Bou Khalil Rami, Richa Sami
Hotel Dieu de France Hospital, Beirut, Lebanon.
Clin Neuropharmacol. 2011 Nov-Dec;34(6):248-55. doi: 10.1097/WNF.0b013e31823429a7.
Because many patients with mental illness take more than one psychotropic drug, an understanding of the effects of every class of these drugs is very important to manage any thyroid abnormalities that can happen with these patients.
A systematic review of all the published literature was made via Medline. Keywords used for the search were "thyroid side effects" in association with one of the following: "antipsychotics," "antidepressants," "lithium," "anticonvulsants," "benzodiazepines," "anticholinergics," "antihistaminergics," "cholinesterase inhibitors," "stimulants," "methadone," and "naltrexone."
Phenothiazines, which are antipsychotics, mainly alter iodine capture, complex and deactivate it, as well as decrease thyroid-stimulating hormone's (TSH's) response to thyroid-releasing hormone (TRH). Nonphenothiazines, typical antipsychotics, can induce the formation of thyroid autoantibodies and can elevate TSH levels. Atypical antipsychotics may decrease TRH-stimulated TSH. Tricyclic antidepressant drugs complex with iodine and thyroid peroxidase and deactivate them, induce deiodinase activity and interfere with the hypothalamo-pituitary-thyroid (HPT) axis by decreasing TSH response to TRH. The main effect with other antidepressant drugs is a decrease in circulating thyroid hormone levels. Lithium inhibits thyroid hormone release and increases TRH-stimulated TSH, inducing goiter, clinical and subclinical hypothyroidism, and hyperthyroidism. Carbamazepine mainly reversibly decreases serum thyroid hormone levels. Other psychotropic drugs such as valproic acid, benzodiazepines, opiates, anticholinergic and antihistaminergic drugs, and stimulants have minor interferences with thyroid functions.
Patients receiving lithium, phenothiazines, and tricyclic antidepressants TCA should be closely monitored for the development of thyroid function abnormalities. Only patients at risk for developing thyroid function abnormalities should be monitored when they receive typical and/or atypical antipsychotic drugs, nontricyclic antidepressant drugs, and carbamazepine. No specific recommendations are proposed as toward thyroid function monitoring for patients receiving any other psychopharmacologic drug.
由于许多精神疾病患者服用不止一种精神药物，了解每类药物的作用对于处理这些患者可能出现的任何甲状腺异常非常重要。
通过医学数据库（Medline）对所有已发表的文献进行系统综述。用于检索的关键词是“甲状腺副作用”，并与以下之一相关联：“抗精神病药”、“抗抑郁药”、“锂盐”、“抗惊厥药”、“苯二氮䓬类药物”、“抗胆碱能药物”、“抗组胺能药物”、“胆碱酯酶抑制剂”、“兴奋剂”、“美沙酮”和“纳曲酮”。
作为抗精神病药的吩噻嗪类主要改变碘的摄取，使其络合并失活，还会降低促甲状腺激素（TSH）对促甲状腺激素释放激素（TRH）的反应。非吩噻嗪类典型抗精神病药可诱导甲状腺自身抗体的形成并可升高TSH水平。非典型抗精神病药可能会降低TRH刺激的TSH。三环类抗抑郁药与碘和甲状腺过氧化物酶络合并使其失活，诱导脱碘酶活性，并通过降低TSH对TRH的反应来干扰下丘脑 - 垂体 - 甲状腺（HPT）轴。其他抗抑郁药的主要作用是循环甲状腺激素水平降低。锂盐抑制甲状腺激素释放并增加TRH刺激的TSH，导致甲状腺肿大、临床和亚临床甲状腺功能减退以及甲状腺功能亢进。卡马西平主要可逆性降低血清甲状腺激素水平。其他精神药物，如丙戊酸、苯二氮䓬类药物、阿片类药物、抗胆碱能和抗组胺能药物以及兴奋剂对甲状腺功能有轻微干扰。
接受锂盐、吩噻嗪类和三环类抗抑郁药（TCA）治疗的患者应密切监测甲状腺功能异常的发生。当患者接受典型和/或非典型抗精神病药、非三环类抗抑郁药和卡马西平时，仅应监测有发生甲状腺功能异常风险的患者。对于接受任何其他精神药物治疗的患者，未提出关于甲状腺功能监测的具体建议。
