2 Lab test (reference range) Homocysteine (3.7–13.9 Umol/L) Anticardiolipin IgG (<23.0 GLP Units) Anticardiolipin IgM (<11.0 MPL Units) Anticardiolipin IgA (<22.0 APL units) ANA Factor V leiden Antithrombin III activity (>75%) Antithrombin III functionality (218–310 mg/L) Lupus anticoagulant (<1.2) Protein C activity (>69%) Protein C antigen (65–140%) Protein S activity (>59%) Prothrombin time (8.9–11.9) INR (0.9–1.1) C3, C4 and CH50 Partial thromboplastin time (23–33 seconds) C-ANCA and P-ANCA Prothrombin mutation Blood cultures on two separate occasions Table 1: Results of diagnostic workup. Case Reports in Medicine Result 13.7 10.4 1.8 9.5 Negative Negative 84 195 1.23 69 85 65 11.4 1.1 Within normal limits 32 Negative Heterozygous G20210A prothrombin gene mutation All negative nonhealing skin ulcers over her malleoli bilaterally and shin swelling present for approximately 1 year. Her clinical condi- tion worsened over the last several weeks. The patient denied any fever, chills, shortness of breath, chest pain, cough, abdominal pain, diarrhea, or constipation. The patient does not have past medical history of thrombotic events. Past medical history is relevant for arterial hypertension, hyperlipidemia, and a resection of a right middle lobe lung mass more than 10 year ago. The patient was using spironolactone, allopurinol, aspirin, carvedilol, rosuvastatin, and pentoxyﬁlline prior to admission. On a physical examination, there were two bilateral and laterally located ulcers over malleoli with a depth of approximately 1 millimeter (mm), height of 1 centimeter (cm), diameter of 0.8 mm, and sharp margins. There was no discharge; the margins of the ulcers were sharp and slightly erythematous without overt induration. Lower venous vari- cosities and shin swelling were present bilaterally, without local warmth and calf pain. Homan sign was negative bilaterally. Pulses were palpable over arteria dorsalis pedis and arteria femoralis posterior bilaterally. Cardiovascular, chest, abdominal, neurological, HEENT, and eye exams were grossly normal. Several potential diagnoses were considered: chronic venous insuﬃciency and lower extremities deep venous thrombosis (DVT) with an emphasis of hypercoagulable state because of a history of pulmonary mass, vasculitis, LV, and skin infection. Complete blood count (CBC), comprehensive metabolic proﬁle (CMP), homocysteine, folic acid, vitamin B12, anticardiolipin antibodies, lupus antico- agulant, factor V Leiden, Protein C activity and Protein C antigen, Protein S activity, D-Dimer, prothrombin mutation, prothrombin time and INR, partial thromboplastin time, blood, and wound cultures were drawn. Relevant diagnostic test results are present in Table 1. Chest X-ray was done and showed 2.5 cm nodular density over the right hilum and chest CT scan without contrast (the contrast was not given because of compromised renal func- tion present at baseline) showed a 6 mm right cardiophrenic lymph node but did not add additional knowledge regarding the right hilar nodule. However, her past CXR 1 year ago was similar and the recent chest imaging did not ﬁnd any change from her baseline. The patient denied undergoing pulmonary biopsy and further workup for lung mass at this time. Lower extremities venous and arterial Doppler ultra- sound did not show any evidence of venous and arterial disease, respectively. Heterozygous G20210A Prothrombin gene mutation was found (please see the Table 1), and the patient was started on enoxaparin 1 mg/kg once a day and 1 day after warfarin was added to the regimen. The skin biopsy was performed and periodic acid-Schiﬀ staining was used, which showed histopathologic ﬁndings characteristic for livedoid vasculopathy, such as deposition of ﬁbrinoid material with the proliferation of endothelial cells with few lymphatic cells. The patient’s INR was therapeutic on the ﬁfth hospital day (INR = 2.1) and 1 day after this enoxaparin was discontinued. On a followup visit after 5 months, the malleoli ulcers were healed, her INR was within the therapeutic range, and the patient did not experience any bleeding or thrombotic episode. 3. Discussion LV is relatively uncommon disorder, which can be in part explained by nonspeciﬁc clinical presentation. Painful skin