Department of Clinical Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Department of Psychiatry and Psychotherapy, School of Medicine, Technical University of Munich, Munich, Germany.
Schizophr Bull. 2021 Apr 29;47(3):672-681. doi: 10.1093/schbul/sbaa163.
An association between antipsychotic drugs and pneumonia has been demonstrated in several studies; however, the risk for pneumonia caused by specific antipsychotics has not been extensively studied. The underlying mechanism is still unknown, and several receptor mechanisms have been proposed. Therefore, using a combined pharmacovigilance-pharmacodynamic approach, we aimed to investigate safety signals of US Food and Drug Administration (FDA)-approved antipsychotics for reporting pneumonia and the potential receptor mechanisms involved. A disproportionality analysis was performed to detect a signal for reporting "infective-pneumonia" and "pneumonia-aspiration" and antipsychotics using reports submitted between 2004 and 2019 to the FDA adverse events spontaneous reporting system (FAERS) database. Disproportionality was estimated using the crude and the adjusted reporting odds ratio (aROR) and its 95% confidence interval (CI) in a multivariable logistic regression. Linear regressions investigated the relationship between aROR and receptor occupancy, which was estimated using in vitro receptor-binding profiles. Safety signals for reporting infective-pneumonia were identified for clozapine (LL = 95% 3.4, n = 546 [aROR: 4.8]) as well as olanzapine (LL = 95% 1.5, n = 250 [aROR: 2.1]) compared with haloperidol, while aRORs were associated with higher occupancies of muscarinic receptors (beta = .125, P-value = .016), yet other anti-muscarinic drugs were not included as potential confounders. No safety signals for reporting pneumonia-aspiration were detected for individual antipsychotics. Multiple antipsychotic use was associated with both reporting infective-pneumonia (LL 95%: 1.1, n = 369 [aROR:1.2]) and pneumonia-aspiration (LL 95%: 1.7, n = 194 [aROR: 2.0]). Considering the limitations of disproportionality analysis, further pharmacovigilance data and clinical causality assessment are needed to validate this safety signal.
抗精神病药物与肺炎之间的关联已在多项研究中得到证实;然而,特定抗精神病药物引起肺炎的风险尚未得到广泛研究。其潜在机制尚不清楚,并且已经提出了几种受体机制。因此,我们使用药物警戒-药效学联合方法,旨在研究美国食品和药物管理局 (FDA) 批准的抗精神病药物报告肺炎的安全信号以及涉及的潜在受体机制。进行了不均衡性分析,以检测报告“感染性肺炎”和“肺炎吸入”以及 2004 年至 2019 年期间向 FDA 不良事件自发报告系统 (FAERS) 数据库提交的抗精神病药物的信号。使用多变量逻辑回归,使用未调整的报告比值比 (aROR) 和 95%置信区间 (CI) 来估计比例失调。线性回归调查了 aROR 与受体占有率之间的关系,该占有率使用体外受体结合谱来估计。与氟哌啶醇相比,氯氮平 (LL = 95% 3.4,n = 546 [aROR:4.8]) 以及奥氮平 (LL = 95% 1.5,n = 250 [aROR:2.1]) 报告感染性肺炎的信号被确定为安全信号,而 aROR 与毒蕈碱受体的更高占有率相关 (β =.125,P 值 =.016),然而,其他抗毒蕈碱药物并未被包括为潜在的混杂因素。未发现个别抗精神病药物报告肺炎吸入的安全信号。多种抗精神病药物的使用与报告感染性肺炎 (LL 95%:1.1,n = 369 [aROR:1.2]) 和肺炎吸入 (LL 95%:1.7,n = 194 [aROR:2.0]) 均相关。考虑到不均衡性分析的局限性,需要进一步的药物警戒数据和临床因果关系评估来验证这一安全信号。