Abstract
Endothelial progenitor cells (EPCs) have reparative potential in overcoming the endothelial
dysfunction and reducing cardiovascular risk. EPC depletion has been demonstrated
in the setting of established atherosclerotic diseases. We evaluated whether reduced
EPCs population are associated with endothelial dysfunction, subclinical atherosclerosis,
and inflammatory markers in ankylosing spondylitis (AS) patients without any known
traditional cardiovascular risk factor. We performed a cross-sectional study of 30
consecutive AS patients and 25 age- and sex-matched healthy controls. Patients with
traditional cardiovascular risk factors were excluded. Circulating EPCs (CD34+/CD133+) were quantified by flow cytometry. The assessment of endothelial function by brachial
artery flow-mediated dilatation (FMD) and ultrasound assessment of carotid intima-media
thickness (CIMT) was measured in both the groups. EPCs cells were significantly (0.020 ± 0.001
vs. 0.040 ± 0.010%, p < 0.001) reduced in patients with AS compared with healthy controls. Endothelial
function (7.35 ± 2.54 vs. 10.27 ± 1.73, p = 0.002), CIMT (0.63 ± 0.01 vs. 0.35 ± 0.02, p < 0.001), and inflammatory markers were also significantly (p < 0.01) altered as compared with controls. EPCs inversely correlated with tumor necrosis
factor (TNF)-α and C-reactive protein (CRP) and positively correlated with endothelial
function. Present study results demonstrate depleted EPC population in AS patients
compared with controls. Increased level of CRP and TNF-α appears to play a key role
in EPC depletion and the latter contributes to endothelial dysfunction and atherosclerosis
in AS. EPC population would, therefore, represent an attractive measure of endothelial
dysfunction and accelerated atherosclerosis disease associated with AS.
Keywords
ankylosing spondylitis - endothelial progenitor cells - endothelial function - carotid
intima-media thickness - inflammation
