Background Ankylosing Spondylitis (AS) is an inflammatory disease associated with premature atherosclerosis.1 We hypothesized that depleted endothelial progenitor cells (EPCs), mediators of inflammation and Carotid intima media thickness (cIMT) are associated with atherosclerosis in other populations 2 and would be increased and associated with the severity of atherosclerosis in patients with AS.
Objectives The aim of this study was to assess EPC population, and its potential relationships with inflammatory cytokines, vascular function and marker of atherosclerosis in AS.
Methods We compared 30 patients of AS with 22 healthy controls. CD34
+, CD133+, were used to quantify EPCs using flow-cytometry. Flow-mediated dilatation (FMD) was assessed by using Angiodefender™ (Everest Genomic Ann Arbor, MI, United States). Carotid intima media thickness (cIMT) was measured using ultrasonography. Pro-inflammatory cytokines, TNFalpha, IL-1, IL-6, and inflammatory disease activity measures Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Functional ability was monitored by using Bath Ankylosing Spondylitis Functional Index (BASFI) were also assessed.
Results EPCs were significantly decreased in AS patients as compared to healthy controls (p=0.01). We also found significantly increased CIMT in AS group compared with controls (p=0.01). FMD was significantly impaired and inflammatory disease activity measures i.e. BASDAI, BASFI and serum concentrations of IL-6, TNF-α and IL-6 were higher in AS patients than controls (all P<0.05). Total cholesterol and high density lipoprotein cholesterol levels are significantly impaired in AS patients than controls (P<0.05). Significant positive correlation was observed between the percentage of EPCs, FMD and HDL cholesterol (P<0.05) and negative correlation was found between EPC and CIMT, IL-6, and BASDAI.
Conclusions EPCs are significantly associated endothelial dysfunction and subclinical atherosclerosis in AS. EPC depletion in AS possibly results from severe disease and elevated IL-6. Higher CV risk in AS is possibly also contributed by reduced EPCs, altered lipid profile and higher level of pro-inflammatory cytokines. Impaired EPC may lead to accelerated vascular remodelling due to chronic impairment of endothelial function.
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Disclosure of Interest None declared
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