We assessed the effects of 12 months of non-pharmacological and pharmacological therapy on 24-h ambulatory blood pressure, regression of target organ damage (TOD) and metabolic abnormalities in 86 children (14.1 ± 2.4 years) with primary hypertension. Twenty-four hour systolic and diastolic blood pressure (BP) decreased (130 ± 8 vs 126 ± 8, 73 ± 7 vs 70 ± 7, p = 0.0001 and 0.004 respectively). Body mass index (BMI) did not change, but waist-to-hip (0.85 ± 0.07 vs 0.83 ± 0.05, p = 0.01) and waist-to-height ratio (WHtR; 0.49 ± 0.07 vs 0.48 ± 0.05, p = 0.008) decreased. Left ventricular mass index (LVMi; 38.5 ± 10.7 vs 35.2 ± 7.5 g/m^2.7, p = 0.0001), prevalence of left ventricular hypertrophy (46.5% vs 31.4%; p = 0.0001), carotid intima-media thickness (cIMT; 0.44 ± 0.05 vs 0.42 ± 0.04 mm, p = 0.0001), wall cross sectional area (WCSA; 7.5 ± 1.3 vs 6.9 ± 1.2 mm², p = 0.002), hsCRP (1.1 ± 1.0 vs 0.7 ± 0.7 mg/l, p = 0.002), and LDL-cholesterol (115 ± 33 vs 107 ± 26 mg/dl, p = 0.001) decreased. Patients who had lowered BP had a lower cIMT at the second examination (0.41 ± 0.04 vs 0.43 ± 0.04 mm, p = 0.04) and lower initial hsCRP values (0.9 ± 0.7 vs 1.5 ± 1.3 mg/l, p = 0.04) in comparison to non-responders. Regression analysis revealed that the main predictor of LVMi decrease was a decrease in abdominal fat expressed as a decrease in waist circumference (WC) (R ² = 0.280, β = 0.558, p = 0.005), for WCSA-SDS a decrease in WC (R ² = 0.332, β = 0.611, p = 0.009) and for a cIMT-SDS decrease the main predictor was a decrease in hsCRP concentrations (R ² = 0.137, β = 0.412, p = 0.03). Standard antihypertensive treatment lowered BP and led to regression of TOD in hypertensive children. Lean body mass increase and decrease in abdominal obesity correlated with TOD regression.

Idiopathic infantile hypercalcemia (IIH) is a mineral metabolism disorder characterized by severe hypercalcemia, failure to thrive, vomiting, dehydration, and nephrocalcinosis. The periodical increase in incidence of IIH, which occurred in the twentieth century in the United Kingdom, Poland, and West Germany, turned out to be a side effect of rickets over-prophylaxis. It was recently discovered that the condition is linked to two genes, CYP24A1 and SLC34A1. The aim of the study was to search for pathogenic variants of the genes in adult persons who were shortlisted in infancy as IIH caused by “hypersensitivity to vit. D”. All persons were found to carry mutations in CYP24A1 or SLC34A1, nine and two persons respectively. The changes were biallelic, with one exception. Incidence of IIH in Polish population estimated on the basis of allele frequency of recurrent p.R396W CYP24A1 variant, is 1:32,465 births. It indicates that at least a thousand homozygotes and compound heterozygotes with risk of IIH live in the country. Differences in mechanism of developing hypercalcemia indicate that its prevention may vary in both IIH defects. Theoretically, vit. D restriction is a first indication for CYP24A1 defect (which disturbs 1,25(OH)₂D degradation) and phosphate supplementation for SLC34A1 defect (which impairs renal phosphate transport). In conclusion, we suggest that molecular testing for CYP24A1 and SLC34A1 mutations should be performed in each case of idiopathic hypercalcemia/hypercalciuria, both in children and adults, to determine the proper way for acute treatment and complications prevention.

We sought to describe the prevalence of metabolic abnormalities and of metabolic syndrome (MS) and its relationship to target-organ damage in children with primary hypertension (PH). Patients included 113 children with untreated PH at a mean age of 14.6 years (range, 5 to 18 years). The control group consisted of 134 healthy children at a mean age of 13.5 years (range, 5 to 20 years). We performed a cross-sectional assessment of anthropometric and biochemical cardiovascular risk factors, homeostatic metabolic assessment (HOMA-IR), the insulin sensitivity index (ISI[0,120]), and adiponectin. Metabolic syndrome, as defined by classic criteria, was present in 4 of 134 (3%) of controls versus 23 of 113 (20.4%) patients (P = .0001), but when PH was not taken as a criterion of MS, MS was diagnosed in 6.2% of patients (no significance). Left-ventricular hypertrophy (LVH) was found in 46 of 113 patients (40.7%), and severe LVH was found in 14 of 113 patients (12.5%). Patients with LVH had a greater body mass index, greater waist-to-hip-ratio, and greater number of parameters of metabolic syndrome (overall P < .05). Carotid (cIMT) and femoral superficial artery intima-media thicknesses correlated positively with HOMA-IR and negatively with ISI[0.120] and serum adiponectin (P < .05). The main predictor for cIMT was adiponectin (R² = 0.178, β = −0.466, P = .002). Left-ventricular hypertrophy was predicted (R² = 0.332) by body mass index-standard deviation score (β = 0.551, P = .005) and HOMA-IR (β = 0.380, P = .04). Metabolic syndrome, as defined by classic criteria, was diagnosed in 20% of children with PH, but when PH was not a criterion, MS was present in 6.2% of patients. Irrespective of the definition of MS, the applied markers of MS and insulin resistance were the main predictors of target-organ damage. Am J Hypertens 2007;20: 875–882 © 2007 American Journal of Hypertension, Ltd.