California Poison Control System, San Francisco Division, University of California , San Francisco, CA , USA.
Clin Toxicol (Phila). 2013 Dec;51(10):1230-4. doi: 10.3109/15563650.2013.849349. Epub 2013 Oct 17.
Bupropion overdose commonly causes generalized seizures and central nervous system depression. Less commonly, cardiotoxicity has been reported. The toxicity of the parent drug compared to its active metabolite hydroxybupropion is uncertain.
A 31-year-old man presented to the emergency department with altered mental status after an intentional overdose of bupropion. Three hours after admission he developed status epilepticus requiring intubation, and 13 h after admission he developed marked widening of the QRS complex and prolongation of the QTc interval. Serial serum bupropion levels peaked with the onset of cardiotoxicity (334 ng/mL) and fell into the therapeutic range within 24 h, which coincided with normalization of his ECG intervals. Levels of the metabolite hydroxybupropion peaked later (4302 ng/mL) and remained elevated even after neurological and cardiotoxic symptoms resolved.
Cardiotoxicity appears to be caused primarily by bupropion rather than its active metabolite hydroxybupropion.
盐酸安非他酮过量通常会导致全身性癫痫发作和中枢神经系统抑制。较少见的是,已有报道称其会引起心脏毒性。与活性代谢物羟可酮相比,母体药物的毒性尚不确定。
一名 31 岁男性因故意过量服用盐酸安非他酮后出现意识改变,被收入急诊。入院 3 小时后,他出现癫痫持续状态,需要插管治疗,入院 13 小时后,他出现明显的 QRS 波群增宽和 QTc 间期延长。血清安非他酮水平在出现心脏毒性时(334ng/ml)达到峰值,并在 24 小时内降至治疗范围,这与心电图间隔的正常化相吻合。代谢物羟可酮的水平较晚达到峰值(4302ng/ml),即使在神经和心脏毒性症状消退后仍保持升高。
心脏毒性似乎主要是由安非他酮引起的,而不是其活性代谢物羟可酮。