Serum vascular endothelial growth factor (VEGF), soluble VEGF receptor-1 (sVEGFR-1) and sVEGFR-2 in systemic sclerosis patients: Relation to clinical manifestations and capillaroscopy findings

作者
Saeedeh Shenavandeh,Taraneh Tarakemeh,Eskandar Kamali Sarvestani,Mohammad Ali Nazarinia
出处
期刊:The Egyptian Rheumatologist [Elsevier BV]
卷期号:39 (1): 19-24 被引量:19
标识
DOI:10.1016/j.ejr.2016.03.004
摘要

The role of angiogenesis in the pathogenesis of systemic sclerosis (SSc) is well known. The imbalance between vascular endothelial growth factor (VEGF) and their anti-angiogenic soluble receptors (sVEGFR-1 and VEGFR-2) has been proposed as a possible cause of microangiopathy. To determine the levels of VEGF, sVEGFR-1 and sVEGFR-2 and the VEGF/sVEGFR1 and VEGF/sVEGFR2 ratios in SSc patients and to study their relation with clinical manifestations and capillaroscopy findings. The study included 44 SSc patients and 44 controls. The sclerosis severity was assessed by the modified Rodnan skin score (mRss) and capillaroscopy performed in patients. Serum VEGF, sVEGFR-1 and sVEGFR-2 were measured in patients and control. SSc patients had a mean age of 40.7 ± 12.8 years, M:F (1:9) and disease duration was 56.2 ± 60.6 months. 27 patients (61.4%) had diffuse-SSc and 17 (38.6%) limited. The mean VEGF was significantly higher (363.4 ± 133.9 pg/ml) and sVEGFR-2 lower (2039.6 ± 109 pg/ml) in patients compared to control (93.9 ± 25.2 pg/ml and 2366 ± 116.5 pg/ml; p = 0.05 and p = 0.04, respectively). Serum levels of sVEGFR-2 in patients with early, active and nonspecific scleroderma pattern of capillaroscopy was higher in comparison to patients with late scleroderma pattern (p = 0.05). There were no significant differences in the studied parameters between those patients with and without digital ulcerations and interstitial pulmonary fibrosis. A significant correlation was found between mRss and VEGF (p = 0.04). An overproduction of VEGF, a potent angiogenic molecule or down regulated production of its natural inhibitors (sVEGFR-2) might be involved in the development of vasculopathy in SSc patients.

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