Department of Rheumatology, Mater Misericordiae University Hospital, RCSI, Dublin, Ireland.
Rheumatology (Oxford). 2010 Feb;49(2):240-5. doi: 10.1093/rheumatology/kep377. Epub 2009 Dec 4.
To assess the influence of disease activity on platelet function in patients with inflammatory arthritis (IA).
Ninety-six patients with an established diagnosis of IA (RA, PsA, seronegative SpA) were recruited. Patients with a history of cardiovascular disease (CVD), diabetes mellitus or receiving anti-platelet therapy were excluded. Demographic data, traditional CVD risk factors and medication use were recorded. Patients were characterized as active disease (n = 38) or control disease (n = 58) groups, respectively, based on internationally validated measures of disease activity [comprising serological markers (ESR, CRP, fibrinogen), patient measures (visual analogue scale of disease activity), evaluator global assessment and the 28-joint disease activity score]. Platelet function was assessed using a novel assay of platelet reactivity. Platelet aggregation to multiple concentrations of arachidonic acid, collagen, epinephrine, thrombin receptor activating peptide and adenosine diphosphate (ADP) were measured simultaneously using a modification of light transmission aggregometry.
The two groups (active vs control) were similar in terms of demographics and CVD risk factors. Anti-TNF-alpha therapy use was higher in the control group (P = 0.004), whereas NSAID use was higher in the active group (P = 0.001). There was a significant difference between the two groups in platelet response to ADP (P < 0.001). Platelet aggregation, in response to submaximal concentrations of ADP, was increased in the active disease group compared with the control group. There was no difference in platelet reactivity between the groups in response to any of the other agonists.
Patients with active IA demonstrate enhanced platelet reactivity, unique to the ADP pathway. This potential pro-thrombotic bias may contribute to their increased cardiovascular risk.
评估炎症性关节炎（IA）患者的疾病活动度对血小板功能的影响。
共招募了 96 例确诊为 IA（类风湿关节炎、银屑病关节炎、血清阴性脊柱关节炎）的患者。排除有心血管疾病（CVD）、糖尿病或正在接受抗血小板治疗病史的患者。记录人口统计学数据、传统 CVD 危险因素和用药情况。根据国际公认的疾病活动度评估标准[包括血清学标志物（ESR、CRP、纤维蛋白原）、患者评估（疾病活动视觉模拟评分）、评估者整体评估和 28 关节疾病活动度评分]，将患者分为活动期疾病（n=38）和对照组（n=58）。使用血小板反应性的新型检测方法评估血小板功能。使用改良的透光比浊法同时测量血小板对多种浓度的花生四烯酸、胶原、肾上腺素、血栓素受体激活肽和二磷酸腺苷（ADP）的聚集反应。
两组（活动期 vs 对照组）在人口统计学和 CVD 危险因素方面相似。对照组接受 TNF-α 拮抗剂治疗的比例较高（P=0.004），而活动期组接受 NSAIDs 治疗的比例较高（P=0.001）。两组间 ADP 诱导的血小板反应存在显著差异（P<0.001）。与对照组相比，活动期疾病组对 ADP 的血小板聚集反应显著增加（P<0.001）。两组在其他激动剂的血小板反应性方面无差异。
活动期 IA 患者表现出独特的 ADP 途径的血小板反应性增强。这种潜在的促血栓形成倾向可能导致其心血管风险增加。
