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ORIGINAL ARTICLE
Year : 2016  |  Volume : 11  |  Issue : 1  |  Page : 14-20

Endothelial progenitor cell biology in psoriatic arthritis patients in the absence of traditional cardiovascular risk


1 Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India
2 Cardio Rheuma and Healing Touch City Clinic, Chandigarh; Fortis Multi Specialty Hospital, Mohali, India

Correspondence Address:
Pawan Krishan
Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.1016/j.injr.2015.11.001

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Introduction: Endothelial progenitor cells (EPCs) restore dysfunctional endothelium and protect against atherosclerotic vascular disease. EPC population has been assessed in a heterogeneous population with equivocal results in psoriatic arthritis (PsA) patients with confounding factors. The aim of this study was to investigate EPC population in PsA patients in the absence of traditional cardiovascular risk factors. Methods: 22 active PsA patients and 20 age- and sex-matched healthy controls were includ- ed. EPCs (CD34+/CD133+) were assessed by Flow Cytometry. Endothelial function was assessed by measuring flow-mediated dilatation (FMD%) and carotid intima-media thick- ness (CIMT) was assessed by ultrasonography. Inflammatory markers, i.e. erythrocyte sedimentation rate, C-reactive protein (CRP), tumor necrosis factor (TNF)-a, interleukin (IL)-6, and IL-1, were also assessed in all subjects. Results: EPC population was significantly lower in PsA patients compared with controls (mean 0.028% vs. 0.047%, p < 0.001). FMD and inflammatory markers were also significantly (p < 0.05) altered as compared to healthy controls, but there was no significant difference in CIMT (mean 0.65 vs. 0.56, p = 0.068). Specifically, CD34+CD133+cells correlated positively with FMD (r = 0.66, p = 0.002) and inversely correlated with CRP (r = -0.65, p = 0.002), TNF-a (r = -0.58, p = 0.01), IL-6 (r = -0.64, p = 0.003), disease activity measures (DAS-28 (r = -0.63, p = 0.004), and disease activity index for PsA (r = -0.53, p = 0.02)). Conclusions: EPC population is depleted in PsA patients in the absence of traditional cardio- vascular risk. Inflammation appears to play a key role in EPC depletion and the latter contributes to endothelial dysfunction in PsA.


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