Patients with chronic venous disease may develop characteristic changes in the skin of the lower limb known as lipodermatosclerosis (LDS). The affected skin becomes indurated and pigmented and often ulcerates. The degree of induration associated with LDS correlates directly with ulcer formation and leads to a subsequent delayed rate of healing. However, there is limited information regarding the cellular and molecular events that lead from venous dysfunction to LDS development. This article reviews the current knowledge of the clinical progression of chronic venous disease, summarizing the histological findings from these authors' laboratory and other studies on LDS, and offers possible mechanisms to explain the fibrotic changes associated with this condition.
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