ABSTRACT
This chapter includes opinions relating to venous leg ulcers from an Australian and New Zealand Clinical Practice Group. Varicose veins are characterized by patchy damage to all layers of the vein wall which allow the weakened vein to dilate. Increased levels of tissue and plasma matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteineses (TIMP) occur in both varicose vein tissue and the skin of patients affected with varicose disease, indicating a systemic influence. Cytokines mediate the effects of inflammation. Chemokines, interleukins, lymphokines and tumour necrosis factor are involved in varicose disease. Thrombomodulin is an endothelial cell surface glycoprotein receptor that binds thrombin, and the thrombomodulin gene has been related to endothelial injury predisposing to varicose veins. Red blood cell degradation products and interstitial proteins attract cytokines, growth factors and other chemical agents to initiate an inflammatory reaction in the dermis.
