The results of multivariate analysis are shown in Table 5. and of ICAM-1 C uric acid (= 0.430, 95% CI: 0.040-0.819). In 27 children with newly diagnosed PH E-selectin correlated negatively with diastolic blood pressure dipping AZD-5904 (r = C0.54, p = 0.004) and positively with ambulatory arterial stiffness index (r = 0.51, p = 0.012). Conclusions Elevated mean arterial pressure and hyperuricemia are risk factors of endothelial damage in paediatric patients with main hypertension. In children with untreated main hypertension there may be a relation between endothelial damage and disturbed circadian blood pressure profile. Mann-Whitney test, ANOVA, Kruskal-Wallis test, Pearson linear correlation, Spearman rank correlation, and Fishers exact test. Multivariate analysis was performed using a general regression model. Parameters that correlated with markers of endothelial injury with 0.300 in AZD-5904 univariate analysis were included in the final model. A (%)50/27 (64.9/35.1)Duration of arterial hypertension, months17.63 19.09 (5-26)BMI, kg/m2(%)33 (42.9)Calcium channel antagonists24Angiotensin converting enzyme inhibitors15AT1 receptor antagonists3-adrenolytics3Diuretics1-adrenolytics1 Open in a separate windows SBP C systolic blood pressure, DBP C diastolic blood pressure, BMI C body mass index, AT1 C angiotensin II receptor type 1 Table 2 Results of ambulatory blood pressure monitoring in children with main hypertension = 0.600, and 304.29 53.13 vs. 305.67 77.92 vs. 292.02 67.39 [ng/ml], = 0.782, respectively). Also, no relation between treatment with the two most commonly used antihypertensive drugs (calcium channel blockers and angiotensin transforming enzyme inhibitors) and the concentration of markers of endothelial damage was found. E-selectin was significantly higher in 50 males than in 27 ladies (60.02 26.56 vs. 47.49 24.80 [ng/ml], = 0.047), but there was no significant difference in ICAM-1 between boys and girls (312.63 72.44 vs. 282.80 51.86 [ng/ml], = 0.062). Open in AZD-5904 a separate windows Fig. 1 E-selectin in children with main hypertension (p = 0.600) Open in a separate windows Fig. 2 Intercellular adhesion molecule (ICAM-1) in children with main hypertension (p = 0.782) The relation between markers of endothelial injury and selected clinical, biochemical, and inflammatory parameters are depicted in Table 4. In the whole group of 77 patients E-selectin and ICAM-1 concentrations correlated with BMI = 0.29, = 0.038). The results of multivariate analysis are shown in Table 5. In multivariate analysis using a general AZD-5904 regression model the only significant predictors of markers of endothelial injury were mean arterial pressure during 24 hours in ABPM expressed as = 0.042) and uric acid for ICAM-1 ( = 0.430, 95% CI: 0.040-0.819, = 0.031). Table 4 The correlation between markers of endothelial injury and selected clinical, biochemical, and inflammatory indicators in children with main hypertension = C0.54, = 0.004) and positively with AASI (= 0.51, = 0.012). Conversation Our cross-sectional analysis revealed that this strongest predictors of endothelial damage in pediatric patients with main hypertension were MAP in ABPM (for E-selectin) and serum uric acid (for ICAM-1). Additionally, overweight and obesity, low HDL-cholesterol, increased BP variability, and higher degree of subclinical inflammation may also be factors predisposing to endothelial dysfunction in this group of patients. Interestingly, in the subgroup of untreated, newly diagnosed patients we found also positive correlations of E-selectin Rabbit polyclonal to NF-kappaB p65.NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA, or RELB (MIM 604758) to form the NFKB complex. with night-time DBP dipping, and most importantly with stiffness evaluated as AASI. The Stanislas study evaluated the concentration of adhesion molecules in healthy children and adults . Both ICAM-1 and E-selectin were inversely related to age in paediatric patients, but this relationship disappeared in multivariate analysis for E-selectin . There was no relation between sex and level of adhesion molecules. In our cohort we found no relation of these biomarkers with age, and the relationship with sex was not confirmed in multivariate analysis. The discrepancy between our results and results in healthy individuals must be analysed with caution. It is probable that other factors determine endothelial function in hypertensive and normotensive individuals. There is a pathophysiological link between inflammation and concentration of circulating adhesion molecules. Leukocytes secrete cytokines.