Gaillard M C, Reichberg S B, Nogueira C M, Kilroe-Smith T A
Department of Medicine, University of the Witwatersrand Medical School, Johannesburg, South Africa.
Clin Chem. 1993 Apr;39(4):675-9.
Forty-two adult patients with asthma and 30 control subjects were investigated for elastase-binding capacities of alpha 1-protease inhibitor and alpha 2-macroglobulin in plasma. The binding activities of alpha 1-protease inhibitor and alpha 2-macroglobulin in asthmatic patients with the M phenotype for the alpha 1-protease inhibitor differed in their relationship to the values in control subjects with the same phenotype [less alpha 1-protease inhibitor for asthmatics (35.1 +/- 1.8) than for controls (42.9 +/- 2.0 kU/L) (P < 0.001); more alpha 2-macroglobulin for asthmatics (6.9 +/- 0.3) than for control subjects (5.9 +/- 0.4 kU/L) (P < 0.03)]. In contrast, the patients with a deficiency allele (S, V, or Z) for alpha 1-protease inhibitor had lower activities of both alpha 1-protease inhibitor [22.1 +/- 0.1 vs 42.9 +/- 2.0 kU/L (P < 0.001)] and alpha 2-macroglobulin [4.6 +/- 0.6 vs 5.9 +/- 0.4 kU/L (P < 0.001)] than did the control subjects with the M phenotypes. The relevance of the results to the pathogenesis of asthma is discussed.
对42例成年哮喘患者和30名对照者的血浆α1 -蛋白酶抑制剂和α2 -巨球蛋白的弹性蛋白酶结合能力进行了研究。M表型哮喘患者中α1 -蛋白酶抑制剂与α2 -巨球蛋白的结合活性与相同表型对照者的值相比存在差异[哮喘患者的α1 -蛋白酶抑制剂(35.1±1.8)低于对照者(42.9±2.0 kU/L)(P<0.001);哮喘患者的α2 -巨球蛋白(6.9±0.3)高于对照者(5.9±0.4 kU/L)(P<0.03)]。相比之下,α1 -蛋白酶抑制剂存在缺陷等位基因(S、V或Z)的患者,其α1 -蛋白酶抑制剂[22.1±0.1对42.9±2.0 kU/L(P<0.001)]和α2 -巨球蛋白[4.6±0.6对5.9±0.4 kU/L(P<0.001)]的活性均低于具有M表型的对照者。讨论了这些结果与哮喘发病机制的相关性。