Circulating Platelet-Neutrophil Aggregates Play a Significant Role in Kawasaki Disease
Circulating Platelet-Neutrophil Aggregates Play a Significant Role in Kawasaki Disease
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DOI：
10.1253/circj.cj-14-1323
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发表时间：
2015-06-01
影响因子：
3.3
通讯作者：
Kawano, Yoshifumi
中科院分区：
文献类型：
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作者：
Ueno, Kentaro;Nomura, Yuichi;Kawano, Yoshifumi
背景资料：循环血小板-中性粒细胞聚集体在放大急性炎症中起着至关重要的作用，并可能促进涉及血管损伤的不良反应。本研究的目的是评估血小板-中性粒细胞聚集体在川崎（KD）中的作用。方法和结果：40例KD患者（30例静脉注射免疫球蛋白[IVIG]应答者和10例IVIG无应答者），7例细菌感染发热患者和9例正常志愿者进行了分析。33例患儿接受IVIG治疗，7例患儿接受IVIG加泼尼松龙治疗。我们评估了血小板-中性粒细胞聚集率，并测量了血小板因子4（PF 4）和β-血小板球蛋白（β-TG）水平。KD患者血小板-中性粒细胞聚集率明显高于细菌感染组和正常对照组。血小板-中性粒细胞聚集率在冠状动脉异常（CAA）组明显高于无CAA组，且与KD组PF 4和β-TG水平相关。比较时程分析，血小板-中性粒细胞聚集率显着下降，在IVIG加泼尼松龙治疗的患者比在IVIG单独治疗的患者。结论：研究结果表明，血小板-中性粒细胞聚集显着存在于较高的利率，并与CAA在KD的病理发展密切相关。对KD急性期患者进行额外的泼尼松龙治疗可以抑制血小板-中性粒细胞聚集体，表明血小板-中性粒细胞聚集体可以抑制放大的相互血管炎症激活。
Background: Circulating platelet-neutrophil aggregates play a crucial role in amplifying acute inflammation and could promote adverse effects involving vascular injury. The aim of this study was to evaluate the role of platelet-neutrophil aggregates in Kawasaki disease (KD).Methods and Results: Forty patients with KD (30 intravenous immunoglobulin [IVIG] responders and 10 IVIG non-responders), 7 febrile patients with bacterial infections, and 9 normal volunteers were analyzed. Thirty-three patients with KD were treated with IVIG, and 7 were treated with IVIG plus prednisolone. We evaluated the rate of platelet-neutrophil aggregates and measured the platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) levels. The rate of platelet-neutrophil aggregates was significantly higher in patients with KD than those with bacterial infection and normal volunteers. The rate of platelet-neutrophil aggregates was significantly higher in patients with coronary artery abnormalities (CAA) than in those without CAA, and was correlated with PF4 and beta-TG levels in patients with KD. Comparing time-course analysis, the rate of platelet-neutrophil aggregates was significantly decreased in patients treated with IVIG plus prednisolone than in those treated with IVIG alone.Conclusions: The findings demonstrate that platelet-neutrophil aggregates are significantly present in higher rates and are closely related to pathological developments of CAA in KD. Additional prednisolone treatment for patients in the acute phase of KD could suppress platelet-neutrophil aggregates, indicating that platelet-neutrophil aggregates would inhibit amplified reciprocal vascular inflammatory activation.