Anticardiolipin antibodies and ulcerations of the leg.

Abstract

ACA appeared to be significantly associated with venous ulcerations of the leg but not with ulcerations associated with isolated arteritis. None of the patients had typical signs of APS. As for the relation between ACA and venous ulcerations, several hypotheses can be proposed. First, the causes of arteritis-associated and venous ulcers are clearly different; t he former is most frequently related to atherosclerosis.S 8 Venous ulcers have been reported to develop as a consequence of fibrin cuff formation or leukocyte trapping.?' 10 In the first model decreased fibrinolytic activity favors the formation of pericapillary fibrin cuffs impairing the diffusion of oxygen and nutrients. Although ACA could lead to anomalies of the coagulation cascade, a direct role ofsuch antibodies and their appearance as a consequence of the vascular alterations induced by cuff formation seem unlikely in this model. The formation of ACA could more likely be triggered in the leukocyte trapping model. This hypothesis sugThe leg ulcers described in the antiphospholipid syndrome (APS)!' 2 mimic pyoderma gangrenosum or appear as superficial ulcerations surrounded by a purple halo.3, 4 These painful, treatment-resistant lesions occur mostly in young patients with systemic lupus erythematosus. Clinically different types of ulcerations of the leg occur commonly in elderly patients with no clinical or biologic signs of systemic lupus erythematosus.l