Institutional members access full text with Ovid®

Cocaine-Associated Retiform Purpura: A C5b-9Mediated Microangiopathy Syndrome Associated With Enhanced Apoptosis and High Levels of Intercellular Adhesion Molecule-1 Expression

Magro, Cynthia M. MD; Wang, Xuan MD, PhD

American Journal of Dermatopathology: October 2013 - Volume 35 - Issue 7 - p 722–730
doi: 10.1097/DAD.0b013e31827eaf0b
Original Study

Abstract: Cocaine-associated retiform purpura is a recently described entity characterized by striking hemorrhagic necrosis involving areas of skin associated with administration of cocaine. Levamisole, an adulterant in cocaine, has been suggested as the main culprit pathogenetically. Four cases of cocaine-associated retiform purpura were encountered in the dermatopathology practice of C. M. Magro. The light microscopic findings were correlated with immunohistochemical and immunofluorescence studies. All 4 cases showed a very striking thrombotic diathesis associated with intravascular macrophage accumulation. Necrotizing vasculitis was noted in 1 case. Striking intercellular adhesion molecule-1 (ICAM-1)/CD54 expression in vessel wall along with endothelial expression of caspase 3 and extensive vascular C5b-9 deposition was observed in all biopsies examined. Cocaine-induced retiform purpura is a C5b-9–mediated microvascular injury associated with enhanced apoptosis and prominent vascular expression of ICAM-1, all of which have been shown in prior in vitro and in vivo murine models to be a direct effect of cocaine metabolic products. Antineutrophilic cytoplasmic antibody and antiphospholipid antibodies are likely the direct sequelae of the proapoptotic microenvironment. The inflammatory vasculitic lesion could reflect the downstream end point reflective of enhanced ICAM-1 expression and the development of antineutrophilic cytoplasmic antibody. Levamisole likely works synergistically with cocaine in the propagation of this syndromic complex.

Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY.

Reprints: Xuan Wang, MD, PhD, Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, Box 58, Room F-309, 1300 York Avenue, New York, NY 10065 (e-mail: xuw9004@nyp.org).

Supported by the Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY.

The authors declare no conflicts of interest.

© 2013 by Lippincott Williams & Wilkins.