Platelet reactivity in depressed patients treated with paroxetine -: Preliminary findings
Platelet reactivity in depressed patients treated with paroxetine -: Preliminary findings
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DOI：
10.1001/archpsyc.57.9.875
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发表时间：
2000-09-01
影响因子：
--
通讯作者：
Nemeroff, CB
中科院分区：
文献类型：
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作者：
Musselman, DL;Marzec, UM;Nemeroff, CB
背景：先前认为血小板反应性的改变是抑郁症患者更容易患缺血性心脏病（IHD）的基础。本研究旨在确定抗抑郁治疗后与重度抑郁症相关的血小板反应性增加是否会降低。 方法：招募了诊断为 DSM-IV 重度抑郁症的患者 (n= 15)（平均年龄，37+/-7 岁；范围，23-48 岁）和 12 名正常对照受试者（平均年龄，36+/-7；范围，23-48 岁）。对照组或抑郁组均没有 IHD 的证据； 15 名抑郁症患者中有 10 名有 1 种或多种传统 IHD 危险因素。在基础条件下卧床过夜后以及轻度运动挑战后，测量对照组和患者的体内血小板活化、分泌和剂量反应聚集。用选择性5-羟色胺再摄取抑制剂帕罗西汀（20 mg/d）进行6周的开放治疗后，抑郁症患者重新入院，并重复首次普通临床研究中心入院的程序。 结果：与对照组相比，通过单克隆抗体抗配体诱导的结合位点和GA6的血小板结合增加以及基础条件下血小板因子4的血浆浓度增加检测到，抑郁症组表现出更大的促凝血活性。帕罗西汀治疗后，抑郁症患者的所有3个参数均显着降低。结论：血小板活化正常化与帕罗西汀治疗抑郁症患者相关。由于该研究设计无法确定帕罗西汀对血小板功能的影响是否是由药物或安慰剂的直接作用引起，或者是由于抑郁症的恢复，因此包含安慰剂和/或心理治疗组的研究可能会解决这个问题。
Background: Alterations in platelet reactivity have been previously posited to underlie the increased vulnerability of patients with depression to ischemic heart disease (IHD). The present study sought to determine whether the increased platelet reactivity associated with major depression is reduced after antidepressant treatment.Methods: Patients diagnosed as having DSM-IV-major depression (n= 15) (mean age, 37+/-7 years; range, 23-48 years) and 12 normal comparison subjects (mean age, 36+/-7; range, 23-48 years) were recruited. None of the controls or depressed group had evidence of IHD; 10 of 15 patients who were depressed had 1 or more traditional IHD risk factors. In vivo platelet activation, secretion, and dose-response aggregation of the controls and patients was measured after overnight bedrest under basal conditions, and after a mild exercise challenge. After 6 weeks of open-label treatment with the selective serotonin reuptake inhibitor paroxetine (20 mg/d), the patients with depression were readmitted and procedures of the first General Clinical Research Center admission repeated.Results: In comparison with the control group, the depressed group exhibited greater procoagulant activity as detected by increased platelet binding of the monoclonal antibodies anti-ligand-induced binding site and GA6, and increased plasma concentrations of platelet factor 4 under basal conditions. After paroxetine treatment, the patients with depression exhibited significant reductions in all 3 parameters.Conclusions: Normalization of platelet activation is associated with paroxetine treatment of patients with depression. Because this study design did not allow for the determination of whether this effect of paroxetine on platelet function is caused by a direct effect of the drug or placebo or, alternatively, because of recovery from depression, studies containing a placebo and/or psychotherapy treatment arm may resolve this issue.