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 1β, tumor necrosis factor α, 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, ie, elevation of cytokine levels in cutaneous small vessel vasculitis and platelet and, to a certain degree, lymphocytic activation in livedoid vasculopathy. The problem is that, as we expand our capabilities to apply basic investigative laboratory techniques to clinical problems of vasculitis and/or vasculopathy, we will find ourselves increasingly handicapped by our inability to communicate clearly regarding disease classification.
Jorizzo JL. Livedoid Vasculopathy: What Is It? Arch Dermatol. 1998;134(4):491–493. doi:10.1001/archderm.134.4.491
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