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Arch Dermatol. 1998;134:88-89.

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

URTICARIAL VASCULITIS is a form of leukocytoclastic vasculitis defined clinically by urticarial wheals that tend to be painful or to cause a burning sensation, last longer than 24 hours, and resolve with purpura. It is often associated with hypocomplementemia and autoimmune disorders, primarily systemic lupus erythematosus. Those patients with serum hypocomplementemia in particular are more likely to have an associated autoimmune disease. The course of the disease is often chronic and must be differentiated from chronic urticaria. Histologically, urticarial vasculitis shows evidence of small vessel damage, including endothelial swelling, necrosis, and fibrin deposition.¹ These histologic changes characteristically evolve as the lesions develop thus making this disease a suitable model for the study of the early changes in leukocytoclastic vasculitis.

In this issue of the ARCHIVES, Kano et al² have taken advantage of a rare opportunity to study the earliest changes in urticarial vasculitis. Leukocytoclastic vasculitis is a type III immune . . . [Full Text of this Article]

IMMUNE COMPLEX REPOSITION


ACTIVATION OF MAST CELLS

INFLUX AND ACTIVATION OF EOSINOPHILS

PERSISTENT ACTIVATION OF MAST CELLS

NEUTROPHIL INFLUX WITH ENZYME RELEASE AND BLOOD VESSEL DAMAGE

CONCLUSIONS


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