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Index: WOUNDS. 2012;24(7):190–194.

  Abstract: Venous ulcers affect approximately 1% of the world’s population, increasing health care expenditures and decreasing quality of life. Several hypotheses may help explain their origin. Insufficient veins or valves or impaired muscle function may lead to abnormal calf muscle pump function that can elevate ambulatory venous pressure. The aim of this study was to evaluate the efficacy of pentoxifylline in treating chronic venous ulcers. Methods. From May 2009 to March 2010, 40 patients with chronic venous ulcers were randomly assigned to 2 groups: a standard treatment group that received compression therapy or an intervention group that received oral pentoxifylline (400 mg, 3 times daily) in addition to compression therapy. Time duration of wound healing, edema, pain, and ulcer size in the 2 groups were studied. For all tests, P <0.05 was considered significant.

Results. The median duration of complete wound healing was 4 months in the intervention group and 6.25 months in the standard treatment group (P = 0.007). Recovery from pain and edema was not statistically significant after 3 months’ follow-up in either group. After 3 months of treatment, ulcer size decreased more in the intervention group compared to the standard treatment group (P = 0.02). Pentoxifylline in association with compression therapy decreases both time to complete wound healing and ulcer size.

Introduction

  Venous ulcers affect approximately 1% of the world’s population, increasing health care expenditures and decreasing quality of life.¹ Several hypotheses may help explain their origin.^2,3 Insufficient veins or valves (dysfunctional valves in the veins that allow backward blood recirculation due to incomplete valve closure) or impaired muscle function may lead to abnormal calf muscle pump function that can elevate ambulatory venous pressure (venous hypertension).⁴ This hypertension subsequently results in local venous dilatation and pooling, concomitantly trapping leukocytes that may release proteolytic enzymes that destroy tissue. Venous pooling also induces interendothelial pore widening and deposition of fibrin and other macromolecules that trap growth factors within them, rendering them unavailable for wound repair. Compression therapy, the mainstay treatment, reduces edema, reverses venous hypertension, and improves calf muscle pump function. Several treatment options can be employed as adjuvants to compression, such as systemic therapy with pentoxifylline or aspirin, autologous grafts, tissue-engineered skin, growth factor therapy, and/or vein surgery.⁵

  Pentoxifylline is a xanthine derivative used in the treatment of peripheral vascular disease.^6–8 Although it is often classified as a vasodilator, pentoxifylline’s primary action reduces blood viscosity, probably due to its effect on erythrocyte deformability, platelet adhesion, and aggregation.^8–11 Pentoxifylline also inhibits production of cytokine tumor necrosis factor alpha (TNF-a), a property currently under investigation in a number of diseases. The most common adverse effects are nausea, gastrointestinal disturbances, dizziness, and headache.