醫(yī)學(xué)論文范文:過敏性紫癜患兒GPⅡb/Ⅲa、P�策x擇素及vWF檢測的意義

醫(yī)學(xué)論文范文:過敏性紫癜患兒GPⅡb/Ⅲa、P�策x擇素及vWF檢測的意義

【摘要】 目的 檢測過敏性紫癜(HSP)患兒全血中血小板膜糖蛋白GPⅡb/Ⅲa(CD41a/CD61)、P�策x擇素(CD62P)及血漿中血管性假血友病因子(vWF)的表達水平，探討它們在HSP發(fā)病機制中的作用。方法 應(yīng)用流式細胞儀和酶聯(lián)免疫吸附試驗(ELISA)分別檢測HSP患兒(急性期44例，緩解期40例)及健康對照兒童(18例)空腹血CD41a/CD61、CD62P及vWF水平。結(jié)果 HSP患兒急性期CD41a/CD61、CD62P、vWF水平明顯高于緩解期和對照組(P均<0.01);腎受累組CD41a/CD61、CD62P、vWF水平高于非腎受累組(P<0.01)。結(jié)論 血小板的活化及血管內(nèi)皮的損傷在HSP的發(fā)病機制中起著重要作用，CD41a/CD61、CD62P、vWF水平的測定有助于了解HSP患兒早期的凝血異常，為抗凝治療提供依據(jù)。

【關(guān)鍵詞】 紫癜，過敏性;血小板膜糖蛋白類;P�策x擇素;血管性假血友病因子;兒童

ZHANG Hong�瞲ia1, LIU Xue�瞞ei2, LIU Fang�瞖1, LIN Ai�瞱ei2，　DUAN Chun�瞙ong2，　YANG Xiao�瞞ei2

(1. Department of Pediatrics, Second Hospital of Shandong University, Jinan 250033, China;

2. Qilu Children′s Hospital of Shandong University， Jinan 250022, China)

To investigate the role of platelet membrane glycoproteinⅡb/Ⅲa, P�瞫electin and von Willebrane Factor in children with Henoch�睸chonlein purpura (HSP), and to investigate the pathological role of them in HSP. Methods The concentrations of CD41a/CD61 and CD��62P were determined by flow cytometry and the level of vWF by an enzyme�瞝inked immunosorbent assay(ELISA) method in 44 patients with acute HSP, 40 patients in the recovery phase and 18 healthy controls. Results The plasma levels of CD41a/CD61, CD��62P and vWF in the acute phase were significantly higher than those in the recovery phase, were higher than those in healthy controls(P<0.01), and also were higher in the renal damage group than in the non�瞨enal damage group(P<0.01). Conclusion Activation of platelet and damage of vascular endothelium play important roles in the pathological mechanism of HSP. Levels of CD41a/CD61, CD��62P and vWF are helpful in finding the disturbance of blood coagulation，and provide a basis for anti�瞔oagulant treatments醫(yī).學(xué)全.在.線網(wǎng)站zxtf.net.cn.

Key words: Purpura, Henoch�睸chonlein; Platelet membrane glycoproteins; P�瞫electin; von Willebrane factor; Child 過敏性紫癜(henoch�瞫chonlein purpura，HSP)是兒童最常見的血管炎之一。有文獻報道[1]，約20～80%的HSP患兒并發(fā)腎臟損害，導(dǎo)致過敏性紫癜性腎炎(henoch�瞫chonlein purpura nephritis, HSPN)。HSP的發(fā)病機制尚未完全明了，近年來許多研究[2��3]認為，HSP患兒血小板的聚集功能增強，存在血液的 高凝狀態(tài)甚至有微血栓形成。血小板膜糖蛋白(platelet membrane glycoprotein，GP)Ⅱb/Ⅲa是血小板聚集的關(guān)鍵因素，在出血與凝血過程中起著重要作用。P�策x擇素，即CD62P，具有介導(dǎo)活化血小板、血管內(nèi)皮細胞與白細胞粘附的功能[4]，為血小板活化的特異性標(biāo)志。GPⅡb/Ⅲa與P�策x擇素在血循環(huán)中的變化反映了血液凝血狀態(tài)的早期改變。血管性假血友病因子(von willebrane factor, vWF)是血管內(nèi)皮細胞損傷的標(biāo)記物，血管內(nèi)皮細胞受損時可促進血小板的粘附、聚集。本研究旨在觀察HSP患兒GPⅡb/Ⅲa(CD41a/CD61)、P�策x擇素(CD62P)及vWF的變化，探討HSP發(fā)生時凝血狀態(tài)的改變、內(nèi)皮細胞損害與腎臟損害的關(guān)系。

[1] [2] [3] 下一頁