摘要
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 detect the expression of platelet surface glycoproteins GP Ⅱ b/Ⅲa and CD62P and to explore their effect in the pathogenesis of HSP. Methods 29 HSP patients and 27 control cases were enrolled in this study. HSP patients were devided into nephritis group and non-nephritis group. The expression of GP Ⅱ b/Ⅲa and CD62P in platelets were examined by flow cytometry. Results Compared to the control [ （20.67±7.80）% ], the expression of GPⅡ b/Ⅲa in HSP group [（：26.30±10.25）% ] was significantly increased （P 〈 0.05）, and the level of nephrits group was significantly higher than that of non-nephrits group （P 〈 0.05）, while the expression of CD62P in HSP group was not significantly different from that in control （P=0.43）. Conclusions The expression of GP IⅡ b/Ⅲa in HSP group significantly increased, especially in those with renal involvement. The aberrant activation of platelets may play a role in the pathogenesis of HSP and HSPN.
出处
《北京医学》
CAS
2008年第11期661-663,共3页
Beijing Medical Journal
