Dysregulation of angiogenic homeostasis in systemic sclerosis
Article first published online: 2 JUL 2013
© 2013 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd
International Journal of Rheumatic Diseases
Volume 16, Issue 4, pages 448–454, August 2013
How to Cite
Farouk, H. M., Hamza, S. H., El Bakry, S. A., Youssef, S. S., Aly, I. M., Moustafa, A. A., Assaf, N. Y. and El Dakrony, A. H. M. (2013), Dysregulation of angiogenic homeostasis in systemic sclerosis. International Journal of Rheumatic Diseases, 16: 448–454. doi: 10.1111/1756-185X.12130
- Issue published online: 31 AUG 2013
- Article first published online: 2 JUL 2013
- systemic sclerosis;
- vascular endothelial growth factor
Systemic sclerosis (SSc) is a connective tissue disorder characterized by tissue hypoxia and excessive fibrosis of skin and internal organs.
To evaluate the possible role of angiogenesis imbalance in the pathogenesis of SSc.
Subjects and methods
Twenty-five SSc patients and 20 age- and sex-matched healthy controls were included. Assay of serum vascular endothelial growth factor (VEGF) and endostatin was done for all patients and controls using enzyme-linked immunosorbent assay. Patients were subjected to modified Rodnan skin score (mRss), pulmonary function tests (PFTS) and skin biopsies for histopathological skin thickness score assessment.
There was significant increase in the mean levels of serum VEGF and endostatin in SSc patients compared to controls (t = 4.07, P < 0.001). Mean values of serum endostatin was significantly increased in late compared to early stages of disease (t = 6.65, P < 0.01). A significant positive correlation was found between serum levels of endostatin, mRss and histopathological skin thickness score (r = 0.99, 0.94, respectively, P < 0.01). SSc patients with ischemic manifestations had significantly higher levels of serum endostatin compared to those without ischemic manifestations (t = 6.27, P < 0.001). SSc patients with restricted PFTS had significantly higher levels of serum endostatin compared to those without pulmonary manifestations (t = 4.3, P < 0.001).
Angiogenic inhibitor (endostatin) is induced and outweighs angiogenic inducer (VEGF) in late stages of SSc. Increased serum endostatin is associated with skin sclerosis severity and pulmonary fibrosis and favors SSc disease progression.