Denchev K, Radkov M, Lipcheva N
Vutr Boles. 1977;16(2):75-8.
The alfa1-antitrypsin level was followed up in patients with bronchial asthma with different forms and severity of the disease. The latter was found to be elevated in all patient groups with an average of 335,38 mg% as compared with the controls 290.83 mg%, p less than 0,01. The elevated antitrypsin is explained with the allergic process and the secondary bacterial inflammatory reactions, triggering the formation of antienzyme substances, in order to inactivate the enzymes, playing a certain role in the pathogenesis of the first two processes--allergy and bacterial inflammation. In patients, both treated and not with cortisone, antitrypsin is elevated with no manifestation of significant difference for both patient groups. The cortisone preparations very likely do not supress the antienzyme systems in organism. As regards the pathogenetic role of alfa1-antitrypsin deficiency in asthma, the latter is admitted to play an insignificant role only in single cases.
对患有不同类型和严重程度支气管哮喘的患者进行了α1-抗胰蛋白酶水平的随访。结果发现,所有患者组的该水平均升高,平均为335.38mg%,而对照组为290.83mg%,p<0.01。抗胰蛋白酶升高的原因是过敏反应和继发性细菌炎症反应,引发了抗酶物质的形成,以便使在前两个过程(过敏和细菌炎症)的发病机制中起一定作用的酶失活。在接受和未接受皮质醇治疗的患者中,抗胰蛋白酶均升高,两组患者之间无显著差异。皮质醇制剂很可能不会抑制机体中的抗酶系统。至于α1-抗胰蛋白酶缺乏在哮喘中的致病作用,仅在个别病例中被认为起微不足道的作用。