Hindawi Publishing Corporation Case Reports in Medicine Volume 2012, Article ID 910231, 5 pages doi:10.1155/2012/910231 Case Report Painless Livedoid Vasculopathy in a Patient with G20210A Prothrombin Gene Mutation Aibek E. Mirrakhimov, Erwin Velasquez Kho, and Alaa Ali Department of Internal Medicine, Saint Joseph Hospital, 2900 N. Lake Shore, Chicago, IL 60657, USA Correspondence should be addressed to Aibek E. Mirrakhimov, amirrakhimov1@gmail.com Received 29 July 2012; Revised 9 August 2012; Accepted 9 August 2012 Academic Editor: Arduino A. Mangoni Copyright © 2012 Aibek E. Mirrakhimov et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 87 year old Caucasian female with chronic painless non-healing ulcers over malleoli was admitted to the hospital. On a physical examination, there were two bilateral and laterally located malleoli ulcers with no discharge. A thorough work up was done: lower extremities venous and arterial Doppler ultrasound did not show any evidence of venous and arterial disease respectively. Heterozygous G20210A Prothrombin gene mutation was found, and the patient was started on anticoagulation. This case reports highlights a possibility of a painless livedoid vasculopathy presentation in a patient without signiﬁcant past thrombotic events. Therefore, it is important to consider livedoid vasculopathy in the diﬀerential in a patient with painless ulcerative, atrophic and/or nodular skin lesions over the shins and malleoli. 1. Introduction Livedoid vasculopathy (LV) is an underrecognized vascular disorder of the arterial tree, which can be clinically presented with skin ulceration, nodular changes, ankle edema, and plaques with hyperpigmented borders, known as atrophic blanche. Typically, these lesions are painful and are located over the lower shins and ankles [1]. The disease pathophysiology is not entirely understood, but thrombosis is believed to play a leading role and inﬂammation does not seem to contribute to the disease pathogenesis [2–4]. The disease is often incorrectly labeled as vasculitis, whereas, in fact, there is no obvious role of inﬂammation. Another important issue that the disease has several conﬂicting names like livedo vasculitis, livedoid vasculitis, and so forth. These factors could contribute to the poor awareness of LV in the general medical practice. The disease can be missed because of similar presentation in chronic lower extremities venous insuﬃciency, atheroscle- rotic peripheral arterial disease, inﬂammatory vasculitides, pyoderma gangrenosum, and so forth. LV can be due to secondary causes or due to unknown defect-idiopathic, however, the latter presumption should be made only after a rigorous workup for associated conditions such as autoimmune diseases and procoagulant states. Thus, a thorough diagnostic workup is warranted, and if no alternative etiology is present, a skin biopsy should be considered to conﬁrm LV. As was mentioned previously, LV is associated with a procoagulant state, favoring clot formation. Prothrombin, which is also known to be II coagulation factor, has a central role in the hemostasis. Mutations in the prothrombin gene are associated with excessive thrombosis, and cardiovascular risk [5], with G20210A mutation is being the most studied. Prothrombin C20209T [6–8] and A19911G [9] genotypes have also been described, however, their role in the procoag- ulant state is much less clear in comparison to the G20210A mutation. The estimated prevalence of prothrombin gene mutation in the general population is up to 2.6% and up to 8% in patients with a thrombotic event [10]. We report a case of G20210A prothrombin gene muta- tion and painless LV clinically presenting similar to chronic venous insuﬃciency of the lower extremities. 2. Case Presentation The patient is an 87-year-old G0P0 Caucasian female which was admitted to the Hospital, because of chronic painless