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. 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.
Leukocytoclastic vasculitis is a type III immune reaction marked by circulatory immune complexes.
Animal models, such as the arthus reaction, have been used previously to study inducible forms of leukocytoclastic vasculitis. However, the work by Kano et al provides us with information regarding early changes within the inflammatory infiltrate, cytokine expression, and adhesion molecule expression in a human model. In the study by Zax et al, serial punch biopsy specimens were taken from lesional skin of a patient with drug induced leukocytoclastic vasculitis. Biopsy specimens from the initial lesions, present for less than 24 hours, revealed a primarily neutrophilic infiltrate with invasion of vessel walls by neutrophils, leukocytoclasis, and fibrin deposition. At 120 hours the infiltrate had changed to predominantly lymphocytic without leukocytoclasis.