Dvir Yael, Smallwood Patrick
Department of Psychiatry, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Gen Hosp Psychiatry. 2008 May-Jun;30(3):284-7. doi: 10.1016/j.genhosppsych.2007.09.007.
Serotonin syndrome is a potentially life-threatening adverse drug reaction caused by excessive serotonergic agonism in central and peripheral nervous system serotonergic receptors (Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-1120). Symptoms are characterized by a triad of neuron-excitatory features, which include (a) neuromuscular hyperactivity -- tremor, clonus, myoclonus, hyperreflexia and, in advanced stages, pyramidal rigidity; (b) autonomic hyperactivity -- diaphoresis, fever, tachycardia and tachypnea; (c) altered mental status -- agitation, excitement and, in advanced stages, confusion (Gillman PK. Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. Br J Anaesth 2005;95:434-441). It arises when pharmacological agents increase serotonin neurotransmission at postsynaptic 5-hydroxytryptamine 1A and 5-hydroxytryptamine 2A receptors through increased serotonin synthesis, decreased serotonin metabolism, increased serotonin release, inhibition of serotonin reuptake or direct agonism of the serotonin receptors (Houlihan D. Serotonin syndrome resulting from coadministration of tramodol, venlafaxine, and mirtazapine. Ann Pharmacother 2004;38:411-413). The etiology is often the result of therapeutic drug use, intentional overdosing of serotonergic agents or complex interactions between drugs that directly or indirectly modulate the serotonin system (Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-1120). Due to the increasing availability of agents with serotonergic activity, physicians need to more aware of serotonin syndrome. The following case highlights the complex nature in which serotonin syndrome can arise, as well as the proper recognition and treatment of a potentially life-threatening yet easily avoidable condition.
血清素综合征是一种潜在的危及生命的药物不良反应,由中枢和外周神经系统血清素能受体的血清素能激动作用过度引起(博耶EW,香农M。血清素综合征。《新英格兰医学杂志》2005年;352:1112 - 1120)。症状的特征是具有三联征的神经元兴奋特征,包括:(a)神经肌肉活动亢进——震颤、阵挛、肌阵挛、反射亢进,在晚期出现锥体束征强直;(b)自主神经活动亢进——多汗、发热、心动过速和呼吸急促;(c)精神状态改变——激动、兴奋,在晚期出现意识模糊(吉尔曼PK。单胺氧化酶抑制剂、阿片类镇痛药与血清素毒性。《英国麻醉学杂志》2005年;95:434 - 441)。当药物通过增加血清素合成、减少血清素代谢、增加血清素释放、抑制血清素再摄取或直接激动血清素受体,从而增加突触后5 - 羟色胺1A和5 - 羟色胺2A受体处的血清素神经传递时,就会引发血清素综合征(侯利汉D。曲马多、文拉法辛和米氮平合用导致的血清素综合征。《药物治疗学年鉴》2004年;38:411 - 413)。病因通常是治疗性药物使用、血清素能药物故意过量服用或直接或间接调节血清素系统的药物之间复杂的相互作用的结果(博耶EW,香农M。血清素综合征。《新英格兰医学杂志》2005年;352:1112 - 1120)。由于具有血清素能活性的药物越来越容易获得,医生需要更加了解血清素综合征。以下病例突出了血清素综合征可能出现的复杂性质,以及对一种潜在危及生命但易于避免的病症的正确识别和治疗。