Abstract

Sickle Cell Disease (SCD) is an intractable hematologic condition most commonly affecting patients of African ancestry. It is a serious global public health concern as over 300,000 babies are born annually with SCD, with up to 75% residing in Sub-Saharan Africa.[1] Chronic leg ulcers occur in 20-70% of SCD patients, although 75% of Jamaican patients that are homozygous for hemoglobin S are affected.[2] Systemic therapies such as Hydroxyurea and red blood cell transfusions have dramatically increased the life span of SCD patients and as a result more patients are reaching adulthood, where they are at greatest risk of developing leg ulcerations.[1,2] SCD leg ulcers are very resistant to heal and are associated with significant pain, disability, and negative psychosocial and economic impacts.[1,2] Although the mechanism of ulcer development has yet to be fully elucidated, the pathogenesis is believed to be a result of vaso-occlusion following intracellular precipitation of the sickle hemoglobin. This promotes endothelial dysfunction, a hypercoagulable state, inflammation, ischemia reperfusion injury, and associated tissue necrosis. [1,2].

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