Increased soluble selectins as a reflection of activated platelets and endothelium in Legg-Calve-Perthes disease

Legg-Calve-Perthes disease (LCPD) is still an enigma. Hemostatic abnormalities have been indicated in the pathogenesis. We had previously demonstrated enhanced tissue factor pathway inhibitor response, increased global fibrinolytic capacity, and an increase in thrombomodulin in patients with LCPD compared with healthy individuals. These studies emphasized the role of vascular endothelium in pathogenesis of the LCPD. P-selectin is expressed on activated platelets and endothelial cells, and E-selectin is expressed on activated endothelial cells. The aim of this study was to assess circulating E-selectin and P-selectin levels in LCPD patients, which might reflect an endothelium activation and/or injury. The study included 85 pediatric patients. Group I consisted of 55 patients with LCPD and group II (control) consisted of 30 healthy children. Peripheral venous blood concentrations of E-selectin and P-selectin levels were measured with a commercially available assay. Mean age was 8.41±2.73 years in group I and 8.83±2.92 years in group II. Both E-selectin and P-selectin levels were higher in LCPD patients in comparison with the age-matched controls. E-selectin was 54.92±18.84 pg/mL in group I, 45.54±15.31 pg/mL in group II and P-selectin was 46.40±20.35 pg/mL in group I, 36.92±9.84 pg/mL in group II (P=0.022 and P=0.019, respectively). On the basis of our results, two important endothelium and platelet markers, E-selectin and P-selectin, are upregulated in LCPD. Our results suggested that activated platelets and possibly endothelial activation, as reflected by enhanced P-selectin/E-selectin kinetics, might contribute to the microvascular thrombosis and/or inflammation of LCPD.