Abstract

The authors classify aspirin sensitive asthma in connection with eosinophilia in the polyps themselves and in the tissues of the lower respiratory tract and with the obviously lacking formation of specific IgE antibodies as a non-allergy related process. Rather, they say that aspirin sensitive asthma is due to genetic disruptions of the arachidonic acid metabolic pathway, which results in overproduction of cysteinyl leukotrienes with subsequent overproduction of inflammatory mediators. In this process, the eosinophils are included only as the source, especially for LTC4 synthase; this does not do justice to the position of eosinophils in the immune sys tem as per current knowledge. To detect eosinophils in tissue and peripheral blood circulation, the histocytochemical test for the enzyme phenoloxidase, after treatment with methanol, has proved to be suitable. Morphologically, the involvement of eosinophil granulocytes in cytotoxic as well as antibody forming reactions can be proved. Both types of reaction can occur simultaneously and can be triggered by medical drugs (1, 2, 3).

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