Considerable progress has been made in the understanding of dermatomyositis. Banker and Victor1 characterized childhood dermatomyositis as an angiopathy in 1966. Banker then identified distinctive capillary endothelial changes and postulated that these were an early and fundamental lesion in dermatomyositis.2 Subsequently, Carpenter et al3 showed endomysial capillary necrosis and significantly reduced capillary numbers relative to muscle fiber area, providing substantive support for muscle fiber atrophy being a sequel of chronic sublethal ischemia.
See also p 26.
In this issue of the Archives, Kissel et al4 provide still more evidence for the primacy of blood-vessel damage as an early pathologic feature of dermatomyositis. The report by Kissel et al5 followed up on an earlier study from the same group, which showed that membrane attack complex (MAC) was present on muscle biopsy in blood vessels of patients with dermatomyositis. The present study used quantitative histologic methods, combined
Griggs RC, Karpati G. The Pathogenesis of Dermatomyositis. Arch Neurol. 1991;48(1):21–22. doi:10.1001/archneur.1991.00530130029013
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