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Livedoid Vasculitis With Ulcerations: The Role of Antithrombin III Deficiency and Its Therapeutic Consequences
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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Livedoid vasculitis (LV) is a descriptive and still indistinct clinical
term that includes considerable "semantic confusion."1
It covers localized cutaneous vasculopathies presenting a clinical pattern
of livedoid discoloration mainly in distal parts of the lower extremities,
eventually eliciting long-lasting painful ulcers particularly after exposure
to heat or cold.1-2 Histologically,
microthromboses and segmental hyalinization of the subendothelial intima in
blood vessels of the middle and lower dermis are significant findings.2 Besides local factors, systemic hypercoagulopathies
(protein C or factor XII deficiencies, deficient release of tissue plasminogen
activator, elevated tissue plasminogen inhibitor, and increased platelet aggregation)
are under discussion as copathogenetic factors.3-5
Herein, we report, for the first time, 2 cases of LV relating to antithrombin
III (AT-III) deficiency.
Report of Cases
Patient 1
A 47-year-old white woman presented with a 9-year history of recurrent
painful ulcerations on the dorsa of both feet accompanied by livedo racemosa
(Figure 1). Results of skin biopsy
revealed inflammatory . . . [Full Text of this Article] Patient 2
Further Investigations
Therapy and Results
Comment
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
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Livedoid vasculopathy: further evidence for procoagulant pathogenesis.
Hairston et al.
Arch Dermatol 2006;142:1413-1418.
ABSTRACT
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Heterozygous Prothrombin G20210A Gene Mutation in a Patient With Livedoid Vasculitis
Gotlib et al.
Arch Dermatol 2003;139:1081-1083.
FULL TEXT
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