Copyright 1998 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1998
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 VasculopathyWhat Is It?. Arch Dermatol. 1998;134(4):491-493. doi:10.1001/archderm.134.4.491