Commentary
m FINE mi ROBERT M. EINE, M.D.
From the Veterans Hospital and the Department of Dermatology, Cmory University School of Medicine, Atlanta, Ceorgia
(which causes degranulation of IgE coated cells) or ragweed antigen E as compared with normal controls and ragweedallergic individuals. The authors believe that the defective release of eosinophilic chemotactic factor may play a part in perpetuating the symptoms in chronic urticaria since eosinophils have a nodulating role on the inflammatory effect of histamine and inactivate the slow-reacting substance of anaphylaxis. Since the total number of circulating basophils in these patients is normal, they appear to be in a state of desensitization. Whether the "desensitized" state of the basophils may be secondary to the chronic urticaria rather than having a primary role in causing it is not clear. This may indeed be the case since chronic urticaria usually resolves spontaneously after a variable period of time. This would not be so if a permanent functional alteration in the basophil existed.
Chronic Urticaria Although patients with chronic urticaria are not uncommonly seen in clinical practice, there is still little fundamental understanding of the etiology and pathogenesis of this condition. A true allergic cause is proved in only a relatively small number of cases even though the hive (wheal and flare) is the cutaneous prototype of the type I reaction (Gell and Coombs). The reaction is mediated by the release of histamine (and other mediators) from mast cells in the skin, and can be triggered by numerous antigens combining with specific IgE coating the mast cell or basophil. Certain chemicals (48/80, polymyxins) are obligatory mast cell degranulators unrelated to the IgE mechanism. In an effort to explain the basic defect in chronic urticaria, Czarnetzki et al.^ have studied histamine and eosinophilic chemotactic factor release from peripheral leukocytes (basophils) from individuals with this condition. Twelve of 15 showed defective release of these 2 mediators following exposure to anti IgE
References 1. Czarnetzki, B. M., Kern, F., and Lichtenstein, L. M.: Defective release of eosinophil chemotactic factor from peripheral leucocytes in patients with chronic urticaria. J. Invest. Dermatol. 67:276, 1976. 2. Kern, E., and Lichtenstein, L. M.: Defective histamine release in chronic urticaria. J. Clin. Invest. 57:1369, 1976.
586
m FINE mi ROBERT M. EINE, M.D.
From the Veterans Hospital and the Department of Dermatology, Cmory University School of Medicine, Atlanta, Ceorgia
(which causes degranulation of IgE coated cells) or ragweed antigen E as compared with normal controls and ragweedallergic individuals. The authors believe that the defective release of eosinophilic chemotactic factor may play a part in perpetuating the symptoms in chronic urticaria since eosinophils have a nodulating role on the inflammatory effect of histamine and inactivate the slow-reacting substance of anaphylaxis. Since the total number of circulating basophils in these patients is normal, they appear to be in a state of desensitization. Whether the "desensitized" state of the basophils may be secondary to the chronic urticaria rather than having a primary role in causing it is not clear. This may indeed be the case since chronic urticaria usually resolves spontaneously after a variable period of time. This would not be so if a permanent functional alteration in the basophil existed.
Chronic Urticaria Although patients with chronic urticaria are not uncommonly seen in clinical practice, there is still little fundamental understanding of the etiology and pathogenesis of this condition. A true allergic cause is proved in only a relatively small number of cases even though the hive (wheal and flare) is the cutaneous prototype of the type I reaction (Gell and Coombs). The reaction is mediated by the release of histamine (and other mediators) from mast cells in the skin, and can be triggered by numerous antigens combining with specific IgE coating the mast cell or basophil. Certain chemicals (48/80, polymyxins) are obligatory mast cell degranulators unrelated to the IgE mechanism. In an effort to explain the basic defect in chronic urticaria, Czarnetzki et al.^ have studied histamine and eosinophilic chemotactic factor release from peripheral leukocytes (basophils) from individuals with this condition. Twelve of 15 showed defective release of these 2 mediators following exposure to anti IgE
References 1. Czarnetzki, B. M., Kern, F., and Lichtenstein, L. M.: Defective release of eosinophil chemotactic factor from peripheral leucocytes in patients with chronic urticaria. J. Invest. Dermatol. 67:276, 1976. 2. Kern, E., and Lichtenstein, L. M.: Defective histamine release in chronic urticaria. J. Clin. Invest. 57:1369, 1976.
586
