• Sao Paulo Med J · Nov 2018

    Vascular endothelial growth factor, endostatin levels and clinical features among patients with ulcerative colitis and irritable bowel syndrome and among healthy controls: a cross-sectional analytical study.

    • Evrim Kahramanoğlu Aksoy, Hülya Çetinkaya, Berna Savaş, Arzu Ensari, Murat Torgutalp, and Cumali Efe.
    • MD. Physician, Department of Gastroenterology, Keçiören Training and Research Hospital, Ankara, Turkey.
    • Sao Paulo Med J. 2018 Nov 1; 136 (6): 543550543-550.

    BackgroundIncreased angiogenetic activity in inflammatory bowel disease (IBD) has been shown in previous studies. The aim of this study was to evaluate the relationship of serum vascular endothelial growth factor (VEGF) and endostatin levels with clinical features and mucosal expression in patients with ulcerative colitis (UC).Design And SettingCross-sectional analytical study conducted in a tertiary-level public hospital.MethodsSerum VEGF and endostatin levels were determined in 82 individuals: 39 with UC, 28 with irritable bowel syndrome (IBS) and 15 healthy controls (HCs), using enzyme-linked immunosorbent assays (ELISA). VEGF and endostatin expressions were studied using immunohistochemistry (IHC).ResultsMean serum VEGF and endostatin levels were significantly higher in patients with UC than in patients with IBS and in HCs (511.9 ± 377.5 pg/ml, 305.0 ± 121.42 pg/ml and 36.1 ± 40.6 pg/ml; P = 0.001 for VEGF; and 155.50 ± 59.8 ng/ml, 116.9 ± 23.8 ng/ml and 102.2 ± 22.4 ng/ml; P < 0.001 for endostatin, respectively). There was a positive correlation between serum VEGF and endostatin levels (r = 0.422; P < 0.01). Mean H-scores for VEGF expression were higher in the active UC group than in the inactive UC and IBS groups, in the stroma, endothelium and epithelium. Mean H-scores for endostatin expression were higher in the active UC group than in the inactive UC and IBS groups, in the stroma and endothelium. There was no endostatin expression in the epithelium.ConclusionIncreased endostatin appears to be a defensive reaction to increased VEGF in patients with UC.

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