Introduction:Livedoid vasculopathy is a chronic noninflammatory skin disease secondary to hypercoagulable states.No therapeutic guideline has yet been established for livedoid vasculopathy.We herein report a case of l...Introduction:Livedoid vasculopathy is a chronic noninflammatory skin disease secondary to hypercoagulable states.No therapeutic guideline has yet been established for livedoid vasculopathy.We herein report a case of livedoid vasculopathy secondary to protein C deficiency that was successfully treated with rivaroxaban.Case presentation:A 31-year-old Thai woman who had been diagnosed with livedoid vasculopathy 10 years previously presented with a 2-month history of worsening leg ulcers and failure to respond to aspirin,colchicine,and pentoxifylline.Further investigations confirmed protein C deficiency.Rivaroxaban was initiated,and clinical improvement was achieved in 8 weeks.Discussion:When livedoid vasculopathy is confirmed by skin biopsy,additional investigations for hypercoagulable states should be performed to exclude secondary causes.Identification of the causes of livedoid vasculopathy can direct physicians to therapeutic options based on previously reported cases of successful treatment.Our patient,whose livedoid vasculopathy was caused by protein C deficiency,responded well to rivaroxaban.Conclusion:Protein C deficiency results in a hypercoagulable state,and affected patients can present with livedoid vasculopathy.The anticoagulant rivaroxaban has been beneficial in the treatment of livedoid vasculopathy.展开更多
文摘Introduction:Livedoid vasculopathy is a chronic noninflammatory skin disease secondary to hypercoagulable states.No therapeutic guideline has yet been established for livedoid vasculopathy.We herein report a case of livedoid vasculopathy secondary to protein C deficiency that was successfully treated with rivaroxaban.Case presentation:A 31-year-old Thai woman who had been diagnosed with livedoid vasculopathy 10 years previously presented with a 2-month history of worsening leg ulcers and failure to respond to aspirin,colchicine,and pentoxifylline.Further investigations confirmed protein C deficiency.Rivaroxaban was initiated,and clinical improvement was achieved in 8 weeks.Discussion:When livedoid vasculopathy is confirmed by skin biopsy,additional investigations for hypercoagulable states should be performed to exclude secondary causes.Identification of the causes of livedoid vasculopathy can direct physicians to therapeutic options based on previously reported cases of successful treatment.Our patient,whose livedoid vasculopathy was caused by protein C deficiency,responded well to rivaroxaban.Conclusion:Protein C deficiency results in a hypercoagulable state,and affected patients can present with livedoid vasculopathy.The anticoagulant rivaroxaban has been beneficial in the treatment of livedoid vasculopathy.
