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What Is It?

Arch Dermatol. 1998;134:491-493.

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

IN THIS issue of the ARCHIVES, Papi et al¹ report an exciting advancement in that modern investigative methods, including assessments of surface expression of platelet P-selectin and circulating levels of interleukin 1, tumor necrosis factor , interleukin 8, interleukin 2, and soluble interleukin 2 receptor, were used to study and compare 2 patient groups, one with livedoid vasculopathy and the other with cutaneous small vessel vasculitis, with a group of healthy controls. Livedoid vasculopathy and cutaneous small vessel vasculitis have been confused because of semantic and classification problems. Papi and colleagues compare a group of patients who most likely had vessel-based disease with an immune-mediated pathogenesis (cutaneous small vessel vasculitis) with a group of patients with a disease with a more vague pathogenesis (livedoid vasculopathy), possibly related to platelet and local endothelial factors. Their data support the hypothesis that different mechanisms have a role in the 2 disease entities, . . . [Full Text of this Article]

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