RESUMO
Livedoid vasculopathy is a chronic disorder characterised by recurrent reticulated purpura on lower extremities, associated with painful purpuric or necrotic macules and ulcerations. Current knowledge indicates LV to be a thrombo-occlusive vasculopathy of cutaneous blood vessels; exact pathogenesis is yet to be understood. Elevated levels of lipoprotein(a) have been found in LV patients. To date, elevated plasma levels of lipoprotein(a) are considered an independent and causal genetic risk factor for the development of cardiovascular disease, as well as a relevant factor in hypercoagulable states. Because of its structural homology with plasminogen, Lp(a) might have important anti-fibrinolytic properties. Altered endothelial function and participation in immune and autoimmune processes, such as antiphospholipid syndrome, are also potential mechanisms of Lp(a) involvement in LV pathogenesis. Lp(a) is part of the wound healing process; the possibility of Lp(a) serum elevation to reflect an acute-phase reagent in LV scenario is also considered. The objective of this review is to examine the possible association of lipoprotein(a) with LV pathogenesis, based on its effects on thrombogenesis, fibrinolysis and autoimmunity.
