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Robert C. Griggs, MD; George Karpati, MD

Arch Neurol. 1991;48(1):21-22.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
Rochester, NY; Montréal, Québec

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