下肢慢性静脉功能不全发病机理的临床研究

Clinical Study on the Pathogenesis of Chronic Venous Insufficiency in the Lower Extremities

目的 探讨下肢慢性静脉功能不全 (CVI)时细胞因子水平和粘附分子表达与皮肤损伤的关系。方法 采用酶联免疫吸附法 (ELISA法 )检测血浆TNF α、IL 1β和IL 2R水平 ,免疫组织化学法 (SP法 )检测血浆白细胞粘附分子(EC ICAM 1、PMN CD18及PMN CD11b)的表达 ,并在电镜下观察 3 2例CVI患者和 8例正常对照组下肢皮肤标本的超微结构改变。结果 ①CVIClass 2～ 3级血浆TNF α和IL 1β水平分别为( 194.66± 2 2 1.90 )pmol/L和 ( 10 0 .60± 19.43 )pmol/L ,明显高于对照组的 ( 3 4.3 8± 9.74) pmol/L和 ( 67.62± 17.2 0 )pmol/L(P <0 .0 5 ) ,Class 2～ 3级和 1级血浆IL 2R水平分别为 ( 14 9.79± 85 .77) pmol/L和 ( 98.2 2± 3 8.5 5 )pmol/L ,与对照组的 ( 94.67± 13 .0 1) pmol/L相比较 ,差异无显著性意义 (P>0 .0 5 ) ;②Class 2～ 3级EC ICAM 1、PMN CD18和PMN CD11b表达阳性率分别为 ( 0 .70± 0 .14 ) %、( 0 .12± 0 .0 3 ) %和 ( 0 .16± 0 .0 2 ) % ,明显高于对照组的 ( 0 .15± 0 .0 9) %、( 0 .0 4± 0 .0 1) %和 ( 0 .0 5± 0 .0 1) % (P<0 .0 5 ) ;③相关分析显示ICAM 1表达与CD11b和CD18表达呈显著正相关 ,r值分别为 0 .845 4和 0 .5 63 9(P<0 .0 5 ) ;④电镜超微结构见中性粒细胞 (PMN)

Objective To explore the relationship among plasma cytokines’ level, adhesion molecules expression and skin damage in patients with chronic venous insufficiency (CVI) of lower extremities.Methods In 32 patients with CVI and 8 normal individuals as control, blood TNF α, IL 1β and IL 2R were assayed with ELISA method; serum endothelial cell intercellular adhesion molecule 1(EC ICAM 1), polymorphonuclear CD 18 (PMN CD 18 ) and polymorphonuclear CD 11b (PMN CD 11b ) were assayed with immunohistochemical method; and ultrastructure of diseased veins was examined by electroscope.Results The results showed that the level of plasma TNF α and IL 1β increased remarkably in Class 2-3 compared with Class 1 and control ( P <0.05), IL 2R had no difference in Class 1,2,3 ( P >0.05) . The index of EC ICAM 1 and PMN CD 11b positively expression increased remarkably in Class 2-3 compared with that in Class 1 and control. The index of PMN CD 18 expression in Class 2-3 and Class 1 was greatly higher than that in control ( P <0.05). The expression of ICAM 1 was positively correlated with that of CD 11b /CD 18 . Electron microcopy showed that the change in microvessel was mainly PMN adhesion with endothelial cells (ECs) and trapped in microvessels.Conclusion The results suggest that activated monocyte may release TNF α and IL 1β, upregulate ICAM 1 and CD 11b /CD 18 expression, and mediate the PMN adhesion to ECs, thus causing ECs and tissue damage. It may be one of important mechanism of venous ulcer.