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    Cytokine profile in psoriatic arthritis: search for relationships with inflammation and blood rheological properties

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    Objective. To estimate the serum levels of interleukins (IL) 6 and 10, tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in patients with psoriatic arthritis (PSA) and their relationship with the clinical and laboratory parameters of inflammation and with erythrocyte aggregation (EA). Material and methods. The authors measured the serum levels of C-reactive protein (CRP) by immunonephelometry (BN, ProSPEC, Siemens) and those of TNF-α, IL-6 and IL-10, and VEGF by X-MAP technology using a BioPlex-200 system (Panel Human 27-Plex Bio-Rad, USA) in 80 patients with PSA [45 women and 35 men; mean age 41.7±10.5 years, mean duration of PSA and psoriasis was 5.0 (2.0; 12,5) and 15 (4; 26) years, respectively; DAS 3.9 (3.09; 5.16)]. The blood samples from 16 healthy donors matched to the examinees for gender and age served as a control. The parameters of EA [Т1(с); Кt (arb. units); β (с-1), I2,5 (%)] were estimated, by recording the rate of back light scattering. The median (Me) and interquartile range [Q25; Q75], and mean and standard deviations (M±σ) were calculated; the indicators were compared by the Mann-Whitney test and Student's t test. Correlation analysis was made using the Spearman rank correlation coefficient (R); p < 0.05 was considered statistically significant. Results. There were significantly higher serum levels of IL-6 and IL-10, TNF-α, and VEGF in patients with PSA than in the controls, and impaired blood rheological properties. There were significant correlations of the level of most cytokines (IL-6 and IL-10, VEGF) with both the values of the clinical and laboratory activity of PSA (self-rated pain, the number of swollen and tender joints, a physician's assessment of disease activity, DAS, erythrocyte sedimentation rate, and fibrinogen) and most parameters of EA (Т1, Kt и I2.5). No significant relationships were found between VEGF and CRP. Conclusion. The enhanced clinical and laboratory activity of PSA is attended by the systemic activation of immunological mediators of inflammation and neoangiogenesis and by impaired blood rheological properties, which supports the interaction of these factors in the immunopathogenesis of the diseases
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