Citalopram is a more potent platelet function inhibitor than paroxetine in a case-control study

摘要

Serotonin is a major component of platelet dense granules [1]. It mediates vasoconstriction and supports platelet activation via platelet 5-hydroxytryptamine receptors [2,3]. Platelets take up serotonin via serotonin transporters in their membranes. This uptake is inhibited by selective serotonin reuptake inhibitors (SSRIs) [4], which thereby affect platelet function [4-6]. Some studies have shown that SSRIs reduce the risk of cardiovascular disease events [7-10], although there is still some controversy on the subject [11,12]. In line with this, numerous studies have shown an increased bleeding risk with SSRI use, although not all studies could confirm this (for an overview of the literature, see [13]). Studies on the influence of SSRIs on platelet function have been performed mainly ex vivo [14-16] or in patient groups treated with with different SSRIs, but analyzed together [5,6,17]; different types of SSRI have been reported to differ in therapeutic efficacy [18]. We compared the effects of paroxetine and citalopram on platelet responsiveness in a case-control study of 13 patients with a platelet function analyzer, and a platelet responsiveness assay to investigate the hypothesis that these SSRIs have different effects on platelet function.