Journal
PLATELETS
Volume 20, Issue 7, Pages 493-497Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/09537100903165174
Keywords
Psoriatic arthritis; psoriasis; platelet-monocyte complexes; CD40L; E-selectin; inflammation
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We evaluated platelet and endothelial activation parameters in psoriatic arthritis (PsA), a disease reported to be associated with the development of endothelial dysfunction and increased atherosclerotic complications. Twenty patients with PsA, eight psoriasis and 20 healthy controls were included into the study. The patients' clinical features and acute phase parameters were assessed. In all patients and controls, platelet-monocyte complexes (PMC), platelet-neutrophil complexes (PNC), and basal and ADP-stimulated P-selectin expression were determined with flow cytometry; soluble E-selectin (sE-selectin) and soluble CD40L (sCD40L) were determined with ELISA. Patterns of joint involvement and degrees of skin involvement in PsA patients were assessed. PMC in PsA patients were significantly higher than in the control group (p = 0.02). PNC were not significantly different among the three groups (p values > 0.05). sE-selectin levels in both PsA and psoriasis groups were significantly higher than in healthy controls (p values, respectively, <0.001 and 0.023). Basal and ADP-stimulated CD62P expression and sCD40L level were similar in all groups (p values > 0.05). Polyarticular PsA patients had significantly higher sCD40L than oligoarticular plus spondylitic PsA groups (p = 0.04). sCD40L level was higher in active PsA group than in inactive PsA group (p = 0.03). Groups with limited and extensive skin involvement did not differ significantly in the evaluated parameters. C-reactive protein (CRP) level in PsA patients correlated with sCD40L (r = 0.69, p = 0.012), basal CD62P expression (r = 0.89, p < 0.001) and ADP-stimulated CD62P expression (r = 0.73, p = 0.001). Endothelial activation might be have a role in the pathogenesis of both psoriasis and PsA. Among parameters of platelet activation, only PMC might play a role in the pathogenesis of PsA.
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