Mechanisms
Lp(a) may drive livedoid vasculopathy through thrombosis, fibrinolysis inhibition and autoimmunity, a hypothesis review (Med Hypotheses 2015)
Original title: Lipoprotein(a) and livedoid vasculopathy: A new thrombophilic factor?
This review by Criado, Espinell, Barreto, Di Giacomo and Sotto examines a possible link between Lp(a) and livedoid vasculopathy (LV), a chronic thrombo-occlusive disorder of cutaneous blood vessels causing recurrent reticulated purpura, painful ulcerations and necrotic macules on the lower extremities, whose exact pathogenesis remains unclear. Elevated Lp(a) has been found in LV patients, and given its established role as a causal cardiovascular risk factor and hypercoagulability marker, its structural homology with plasminogen could confer anti-fibrinolytic properties relevant to LV. The authors also consider altered endothelial function, involvement in autoimmune processes like antiphospholipid syndrome, and Lp(a) role in wound healing as potential mechanisms, proposing Lp(a) elevation in LV patients may partly reflect an acute-phase response.
Original abstract
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.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.