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两例安非他酮过量致血清素综合征患者用赛庚啶治疗。

Two Cases of Serotonin Syndrome After Bupropion Overdose Treated With Cyproheptadine.

机构信息

Department of Emergency Medicine, Wright State Boonsoft School of Medicine, Dayton, Ohio.

Emory University School of Medicine, Atlanta, Georgia.

出版信息

J Emerg Med. 2021 Apr;60(4):e67-e71. doi: 10.1016/j.jemermed.2020.10.039. Epub 2020 Dec 8.

Abstract

Bupropion is not known to have direct serotonin agonism or inhibit serotonin reuptake. In spite of this, it has been implicated as a causative agent of serotonin syndrome. We highlight two cases of single-agent bupropion overdose that subsequently met the diagnosis of serotonin syndrome by the Hunter criteria, despite the absence of direct serotonergic agents. CASE 1: A 14-year-old boy intentionally ingested an estimated 30 bupropion 75-mg immediate-release tablets. He presented in status epilepticus, was intubated, and was placed on midazolam and fentanyl infusions. He developed tremor, ankle clonus, and agitation. He was administered cyproheptadine for presumed serotonin syndrome with temporal improvement in his symptoms. CASE 2: A 19-year-old woman intentionally ingested an estimated 53 bupropion 150-mg extended-release tablets. She had a seizure and required sedation and intubation. During her course, she developed hyperthermia, inducible clonus, and hyperreflexia. She was treated with cyproheptadine without temporal improvement of symptoms but improved the following day. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Although bupropion is not known to be directly serotonergic, it has been implicated as the single causative agent after overdose. This may be due to an indirect increase in activity of serotonergic cells. In these cases, bupropion overdose resulted in a clinical presentation consistent with serotonin syndrome, with the first having a temporal improvement after treatment with cyproheptadine. Physicians need to be aware of the potential serotonergic activity of bupropion for accurate assessment and treatment of this dangerous condition.

摘要

安非他酮没有直接的血清素激动作用,也不会抑制血清素再摄取。尽管如此,它还是被认为是血清素综合征的一个致病因素。我们强调了两例单药安非他酮过量的病例,尽管没有直接的血清素能药物,但根据亨特标准,这些病例随后被诊断为血清素综合征。

病例 1:一名 14 岁男孩故意摄入了约 30 片安非他酮 75mg 速释片。他出现癫痫持续状态,被插管,并给予咪达唑仑和芬太尼输注。他出现震颤、踝阵挛和激越。他被给予赛庚啶治疗,认为是血清素综合征,症状暂时改善。

病例 2:一名 19 岁女子故意摄入了约 53 片安非他酮 150mg 缓释片。她癫痫发作,需要镇静和插管。在她的病程中,她出现了高热、诱导性阵挛和反射亢进。她接受了赛庚啶治疗,但症状没有暂时改善,但第二天有所改善。

为什么急诊医生应该知道这一点?:尽管安非他酮不是直接的血清素能药物,但它被认为是过量后的单一致病因素。这可能是由于血清素能细胞的间接活性增加。在这些情况下,安非他酮过量导致的临床表现与血清素综合征一致,其中第一个病例在接受赛庚啶治疗后症状暂时改善。医生需要意识到安非他酮的潜在血清素活性,以便对这种危险情况进行准确评估和治疗。

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