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

Abstract

BACKGROUND: Increased 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 SETTING: Cross-sectional analytical study conducted in a tertiary-level public hospital. METHODS: Serum 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). RESULTS: Mean 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. CONCLUSION: Increased endostatin appears to be a defensive reaction to increased VEGF in patients with UC.

Association of Circulating Vascular Endothelial Growth Factor Levels With Autoimmune Diseases: A Systematic Review and Meta-Analysis

“…Among 241 eligible studies meeting the inclusion criteria, 76 articles were excluded due to unextractable data, insufficient data on HCs, irrelevant VEGF sample type (urine/synovial fluid/tear fluid), or inappropriate disease control groups. Finally, 165 studies were included in the meta-analysis, with 28, 29, 40, 13, 8, 12, 16, 23, and six studies on SLE ( 20 , 21 , 26 – 51 ), RA ( 12 , 22 – 24 , 38 , 43 , 52 – 74 ), SSc ( 11 , 38 , 39 , 64 , 75 – 110 ), BD ( 111 – 123 ), KD ( 18 , 124 – 130 ), AS ( 55 , 73 , 131 – 140 ), IBD ( 141 – 156 ), PsA ( 12 , 14 , 135 , 136 , 157 – 175 ) and GD ( 10 , 176 – 180 ), respectively. The main study characteristics are summarized in Table 1 and Appendix 1 .…”

“…VEGF was reported to be overexpressed in the skin and peripheral blood of patients with PsA (14). Serum VEGF levels were shown to be elevated and to correlate with disease activity and severity in PsA, SLE, BD, IBD, KD, and AS (14)(15)(16)(17)(18)(19). These findings suggest VEGF as a potential pathogenic factor with promising diagnostic value in ADs.…”

Submucosal Clustered Brownish Microvessels Based on NBI Endoscopy: A Characteristic of LPR

“…The reflux of stomach contents during LPR can induce the expression of various inflammatory mediators in local tissues, such as IL‐8 and VEGF 34 . VEGF, as the most effective angiogenic growth factor, is associated with the aggravation of inflammation and is statistically correlated with microvessel density in inflammatory bowel disease 35 . Hence, it may play an important role in the differential appearance of submucosal CBMs and SBMs.…”

“…34 VEGF, as the most effective angiogenic growth factor, is associated with the aggravation of inflammation and is statistically correlated with density in inflammatory bowel disease. 35 Hence, it may play an important role in the differential appearance of submucosal CBMs and SBMs. In addition, the results of our study showed that the special submucosal microvascular morphology was mostly found in the PCA, which was adjacent to the entrance of the esophagus and thus more susceptible to reflux contents.…”

Thromboembolic and atherosclerotic cardiovascular events in inflammatory bowel disease: epidemiology, pathogenesis and clinical management

“…109 , 110 Both human and animal models provide evidence for upregulation of circulating and local intestinal adhesion molecules in IBD, together with vascular endothelial growth factor (VEGF), ICAM-1, MADCAM-1, and E-selectin. 111 – 113 The expression of these molecules is correlated to disease activity, shown by a fall in the concentration of ICAM-1 and VCAM-1 after treatment. 114 The expression of VEGF correlated with advancement of atherosclerotic lesions.…”