醫(yī)學(xué)論文范文:過(guò)敏性紫癜患兒GPⅡb/Ⅲa、P選擇素及vWF檢測(cè)的意義
【摘要】 目的 檢測(cè)過(guò)敏性紫癜(HSP)患兒全血中血小板膜糖蛋白GPⅡb/Ⅲa(CD41a/CD61)、P選擇素(CD62P)及血漿中血管性假血友病因子(vWF)的表達(dá)水平,探討它們?cè)贖SP發(fā)病機(jī)制中的作用。方法 應(yīng)用流式細(xì)胞儀和酶聯(lián)免疫吸附試驗(yàn)(ELISA)分別檢測(cè)HSP患兒(急性期44例,緩解期40例)及健康對(duì)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(duì)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(jī)制中起著重要作用,CD41a/CD61、CD62P、vWF水平的測(cè)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(guò)敏性;血小板膜糖蛋白類;P選擇素;血管性假血友病因子;兒童
ZHANG Hongxia1, LIU Xuemei2, LIU Fange1, LIN Aiwei2, DUAN Chunhong2, YANG Xiaomei2
(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, Pselectin and von Willebrane Factor in children with HenochSchonlein purpura (HSP), and to investigate the pathological role of them in HSP. Methods The concentrations of CD41a/CD61 and CD62P were determined by flow cytometry and the level of vWF by an enzymelinked 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, CD62P 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 nonrenal 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, CD62P and vWF are helpful in finding the disturbance of blood coagulation,and provide a basis for anticoagulant treatments醫(yī).學(xué)全.在.線網(wǎng)站m.payment-defi.com.
Key words: Purpura, HenochSchonlein; Platelet membrane glycoproteins; Pselectin; von Willebrane factor; Child 過(guò)敏性紫癜(henochschonlein purpura,HSP)是兒童最常見(jiàn)的血管炎之一。有文獻(xiàn)報(bào)道[1],約20~80%的HSP患兒并發(fā)腎臟損害,導(dǎo)致過(guò)敏性紫癜性腎炎(henochschonlein purpura nephritis, HSPN)。HSP的發(fā)病機(jī)制尚未完全明了,近年來(lái)許多研究[23]認(rèn)為,HSP患兒血小板的聚集功能增強(qiáng),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(guò)程中起著重要作用。P選擇素,即CD62P,具有介導(dǎo)活化血小板、血管內(nèi)皮細(xì)胞與白細(xì)胞粘附的功能[4],為血小板活化的特異性標(biāo)志。GPⅡb/Ⅲa與P選擇素在血循環(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(xì)胞損傷的標(biāo)記物,血管內(nèi)皮細(xì)胞受損時(shí)可促進(jìn)血小板的粘附、聚集。本研究旨在觀察HSP患兒GPⅡb/Ⅲa(CD41a/CD61)、P選擇素(CD62P)及vWF的變化,探討HSP發(fā)生時(shí)凝血狀態(tài)的改變、內(nèi)皮細(xì)胞損害與腎臟損害的關(guān)系。