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目的了解过敏性紫癜(HSP)患儿血小板表面黏附分子CD62P、GPⅡb/Ⅲa的表达情况,探讨其在HSP发病机制中的作用。方法选择2006年3~11月我院收治的29例HSP患儿,选择同期27例外科非感染性疾病患儿作为对照,应用流式细胞仪检测外周血小板黏附分子CD62P、GPⅡb/Ⅲa的水平。结果与对照组比较,HSP组血小板GPⅡb/Ⅲa表达水平为(26.30±10.25)%,比对照组的(20.67±7.80)%明显增高(P﹤0.05),且HSP肾炎者[(29.43±10.10)%]明显高于HSP非肾炎者[(21.18±8.72)%,P﹤0.05];HSP组与对照组CD62P分子的表达水平分别为(1.33±0.40)%和(1.24±0.41)%,两组比较无显著性差异(P=0.43)。结论HSP患儿血小板GPⅡb/Ⅲa表达增加,尤以合并肾脏损害时明显。血小板的异常活化参与了HSP、过敏性紫癜肾炎(HSPN)发病的病理生理过程。
Objective To investigate the expression of platelet surface adhesion molecule CD62P and GPⅡb / Ⅲa in children with Henoch-Schonlein Purpura (HSP) and to explore its role in the pathogenesis of HSP. Methods Totally 27 children with HSP who were treated in our hospital from March to November 2006 were selected as the control. Twenty-seven children with surgical noninfectious disease were selected as controls. The levels of CD62P and GPⅡb / Ⅲa in peripheral platelets were detected by flow cytometry. Results Compared with the control group, the GPⅡb / Ⅲa expression level in HSP group was (26.30 ± 10.25)%, significantly higher than that in control group (20.67 ± 7.80)%, and HSP nephritis group was (29.43 ± 10.10) (21.18 ± 8.72)%, P <0.05]. The expression levels of CD62P in HSP group and control group were (1.33 ± 0.40)% and (1.24 ± 0.41)%, respectively There was no significant difference (P = 0.43). Conclusion The expression of platelet GPⅡb / Ⅲa in children with HSP increased, especially when combined with renal damage. Abnormal platelet activation is involved in the pathogenesis of HSP and HSPN.