Faculty of Natural Sciences and Mathematics, "Ss. Cyril and Methodius" University, Arhimedova 3, P.O. Box 162, 1000 Skopje, Macedonia.
Institute of Transfusion Medicine, Department for Hemostasis and Thrombosis, Mother Teresa 17, 1000 Skopje, Macedonia.
Thromb Res. 2018 May;165:24-32. doi: 10.1016/j.thromres.2018.03.006. Epub 2018 Mar 10.
Adverse effects with bleeding disorders are often associated with the administration of SSRI in depression, although the exact mechanisms remain contradicting. This study is aimed at detecting and exploring the mechanisms of SSRI-induced changes in platelet reactivity in non-responding patients with Recurrent Depressive Disorder (RDD) and life-long exposure to antidepressants.
Thirty-one patients and thirty-one healthy controls were included in the study. A comprehensive approach which includes evaluation of peripheral markers and microscopic analyses of platelet morphology changes has been used.
RDD SSRI patients have shown blunted aggregatory responses towards collagen and epinephrine. Evident differences in the microscopic evaluation of platelet morphology were observed between the groups, with inherent absence of micro-aggregates and platelet shape changes within the patients; after quantification, the sensitivity and specificity of this method were assessed as high. The abnormalities were found in association with lower platelet serotonin content and high fluctuations of free plasma serotonin levels. Changes in the levels of CRP, fibrinogen and nitric oxide were not observed. Macroplatelets were also detected within RDD SSRI patients via increased MPV, PDW and P-LCR, which were associated with discoid shape and without procoagulant activity.
The microscopic evaluation might be useful as a simple method for detection of SSRI-reduced platelet function for research purposes or systematic correlations with other biochemical parameters. The mechanisms involved in SSRI-reduced platelet function in non-responding RDD patients are complex, including combined effects of lower platelet serotonin content, high fluctuations in plasma serotonin concentration and abnormal α-AR function.
尽管确切的机制仍存在争议,但抗抑郁药治疗中出现的出血性疾病不良反应通常与 SSRIs 的使用有关。本研究旨在检测和探索复发性抑郁障碍(RDD)患者对 SSRI 无反应且终生暴露于抗抑郁药的情况下,SSRIs 诱导的血小板反应性变化的机制。
本研究纳入了 31 名患者和 31 名健康对照者。我们采用了一种综合方法,包括外周标志物的评估和血小板形态变化的微观分析。
RDD SSRI 患者对胶原和肾上腺素的聚集反应明显减弱。两组之间观察到血小板形态微观评估的明显差异,患者体内固有缺乏微聚集物和血小板形态变化;经定量后,评估了该方法的灵敏度和特异性,结果显示均较高。这些异常与血小板 5-羟色胺含量降低和游离血浆 5-羟色胺水平波动高有关。未观察到 CRP、纤维蛋白原和一氧化氮水平的变化。通过增加 MPV、PDW 和 P-LCR,也在 RDD SSRI 患者中检测到巨血小板,其与盘状形状和无促凝活性有关。
微观评估可能是一种有用的方法,可用于研究目的检测 SSRI 降低的血小板功能,或与其他生化参数进行系统相关性分析。非反应性 RDD 患者中 SSRI 降低血小板功能的机制较为复杂,包括血小板 5-羟色胺含量降低、血浆 5-羟色胺浓度波动高以及 α-AR 功能异常的综合影响。