The Use of Antidepressants and the Risk of Idiopathic Pulmonary Arterial Hypertension
The Use of Antidepressants and the Risk of Idiopathic Pulmonary Arterial Hypertension
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DOI：
10.1016/j.cjca.2014.09.031
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发表时间：
2014-12-01
影响因子：
6.2
通讯作者：
Suissa, Samy
中科院分区：
文献类型：
--
作者：
Fox, Benjamin D.;Azoulay, Laurent;Suissa, Samy
背景：血清素与特发性肺动脉高压（IPAH）的发展有关。包括抗抑郁药在内的调节血清素通路的药物与IPAH的发病率有关，但关于其作用方向的报道相互矛盾。我们的目的是确定抗抑郁药物暴露是否与IPAH的发病率有关。方法：在1988年1月1日至2011年9月30日期间，使用英国临床实践研究数据链和医院事件统计库进行巢式病例对照研究。确定IPAH事件病例，并将其与病例风险设置中的所有对照进行匹配，包括年龄、性别、一般做法和注册日期。在诊断前18个月的滞后期，估计使用抗抑郁药对IPAH风险的比率比（rr）和95%置信区间（ci）。结果：共发现IPAH病例195例（发病率3.84/百万/年）。使用任何抗抑郁药与IPAH风险增加67%相关（RR, 1.67; 95% CI, 1.17-2.37）。IPAH的发生率在抗抑郁药类别中相似，无论是选择性血清素再摄取抑制剂（SSRIs） （RR, 1.67; 95% CI, 1.09-2.57）还是非ssri抗抑郁药（RR, 1.66; 95% CI, 1.07-2.59）。在敏感性和探索性分析中，没有观察到不同延迟时间、血清素转运体亲和力或暴露时间对风险的影响。结论：抗抑郁药的使用与IPAH的风险显著增加相关。然而，这种风险在所有抗抑郁药中都是一致的，而且没有剂量-反应关系，这表明存在非因果关系。
Background: Serotonin has been implicated in the development of idiopathic pulmonary arterial hypertension (IPAH). Drugs modulating serotonin pathways, including antidepressants, have been associated with the incidence of IPAH, with conflicting reports as to the direction of the effect. We aimed to determine whether antidepressant exposure is associated with the incidence of IPAH.Methods: A nested case-control study was conducted using the United Kingdom Clinical Practice Research Datalink and the Hospital Episodes Statistics repository between January 1, 1988 and September 30, 2011. Incident cases of IPAH were identified and matched to all controls in the case's risk set on age, sex, general practice, and date of registration with the practice. Rate ratios (RRs) and 95% confidence intervals (CIs) were estimated for the use of antidepressants on the risk of IPAH, with an 18-month lag period before the diagnosis.Results: One hundred ninety-five IPAH cases were identified (incidence 3.84/million per year). Use of any antidepressant was associated with a 67% increased risk of IPAH (RR, 1.67; 95% CI, 1.17-2.37). The rate of IPAH was similar across antidepressant classes, whether with selective serotonin reuptake inhibitors (SSRIs) (RR, 1.67; 95% CI, 1.09-2.57) or non-SSRI antidepressants (RR, 1.66; 95% CI, 1.07-2.59). In sensitivity and exploratory analyses, no change in risk was observed with different lag times, serotonin transporter affinities, or durations of exposure.Conclusions: The use of antidepressants was associated with a significantly increased risk of IPAH. However, the consistency of this risk across all antidepressants and absence of a dose-response relationship suggests a noncausal association.