INTRODUCTION: vascular endothelial growth factor (VEGF) and tumour necrosis factor alpha (TNF(alpha)) have been specifically implicated in the tissue damage associated with chronic venous disease (CVD). Furthermore, production of both factors is known to be upregulated in vessel wall cells subject to hypertension. The aim of this study was to determine the local venous levels of VEGF and TNF(alpha) in limbs with venous ulcers before and after treatment with graduated compression. PATIENTS AND METHODS: eight patients with venous ulcers and 8 patients with varicose veins only were included in the study. For ulcer patients, serum samples were taken from the superficial veins in lower limbs and repeated after 4 weeks of treatment with 4-layered graduated compression. Serum from the arms of the same patients served as controls. Determination of the concentrations of VEGF and TNF(alpha) proteins were performed with sandwich enzyme-linked immunosorbent assays. RESULTS: both groups of patients had elevated levels of VEGF and TNF(alpha). In patients with venous ulcers there was a reduction in the levels of both cytokines to below control values with treatment. These changes correlated with healing of the ulcers as determined by reduction in ulcer size. CONCLUSION: these data, for the first time, suggest a central role for both TNF(alpha) and VEGF in the pathogenesis of venous ulceration which may constitute a causative link between venous hypertension and tissue pathology. Copyright 2002 Harcourt Publishers Limited.
INTRODUCTION:vascular endothelial growth factor (VEGF) and tumour necrosis factor alpha (TNF(alpha)) have been specifically implicated in the tissue damage associated with chronic venous disease (CVD). Furthermore, production of both factors is known to be upregulated in vessel wall cells subject to hypertension. The aim of this study was to determine the local venous levels of VEGF and TNF(alpha) in limbs with venous ulcers before and after treatment with graduated compression. PATIENTS AND METHODS: eight patients with venous ulcers and 8 patients with varicose veins only were included in the study. For ulcerpatients, serum samples were taken from the superficial veins in lower limbs and repeated after 4 weeks of treatment with 4-layered graduated compression. Serum from the arms of the same patients served as controls. Determination of the concentrations of VEGF and TNF(alpha) proteins were performed with sandwich enzyme-linked immunosorbent assays. RESULTS: both groups of patients had elevated levels of VEGF and TNF(alpha). In patients with venous ulcers there was a reduction in the levels of both cytokines to below control values with treatment. These changes correlated with healing of the ulcers as determined by reduction in ulcer size. CONCLUSION: these data, for the first time, suggest a central role for both TNF(alpha) and VEGF in the pathogenesis of venous ulceration which may constitute a causative link between venous hypertension and tissue pathology. Copyright 2002 Harcourt Publishers Limited.
Authors: Ewa A Burian; Lubna Sabah; Tonny Karlsmark; Klaus Kirketerp-Møller; Christine J Moffatt; Jacob P Thyssen; Magnus S Ågren Journal: Int J Mol Sci Date: 2022-06-10 Impact factor: 6.208
Authors: Javier Barallobre-Barreiro; Rahmi Oklu; Marc Lynch; Marika Fava; Ferheen Baig; Xiaoke Yin; Temo Barwari; David N Potier; Hassan Albadawi; Marjan Jahangiri; Karen E Porter; Michael T Watkins; Sanjay Misra; Julianne Stoughton; Manuel Mayr Journal: Cardiovasc Res Date: 2016-04-11 Impact factor: 10.787