Vascular endothelial growth factor and monocyte chemoattractant protein-1 in Behçet's patients with venous thrombosis

• Published in: Clinical and experimental rheumatology 2005-07, Vol.23 (4 Suppl 38), p.S42-S48
• Main Authors: Bozoglu, E, Dinc, A, Erdem, H, Pay, S, Simsek, I, Kocar, I H
• Format: Article
• Language: English
• Subjects: Acute Disease; Acute-Phase Proteins - analysis; Adult; Behcet Syndrome - blood; Behcet Syndrome - complications; Behcet Syndrome - pathology; Chemokine CCL2 - blood; Chronic Disease; Female; Genital Diseases, Female - blood; Genital Diseases, Female - etiology; Genital Diseases, Female - pathology; Genital Diseases, Male - blood; Genital Diseases, Male - etiology; Genital Diseases, Male - pathology; Humans; Male; Oral Ulcer - blood; Oral Ulcer - etiology; Oral Ulcer - pathology; Tumor Necrosis Factor-alpha - analysis; Vascular Endothelial Growth Factor A - blood; Venous Thrombosis - blood; Venous Thrombosis - complications; Venous Thrombosis - pathology
• ISSN: 0392-856X

Vascular lesions can involve both arterial and venous systems which are often the major causes complicating the disease course of Behçet's disease (BD). Vascular endothelial growth factor (VEGF) is a stimulant of angiogenesis secondary to ischemia while monocyte chemoattractant protein 1 (MCP-1) is induced by shear stresses leading to vascular collateral development. MCP-1 has been also shown to contribute to the recanalization of venous thrombi. Tumor necrosis factor-alpha (TNF-alpha) is known to play a major role in the pathogenesis of BD. Furthermore, up-regulation of secreted MCP-1 and VEGF was observed following stimulation with TNF-alpha. In view of the above functions of VEGF, MCP-1 and TNF-alpha, we hypothesized that these factors may be important in the pathogenesis of thrombosis seen in BD. A total of 36 patients with a diagnosis of BD were studied. BD patients were separated into 3 groups with respect to vascular involvement. Group BD-AT (n = 9) with acute thrombosis, BD-CT (n = 12) with chronic thrombosis and BD-MC (n = 15) with mucocutaneous involvement only. The control group (group H) was comprised of 20 healthy persons. In addition, patients with acute, DC-AT (n= 11) and patients with chronic DC-CT (n = 9) thrombosis without BD served as disease controls. Serum measurements of VEGF MCP-1 and TNF-alpha were performed by quantitative sandwich ELISA. The acute phase reactants, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were also measured. The levels of VEGF were significantly higher in the patients in group BD-AT than either in group BD-CT or BD-MC (p = 0.03 and p < 0.001, respectively). However, no significant difference was found for VEGF levels of thrombotic patients regarding the cause (BD-AT vs. DC-AT, p = 0.063; BD-CT vs. DC-CT, p = 0.084) or the stage of thrombosis (DC-AT vs. DC-CT, p > 0.05). Both BD patients and disease controls with acute thrombosis had significantly higher levels of MCP-1 as compared to corresponding chronic thrombosis patients (BD-AT vs. DC-CT; p < 0.001; DC-AT vs. DC-CT, p < 0.001). Patients with BD and disease controls had significantly higher serum TNF-alpha level when compared with healthy subjects. No significant difference with respect to serum TNF-alpha level was noted when patient subgroups with BD and disease controls were compared with each other Serum levels of VEGF, MCP-1, and TNF-alpha were not found to be correlated with either ESR or CRP (p > 0.05). Increased levels o