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

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• 作者：Inderjeet Verma^a ; Ashit Syngle^b ; ^c ; Pawan Krishan^a ; ^{pawankrishan45@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Psoriatic arthritis ; Endothelial progenitor cells ; Endothelial function ; Sub-clinical atherosclerosis ; Inflammatory cytokines
• 刊名：Indian Journal of Rheumatology
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：11
• 期：1
• 页码：14-20
• 全文大小：761 K

文摘

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 included. EPCs (CD34⁺/CD133⁺) were assessed by Flow Cytometry. Endothelial function was assessed by measuring flow-mediated dilatation (FMD%) and carotid intima-media thickness (CIMT) was assessed by ultrasonography. Inflammatory markers, i.e. erythrocyte sedimentation rate, C-reactive protein (CRP), tumor necrosis factor (TNF)-α, 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-α (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 cardiovascular risk. Inflammation appears to play a key role in EPC depletion and the latter contributes to endothelial dysfunction in PsA.