VEGF、ICAM-1和ADA在良恶性胸腔积液中的鉴别诊断

Role of VEGF,ICAM-1 and ADA in pathogenesis of benign and malignant pleural effusions

目的:研究血管内皮生长因子(VEGF)、细胞间黏附分子1(ICAM-1)和ADA在良恶性胸腔积液形成过程中的作用。方法:81例胸腔积液患者分成4组:27例胸液细胞学检查阳性的肺癌患者、16例胸液细胞学检查阴性的肺癌患者、26例结核性胸腔积液,12例其它病因(8例低蛋白血症、4例心衰)患者。采用双抗体夹心法(ELISA)分别检测胸液中可溶性血管内皮生长因子(sVEGF)、可溶性细胞间黏附分子1(sICAM-1)和ADA的表达水平。结果:胸液中sVEGF、sICAM-1和ADA的含量为,肺癌恶性胸液细胞学检查阳性组[(1017±730)pg/ml,(1510±597)ng/ml,(149±102)ng/ml]、肺癌恶性胸液细胞学检查阴性组[(610±520)pg/ml,(951±390)ng/ml,(118±82)ng/ml]、结核性胸液组[(449±522)pg/ml,(1037±371)ng/ml,(179±132)ng/ml]和其它病因组[(126±78)pg/ml,(88±43)ng/ml,(39±12)ng/ml]。各组之间的sVEGF相比均差异有显著性(P<0.05),而恶性与结核性胸液中的sICAM-1和ADA均明显高于其它病因组(P<0.01)。胸液中的sVEGF和sICAM-1与乳酸脱氢酶(LDH)水平呈显著性正相关(r=0.58,0.38;P<0.05),ADA与腺苷脱苷酶(ADA)呈正相关(r=0.38,P<0.05)。结论:恶性胸腔积液的形成与VEGF密切相关,同时ICAM-1和ADA也在恶性胸液的形成机制中起着重要的作用,而ADA可能与结核性胸膜炎的纤维化形成的组织重建有关。

Objective：To study the role of VEGF,ICAM-1 and ADA in the pathogenesis of benign and malignant pleural effusions. Methods：Eighty-one patients with pleural effusion were categorized into 4 groups：27 cases of lung cancer with malignant pleural effusion,16 cases of lung cancer with pleural effusion of negative cytological findings,26 cases of tuberculosis and 12 cases of other diseases （including 8 cases with hypoproteinemia and 4 cases with congestive heart failure with pleural effiesou）.The levels of soluble VEGF sVEGF,sICAM-1 and ADA pleural fluid were mearured by enzyme-linked immunosorbent assay （ ELISA）.Results：The values of sVEGF in the 4 groups were （1017±730）,（610±520）,（458±531）,（116±78）pg/mL,respectively,with significant differences amony the 4 groups （P〈0.05）.The values of sICAM-1 were （1510±597）,（951±390）,（1037±371）,（88±43）ng/mL,respectively,the values of ADA were （149± 102）,（126±78）,（179±132）,（39±12）ng/mL,respectively.sICAM-1 and ADA were found to be significantly higher in the patients with lung cancer and tuberculosis （P〈0.01）.sVEGF and sICAM-1 were correlated closely with LDH level （r=0.58,0.38;P〈0.05） and ADA correlated closely with ADA （r=0.38,P〈0.05）.Conclusion：VEGF is closely related to malignant pleural effusion,while ICAM-1 and ADA may also play a role in the pathogenesis of malignant pleural effusion. Moreover,ADA may be responsible for the tissue reconstruction during the fibrotic process of tuberculosis pleuritis.