Immunological mechanisms of arterial damage in pediatric patients with primary hypertension.

Primary hypertension is a disease that is being diagnosed with increasing frequency in pediatric patients, and many of them are found to have hypertension-mediated organ damage (HMOD), including arterial damage. The pathophysiology of primary hypertension and the formation of HMOD is multifactorial. One mechanism studied in recent years is the subclinical inflammation accompanying the elevation of blood pressure. Experimental studies, studies in adults and children, revealed the involvement of immune mechanisms in the formation of vascular lesions in the course of primary hypertension. The paper summarizes the current knowledge on this subject and points to possible therapeutic targets. Particular emphasis is placed on data from pediatric patients with primary hypertension, as a relation between arterial damage (early vascular aging) and immune system activation had already been found in children. The correct identification of immunological mechanisms may not only broaden our understanding of primary hypertension as a disease but also, more importantly, lead to the most effective methods of its treatment.

24-hour central blood pressure and immune system activation in adolescents with primary hypertension - a preliminary study.

Introduction: Adult and pediatric data suggest a positive relationship between the extent of subclinical inflammation, blood pressure, and hypertension-mediated organ damage (HMOD) in primary hypertension (PH). 24-hour (24-h) ambulatory blood pressure (ABPM) and central blood pressure (CBP) are strong predictors of HMOD. Our study aimed to analyze the relationship between 24-h central ABPM, subclinical inflammation, and clinical data in adolescents with PH. Material and methods: In 28 untreated adolescents with PH (14.50 ±2.27 years) and 25 healthy peers (14.76 ±2.83 years), we analyzed 24-h peripheral and central ABPM, markers of subclinical inflammation (neutrophil-to-lymphocyte ratio - NLR, platelet-to-lymphocyte ratio - PLR, mean platelet volume - MPV), and clinical and biochemical data. Results: Patients with PH had higher 24-h peripheral and central blood pressure than healthy peers. In all 53 patients, we found significant (p < 0.05) positive correlations between NLR, PLR and 24-h central systolic, diastolic, and mean blood pressure (24-h cSBP, 24-h cDBP, 24-h cMAP), between 24-h central augmentation index corrected for heart rate 75 (24-h cAIx75HR) and platelet count. In 28 patients with PH, 24-h cAIx75HR correlated with low-density lipoprotein (LDL) cholesterol (R = 0.442), and ambulatory arterial stiffness index with body mass index (BMI) (R = 0.487), uric acid (R = 0.430), and high-density lipoprotein (HDL) cholesterol (R = -0.428). Conclusions: Increased central 24-h blood pressure may be associated with immune system activation in adolescents with primary hypertension. In adolescents with primary hypertension, dyslipidemia and hyperuricemia are risk factors for increased arterial stiffness. Further studies on central and peripheral blood pressure in terms of their relationship with inflammation in these patients are needed.