With respect to the observation by Kano et al1 on cellular and molecular dynamics in exercise-induced urticarial vasculitis lesions, and to the editorial by Mehregan,2 we would like to offer the following comments.
In their observation, Kano et al note that eosinophil was the first cell type that appeared around vessels in the induced lesion of urticarial vasculitis when intense expression of E-selectin was noted on endothelial cells. E-selectin is a molecule implicated in the initial adhesion of neutrophils, eosinophils, basophils, and memory T cells.3 Mehregan suggests that the expression of adhesion molecules found by Kano et al is similar to the findings that we reported in a study undertaken to investigate the sequential expression of adhesion molecules on endothelial and infiltrating inflammatory cells in 42 lesions of cutaneous leukocytoclastic vasculitis of between 24 and 72 hours' duration.4 In this study we observed that E-selectin expression on activated endothelium was inversely related to the duration of the lesion. This expression was also significantly associated with positive results of a direct immunofluorescence test and with predominance of neutrophils expressing CD11b (Mac1) in the inflammatory infiltrate but not with the infiltrating eosinophils noted by Kano et al. Endothelial vascular cell adhesion molecule-1 (VCAM-1) expression was absent in most vasculitis specimens in our study, and the 5 lesions that showed VCAM-1 endothelial immunoreactivity were of greater than 24 hours' duration and showed a lymphocytic infiltrate. Such sequential expression of adhesion molecules is not observed by Kano et al, and in our opinion it is difficult to attribute the ordered accumulation of eosinophils and neutrophils in the urticarial vasculitis lesions to the pattern of adhesion molecules found. In another study, Barlow et al5 investigated the adhesion molecule expression in induced wheals of delayed pressure urticaria and found an up-regulation of E-selectin in all lesions biopsied at 6 and 24 hours, which also correlated with accumulation of infiltrating neutrophils. Eosinophils appeared later in the inflammatory infiltrate. Presence of eosinophils has been demonstrated in cutaneous lesions of leukocytoclastic vasculitis, and their role may be underestimated since their presence in tissue is ephemeral. However, in our opinion, the finding of early infiltrating eosinophils observed by Kano et al in one case of urticarial vasculitis does not allow extrapolation of general conclusions concerning the pathogenesis of leukocytoclastic vasculitis. Moreover, experimental models of vasculitis do not show such eosinophil participation.6 It is known that the biological activity of soluble antigen-antibody complexes depends upon the ratio of antigen–antibody molecules, the binding power of the antibody for the antigen, the class of antibody, and the molecular weight of the antigen. In some instances soluble complexes may induce both anaphylactoid (urticarial) and Arthuslike (vasculitic) reaction, and skin changes of both types of reaction may be seen superimposed in some patients.6 Thus the changes observed at 3 hours by Kano et al may not be necessary in the development of a characteristic purpuric lesion of leukocytoclastic vasculitis, an immunocomplex-mediated disorder in which the neutrophil is known to play a central role (type III immunological reaction).
Sais G, Vidaller A. Pathogenesis of Exercise-Induced Urticarial Vasculitis Lesions: Can the Changes Be Extrapolated to All Leukocytoclastic Vasculitis Lesions? Arch Dermatol. 1999;135(1):87–89. doi:10-1001/pubs.Arch Dermatol.-ISSN-0003-987x-135-1-dlt0199
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