Martin W J, Taylor J C
Am Rev Respir Dis. 1979 Aug;120(2):411-9. doi: 10.1164/arrd.1979.120.2.411.
The interaction of serum alpha 1-antitrypsin with leukocyte elastolytic activity was examined in 71 patients with chronic obstructive pulmonary disease and 46 normal subjects. Residual elastolytic activity was present despite adequate amounts of alpha1-antitrypsin in 33 of the 71 patients compared to 6 of the 46 normal control subjects (P less than 0.001). This elastolytic activity was completely abolished by a specific human leukocyte elastase inhibitor. A crossover study designed to detect the source of this abnormal activity revealed that the plasma fraction containing alpha 1-antitrypsin was responsible for inadequate inhibition in 30 of the 39 cases. The residual elastolytic activity from a given patient did not correlate with the serum alpha 1-antitrypsin concentration, alpha 1-antitrypsin phenotype, or history of smoking. Our data suggest that the abnormal interaction of alhpa 1-antitrypsin with leukocyte elastolytic activity is an important additional variable in the gensis of chronic obstructive pulmonary disease.
在71例慢性阻塞性肺疾病患者和46名正常受试者中,研究了血清α1-抗胰蛋白酶与白细胞弹性蛋白酶活性之间的相互作用。与46名正常对照受试者中的6人相比,71例患者中有33人尽管有足够量的α1-抗胰蛋白酶,但仍存在残余弹性蛋白酶活性(P<0.001)。这种弹性蛋白酶活性被一种特异性人白细胞弹性蛋白酶抑制剂完全消除。一项旨在检测这种异常活性来源的交叉研究表明,在39例病例中的30例中,含有α1-抗胰蛋白酶的血浆部分导致抑制不足。给定患者的残余弹性蛋白酶活性与血清α1-抗胰蛋白酶浓度、α1-抗胰蛋白酶表型或吸烟史无关。我们的数据表明,α1-抗胰蛋白酶与白细胞弹性蛋白酶活性之间的异常相互作用是慢性阻塞性肺疾病发生过程中的一个重要额外变量。