过敏性紫癜患儿瘀血及黏附分子sICAM-1、sVCAM-1表达水平的研究

目的:观察过敏性紫癜(HSP)患儿可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞黏附分子-1(sVCAM-1)表达水平及瘀血状态,分析瘀血与尿中黏附分子及肾脏损伤的关系。方法:HSP患儿80例分为无肾损(NO-HSPN)组、血尿组、血尿加蛋白尿组,正常组(健康儿童10名)。根据中医瘀血症候积分表进行瘀血评分。ELISA法测定sICAM-1、sVCAM-1的表达水平。结果:①与NO-HSPN组比较,血尿加蛋白尿组瘀血积分明显升高(P0.01)。②血清sICAM-1在各组中表达差异无统计学意义,尿sICAM-1在血尿加蛋白尿组明显增加,与正常组和NO-HSPN组比较差异有统计学意义(P0.05,P0.01)。③血清sVCAM-1在各组间表达差异无统计学意义,血尿加蛋白尿组尿sVCAM-1的表达水平明显高于其他3组。④血尿加蛋白尿组尿sICAM-1和sVCAM-1的表达与瘀血积分的评定呈正相关。结论:瘀血参与了HSP肾损害过程。血尿加蛋白尿组HSP患儿尿中sICAM-1、sVCAM-1显著增加。

Clinical research of blood stasis and the level of serous and urinary sICAM-1,sVCAM-1 in henoch-schonlein purpura

Objective: We observed the expression of sICAM-1,sVCAM-1 in serum and urine in HSP,blood stasis and the relationship between blood stasis sICAM-1,sVCAM-1 in urine and kidney damage.Methods: 80 patients with HSP were divided into NO-HSPN(30 cases),hematuria group(23 cases) and proteinuria and hematuria group(27 cases),healthy children(10 cases) as normal group.Blood stasis was scored according to TCM symptoms for blood stasis.The concentration of sVCAM,sVCAM-1 in serum and urine was detected by enzyme 1inked immunosorbent assay(ELISA).Results: ①Blood stasis score in proteinuria and hematuria group was higher than NO-HSPN group(P<0.01).②Serous sICAM-1 was not obvious difference in each groups.Urinary sICAM-1 in proteinuria and hematuria group was higher than normal group and NO-HSPN group(P<0.05,P<0.01).③Serous sVCAM-1 is not significant differences among all the groups.Urinary sVCAM-1 of proteinuria and hematuria group was significant higher than normal group,NO-HSPN group,hematuria group.④A positive correlation can be found between urinary sVCAM-1 and sICAM-1 and blood stasis score in proteinuria and hematuria group.Conclusion: Blood stasis was involved in the renal lesion process in HSP.sICAM-1,sVCAM-1 in urine was increased in proteinuria and hematuria group,while those in serum was not changed compared with other group.These results suggested that blood stasis can increase the expression of sICAM,sVCAM-1 in kidney,and which triggered the cellular adhesion molecule-mediated inflammatory cells infiltration,followed up to increase renal lesion.