险.
- 对于中国儿科IBD患者来说,考虑降低阿扎西奥普林剂量是有必要的,无论他们的药物遗传特征如何.
- 药物基因组查可以帮助预防不良事件,并优化儿科IBD管理中的治疗.
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