4.2 Article

Endothelial progenitor cell levels in juvenile idiopathic arthritis patients; effects of anti-inflammatory therapies

Journal

PEDIATRIC RHEUMATOLOGY
Volume 13, Issue -, Pages -

Publisher

BMC
DOI: 10.1186/s12969-015-0001-4

Keywords

Endothelial progenitor cells; Juvenile idiopathic arthritis; Cardiovascular risk factors; Anti-inflammatory therapies

Funding

  1. Medical University of Bialystok
  2. National Leading Research Centre in Bialystok

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Background: Juvenile idiopathic arthritis (JIA), similarly to other arthritides, can be associated with damage of endothelial layer of which structure and function is dependent on reparative properties of endothelial progenitor cells (EPC). To date, it remained unknown whether EPC numbers are altered in young JIA patients and whether on-going anti-inflammatory therapies could exert positive effects on these progenitor cells. Methods: We performed a quantitative analysis of EPC numbers in 25 patients diagnosed with JIA according to International League of Associations for Rheumatism (ILAR) criteria [age 11.50 (7.50-15.00) years] in a broad context of inflammatory and cardiovascular parameters as well as different types of anti-inflammatory treatments. 11 healthy children [age 13.00 (11.00-14.00) years] were recruited as a control group. Results: We demonstrated that EPC numbers were similar in JIA patients and control subjects (0.02% vs. 0.05%, respectively, p = 0.37). EPC levels in JIA patients were negatively correlated with index of insulin resistance (rho = -0.458, p = 0.021), endogenous insulin (rho = -0.472, p = 0.017), triglyceride (rho = -0.438, p = 0.029) and TNF-alpha levels (rho = -0.446, p = 0.026). Notably, glucocorticoid (GC) therapy, was associated with detection of decreased EPC levels in JIA patients (p = 0.023). In contrast, methothrexate (MTX) and etanercept therapy in JIA patients did not affect EPC levels (p = 0.92 and p = 0.08, respectively). Conclusions: We found that EPC numbers are maintained at normal levels in JIA patients and are not enhanced by disease-specific anti-inflammatory treatments.

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