Features of Churg—Strauss Syndrome Shared with Polyarteritis,Wegener's Granulomatosis,and Hypereosinophilic Syndrome: Is There a Common Role for the Eosinophil?

The clinical pattern of a male between the ages of 20 and 50 years with late-onset asthma, allergic rhinitis, polyposis, systemic vasculitis, and peripheral eosinophilia strongly suggest a diagnosis of Churg—Strauss syndrome. The differentiation between Churg—Strauss syndrome, the vasculitides, and other progressive eosinophilia syndromes is very difficult to make, especially in the initial phases of the disease process. The role of the eosinophil in the pathogenesis of tissue destruction in all of these syndromes, with special emphasis on the ability of the eosinophil to cause damage in different tissues, has been very elusive until recently. The involvement of tissue-fixed antigens and the ability to induce mediators of inflammation may well be only the induction phase of eosinophilia. The production of the cytokines, interleukin-3 and interleukin-5, is probably the cause of the development of "hypodense" eosinophils that are found in such high numbers in these related syndromes.