Livedoid Vasculitis With Ulcerations: The Role of Antithrombin III Deficiency and Its Therapeutic Consequences

Livedoid Vasculopathy

“…It has been described as idiopathic, 5 associated with immune complexassociated diseases, 4 and a result of dermal blood vessel occlusion. 6 Laboratory test result abnormalities have been reported in patients with the disease, including defective release of tissue plasminogen activator, 7 elevated fibrinopeptide A, 8 antithrombin III deficiency, 9 and numerous other thrombophilic abnormalities that are further described in this article. The purpose of our review was to further characterize the clinical features, disease associations, and laboratory test result abnormalities, including coagulation study results, in patients with biopsy-proved livedoid vasculopathy whose conditions were evaluated at the Mayo Clinic, Rochester, Minn, from January 1,1990, to December 31, 2000.…”

Therapeutic effect of autologous platelet-rich plasma (PRP) on recalcitrant cutaneous ulcers in livedoid vasculopathy

“… 4 There is, however, increasing evidence that the condition must be mediated by either coagulation or fibrinolysis disorders. 5 , 6 , 7 Systemic therapeutic recommendations mainly refer to antiplatelet, antithrombotic, anticoagulant, and fibrinolytic medications, which are often unsatisfactory. 1 , 8 , 9 We believe this is the first report of successful treatment of recalcitrant cutaneous ulcers in a patient with livedoid vasculopathy by autologous PRP.…”

Frequency of thrombophilia determinant factors in patients with livedoid vasculopathy and treatment with anticoagulant drugs – a prospective study

“…There is, however, increasing evidence that the condition must be mediated by either coagulation or fibrinolysis disorders 7–10 . Some reports have described its association with inadequate fibrinolytic processes, platelet dysfunction, increase in tissue plasminogen activator (tPA) inhibitor levels, 11 cryofribrinogenaemia, 12 hyperhomocysteinaemia, 12 antithrombin III deficiency, 9 factor V Leiden mutation, 13 and antiphospholipid antibodies 14 . Positive clinical response to fibrinolytic and antiplatelet drugs, and to anticoagulation therapies, is an additional evidence of the role of coagulation disorders in LV’s pathogenesis.…”

“…Idiopathic forms, association with immune complex and dermal blood vessel occlusion have been described 4–6 . There is, however, increasing evidence that the condition must be mediated by either coagulation or fibrinolysis disorders 7–10 . Some reports have described its association with inadequate fibrinolytic processes, platelet dysfunction, increase in tissue plasminogen activator (tPA) inhibitor levels, 11 cryofribrinogenaemia, 12 hyperhomocysteinaemia, 12 antithrombin III deficiency, 9 factor V Leiden mutation, 13 and antiphospholipid antibodies 14 .…”