G L Sayer1, P D C Smith. 1. Department of Vascular Surgery, King's College Hospital, London SE5 9RS, UK. mrgabrielsayer@hotmail.com
Abstract
OBJECTIVES: To characterise the inflammatory cell infiltrate in varicose vein wall, and its relationship to the valve complex. DESIGN: A comparative study of the distribution of inflammatory cells in normal and varicose vein. MATERIALS: Specimens of proximal human long saphenous vein were obtained from patients with duplex Doppler confirmed long saphenous vein reflux (n=14). Control vein was obtained from patients undergoing coronary artery bypass without clinical evidence of venous insufficiency (n=6). Longitudinal 7 microm frozen sections of vein, displaying valve, were prepared. METHODS: Using immunohistochemistry, T-lymphocytes (CD3), macrophage/monocytes (CD68), neutrophils (CD15s) and mast cells (anti-mast cell tryptase) were identified. The number of cells per unit length vein were counted using light microscopy. RESULTS: There were significantly more mast cells and macrophage/monocytes in varicose vein as compared to control. There was a non-significant trend towards more T-lymphocytes in varicose vein. Few neutrophils were present in varicose or normal vein. The distribution of inflammatory cells with respect to the valve was not found to be significant. CONCLUSIONS: Varicose veins display a greater inflammatory cell infiltrate than normal vein. The key role of macrophage/monocytes and mast cells in tissue damage and remodelling should stimulate further research into whether they play a significant role in the development of chronic venous insufficiency.
OBJECTIVES: To characterise the inflammatory cell infiltrate in varicose vein wall, and its relationship to the valve complex. DESIGN: A comparative study of the distribution of inflammatory cells in normal and varicose vein. MATERIALS: Specimens of proximal human long saphenous vein were obtained from patients with duplex Doppler confirmed long saphenous vein reflux (n=14). Control vein was obtained from patients undergoing coronary artery bypass without clinical evidence of venous insufficiency (n=6). Longitudinal 7 microm frozen sections of vein, displaying valve, were prepared. METHODS: Using immunohistochemistry, T-lymphocytes (CD3), macrophage/monocytes (CD68), neutrophils (CD15s) and mast cells (anti-mast cell tryptase) were identified. The number of cells per unit length vein were counted using light microscopy. RESULTS: There were significantly more mast cells and macrophage/monocytes in varicose vein as compared to control. There was a non-significant trend towards more T-lymphocytes in varicose vein. Few neutrophils were present in varicose or normal vein. The distribution of inflammatory cells with respect to the valve was not found to be significant. CONCLUSIONS: Varicose veins display a greater inflammatory cell infiltrate than normal vein. The key role of macrophage/monocytes and mast cells in tissue damage and remodelling should stimulate further research into whether they play a significant role in the development of chronic venous insufficiency.