Abstract
The pathogenesis of livedoid vasculopathy (LV) is still unclear. However, with increasing knowledge of disorders of coagulation over the past few years, the cause of some cases of LV has been elucidated. LV has now been described in association with hyperhomocysteinaemia, activated protein C resistance, and prothombin gene mutations in the absence of significant underlying inflammatory disease. When LV is seen in association with systemic lupus erythematosus or polyarteritis nodosa, it is probably due to the pro-coagulable state induced by these diseases rather than being true vasculitis. We review recent insights into LV provided by published clinical cases and discuss its pathogenesis.
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