Motherisk Program, Division of Clinical Pharmacology and Toxicology, Hospital for Sick Children, 555 University Ave, Toronto, ON, Canada M5G 1X8.
Pediatrics. 2010 Oct;126(4):e986-9. doi: 10.1542/peds.2009-1907. Epub 2010 Sep 13.
Fatal opioid toxicity occurred in a developmentally delayed child aged 5 years 9 months who was inadvertently administered high doses of hydrocodone for a respiratory tract infection. The concentration of hydrocodone in postmortem blood was in the range associated with fatality; however, hydromorphone, a major metabolite catalyzed by cytochrome P450 2D6 (CYP2D6), was not detected when using mass spectrometry. Genetic analysis revealed that the child had a reduced capability to metabolize the drug via the CYP2D6 pathway (CYP2D6*2A/*41). Coadministration of clarithromycin (a potent cytochrome P450 3A4 inhibitor) for an ear infection and valproic acid for seizures since birth further prevented drug elimination from the body. This case highlights the interplay between pharmacogenetic factors, drug-drug interactions, and dose-related toxicity in a child.
一名 5 岁 9 个月大的发育迟缓儿童因呼吸道感染被意外给予大剂量氢可酮,导致致命性阿片类药物中毒。死后血液中氢可酮的浓度处于致死相关范围;然而,当使用质谱法时,未检测到主要由细胞色素 P450 2D6(CYP2D6)催化的代谢物氢吗啡酮。基因分析显示,该儿童通过 CYP2D6 途径(CYP2D6*2A/*41)代谢药物的能力降低。由于耳部感染而同时给予克拉霉素(一种强效细胞色素 P450 3A4 抑制剂)和丙戊酸治疗癫痫,自出生以来进一步阻止了药物从体内消除。该病例强调了遗传药理学因素、药物相互作用和与剂量相关的毒性在儿童中的相互作用。