Complete blood count-derived inflammatory markers in adolescents with primary arterial hypertension: a preliminary report

原发性动脉高血压青少年全血细胞计数衍生炎症标志物:初步报告

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Abstract

AIM OF THE STUDY: The aim of our study was to evaluate selected inflammatory markers in children with untreated primary hypertension and to establish the relation between inflammatory markers and 24-hour ambulatory blood pressure monitoring (ABPM) and clinical and biochemical parameters. MATERIAL AND METHODS: In 54 children (15.12 ±2.02 years) with untreated primary hypertension, with excluded overt inflammation, we evaluated: neutrophils (NEU; 1000/μl), lymphocytes (LYM; 1000/μl), platelets (PLT; 1000/μl), mean platelet volume (MPV; fl), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), ABPM (OSCAR 2 SUNTECH), and selected clinical and biochemical parameters. The control group consisted of 20 healthy children (15.55 ±2.27 years). RESULTS: Children with primary hypertension had (p < 0.01) higher 24-hour systolic, diastolic and mean blood pressure, systolic and diastolic blood pressure loads, and pulse pressure. Hypertensive children did not differ in inflammatory indicators (NEU, LYM, PLT, MPV, NLR, PLR) from the control group. In 54 hypertensive children we found the following correlations: between office systolic and diastolic blood pressure and MPV (r = 0.35, p = 0.011, r = 0.36, p = 0.008), between 24-hour ambulatory mean arterial pressure Z-score and NLR (r = 0.30, p = 0.030), 24-hour systolic blood pressure load and NLR (r = 0.38, p = 0.005), plasma renin activity and neutrophil count, NLR, PLR (r = 0.47, p = 0.016, r = 0.64, p < 0.001, r = 0.42, p = 0.033), urinary albumin loss and neutrophil count, NLR (r = 0.46, p = 0.001 and r = 0.42, p = 0.003). Multivariate analysis revealed that office SBP Z-score was related to MPV (β = 0.35, p = 0.008) and albuminuria to neutrophil count (β = 0.62, p = 0.018). CONCLUSIONS: In children with primary arterial hypertension there may be a relation between blood pressure, urinary albumin loss, and subclinical inflammation.

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