Szczeklik A
Department of Allergy and Clinical Immunology, Copernicus Academy of Medicine, Cracow, Poland.
Clin Allergy. 1988 Jan;18(1):15-20. doi: 10.1111/j.1365-2222.1988.tb02838.x.
A hypothesis is presented which states that aspirin-induced asthma results from chronic viral infection. This type of asthma has, indeed, a highly characteristic clinical course, reminiscent of viral upper respiratory tract infection. It is suggested that, in response to a virus, a long time after the initial exposure, specific cytotoxic lymphocytes are produced. Their activity is suppressed by prostaglandin E2 (PGE2) produced by pulmonary alveolar macrophages. Anti-cyclo-oxygenase analgesics block PGE2 production, and allow cytotoxic lymphocytes to attack and kill their target cells, i.e. the virus-affected cells of the respiratory tract. During this reaction, toxic oxygen intermediates, lysosomal enzymes and mediators are released, which precipitate attacks of asthma. These acute attacks can be prevented by avoidance of all drugs with anti-cyclo-oxygenase activity, however, asthma continues to run a protracted course because of chronic viral infection.
有一种假说认为，阿司匹林诱发的哮喘是由慢性病毒感染引起的。事实上，这类哮喘具有高度典型的临床病程，让人联想到病毒性上呼吸道感染。有人提出，在初次接触病毒后很长一段时间，会产生特异性细胞毒性淋巴细胞以应对病毒。它们的活性受到肺泡巨噬细胞产生的前列腺素E2（PGE2）的抑制。抗环氧化酶镇痛药会阻断PGE2的产生，使细胞毒性淋巴细胞能够攻击并杀死其靶细胞，即呼吸道受病毒感染的细胞。在这个反应过程中，会释放有毒的氧中间体、溶酶体酶和介质，从而引发哮喘发作。通过避免使用所有具有抗环氧化酶活性的药物，可以预防这些急性发作，然而，由于慢性病毒感染，哮喘仍会持续很长时间。
