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硫唑嘌呤疗法在一名小儿硫嘌呤甲基转移酶缺乏患者中——仍然是一种选择。

Azathioprine Therapy in a Pediatric TPMT-Deficient Patient-Still an Option.

作者信息

van Moorsel S A W, Bevers N, Meurs M, van Rossum L K, Hooymans P M, Wong D R

机构信息

*Department of Clinical Pharmacy and Toxicology, Zuyderland Medical Centre, Sittard-Geleen;†Department of Pediatrics, Zuyderland Medical Centre, Heerlen; and‡Department of Clinical Pharmacy and Toxicology, Zuyderland Medical Centre, Heerlen, the Netherlands.

出版信息

Ther Drug Monit. 2017 Feb;39(1):1-4. doi: 10.1097/FTD.0000000000000366.

DOI:10.1097/FTD.0000000000000366
PMID:28081040
Abstract

We describe the case of a pediatric patient on azathioprine therapy with previously undiagnosed homozygote thiopurine S-methyltransferase (TPMT) deficiency, resulting in myelotoxic thiopurine metabolite levels. The patient was successfully treated with a very low azathioprine dose of 50 mg once a week (4% of standard dose), guided by frequent thiopurine metabolite measurement and a close clinical surveillance. We demonstrate that azathioprine therapy still might be an effective and safe therapeutic option in pediatric thiopurine S-methyltransferase-deficient IBD patients.

摘要

我们描述了一例接受硫唑嘌呤治疗的儿科患者,其先前未被诊断出纯合子硫嘌呤甲基转移酶(TPMT)缺乏,导致骨髓毒性硫嘌呤代谢物水平升高。在频繁的硫嘌呤代谢物测量和密切临床监测的指导下,该患者成功地以每周一次50毫克的极低硫唑嘌呤剂量(标准剂量的4%)进行治疗。我们证明,对于儿科硫嘌呤甲基转移酶缺乏的炎症性肠病患者,硫唑嘌呤治疗仍可能是一种有效且安全的治疗选择。

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引用本文的文献

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Indian J Pediatr. 2018 Oct;85(10):918-919. doi: 10.1007/s12098-018-2687-z. Epub 2018 May 12.
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Clinical Pharmacokinetic and Pharmacodynamic Considerations in the Treatment of Inflammatory Bowel Disease.治疗炎症性肠病的临床药代动力学和药效学考虑因素。
Clin Pharmacokinet. 2018 Sep;57(9):1075-1106. doi: 10.1007/s40262-018-0639-4.
3
Risk factors for thiopurine-induced myelosuppression and infections in inflammatory bowel disease patients with a normal TPMT genotype.
炎症性肠病患者中硫唑嘌呤诱导的骨髓抑制和感染的危险因素,这些患者的硫嘌呤甲基转移酶(TPMT)基因型正常。
Aliment Pharmacol Ther. 2017 Nov;46(10):953-963. doi: 10.1111/apt.14323. Epub 2017 Sep 15.