Affiliations: Biologie Vasculaire, Laboratoire de Pharmacologie, Université Victor Segalen Bordeaux 2, Carreire Nord, Bât 1A, 146 rue Léo Saignat, 33076 Bordeaux cedex, France | Hôpital d'Annemasse, Medecine A, 74100 Ambilly, France
Note: [] Corresponding author: Dr. med. Bertrand de la Giclais, Hôpital d'Annemasse, Medecine A, 74100 Ambilly, France. Tel.: +33 614 754 257; E‐mail: [email protected].
Abstract: Disturbances in haemodynamic, biochemical and enzymatic factors have been observed in chronic venous diseases (CVD). These changes lead to the development of varices, telangiectasies and skin disorders. They affect vessels, blood, skin tissues and cells. It is now possible to describe their time course and interdependance of these changes. Orthostatism pressure on vein wall may lead to fluid leakage and oedema, these resulting in vein enlargement. These processes may be further influenced by genetic or acquired risk factors. Skin microvessels suffer more from hypoxia than from hypertension. Indeed, hypoxia affects not only endothelial cells, but also red and white blood cells and modifies particularly, but not exclusively, TGF‐β1 production. This substance is, an important modulator of zinc dependent‐metallo‐proteinases and their tissue inhibitor of metallo‐proteinases (TIMP) in the skin. Imbalance in this enzymatic system seems to lead either to sclerosis or ulcer. Of course, other biochemical events (also in this review) play a role in vessel wall and skin deterioration in CVD. The aim of the present review is to assess the role of pathophysiological factors in CVD and the influence of different therapies, including the venotropic agent calcium dobesilate, on some of these haemodynamic or biochemical aspects.
Keywords: Chronic venous disease, transforming growth factor‐beta‐1/tissue inhibitor of metallo‐proteinases balance, clinical sign and symptoms, calcium dobesilate
