Endothelial dysfunction in ankylosing spondylitis associated with reduced endothelial progenitor cell population

Authors

  • Pawan Krishan Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India
  • Inderjeet Verma Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India
  • Ashit Syngle Cardio Rheuma and Healing Touch City Clinic, Chandigarh and Rheumatologist Fortis Multi Specialty Hospital, Mohali, India

DOI:

https://doi.org/10.15305/ijrci/v3i1/130

Keywords:

Endothelial dysfunction, endothelial progenitor cells, ankylosing spondylitis, cardiovascular risk and inflammation

Abstract

Background: Endothelial dysfunction, and cardiovascular (CV) morbidity and mortality have been documented in patients with ankylosing spondylitis (AS). Endothelial progenitor cells (EPCs) have reparative potential in overcoming the endothelial dysfunction and reducing cardiovascular risk.

Aim: To investigate the relationship between endothelial function and EPCs in patients with AS in a cross-sectional study.

Methods: Circulating EPCs (CD34+/CD133+) were isolated and quantified from peripheral blood samples of AS (n23) and healthy controls (n=20) matched for  age and sex. Endothelium-depended vascular function, i.e. flow-mediated dilation (FMD), was assessed for all subjects. Disease activity was evaluated using Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Functional ability was monitored using Bath Ankylosing Spondylitis Functional Index (BASFI). All subjects were free of any other known traditional CV risk factors.

Results: AS patients had depleted level of circulating %EPCs (0.028 ± 0.001% versus 0.045 ± 0.011%, P <0.001) and reduced FMD% (6.77 ± 2.15 versus 10.06 ± 0.55, P <0.001) than healthy controls. Circulating EPC population significantly positively correlated with FMD% (r 0.538, P = 0.008). Levels of CD34+/CD133+ putative cells showed a significant inverse correlation with disease duration (P = 0.01), BASDAI (P = 0.04), ESR (P = 0.002) and CRP (P = 0.007).

Conclusion: AS patients, free of any other known CV risk factors, demonstrated depleted levels of EPCs and reduced endothelial function. These alterations may cause further deterioration of endothelial function in AS patients. EPC would possibly serve as a novel therapeutic target for preventing cardiovascular risk in AS.

 

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Published

12-06-2015

Issue

Vol. 3 No. 1 (2015)

Section

Original Articles

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