G Model SBMB-4089; No. of Pages 5
ARTICLE IN PRESS Journal of Steroid Biochemistry & Molecular Biology xxx (2013) xxx–xxx
Contents lists available at ScienceDirect
Journal of Steroid Biochemistry and Molecular Biology journal homepage: www.elsevier.com/locate/jsbmb
Review
Vitamin D status, body composition and hypertensive target organ damage in primary hypertension Pawel Pludowski a,∗ , Maciej Jaworski a , Anna Niemirska b , Mieczyslaw Litwin b , ˙ Mieczyslaw Szalecki c,d , Elzbieta Karczmarewicz a , Jacek Michalkiewicz e,f a
Department of Biochemistry, Radioimmunology and Experimental Medicine, The Children’s Memorial Health Institute, Warsaw, Poland Department of Nephrology and Arterial Hypertension, The Children’s Memorial Health Institute, Warsaw, Poland c Department of Endocrinology, The Children’s Memorial Health Institute, Warsaw, Poland d Department of Health Sciences, Jan Kochanowski University, Kielce, Poland e Department of Microbiology and Immunology, The Children’s Memorial Health Institute, Warsaw, Poland f Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, Poland b
a r t i c l e
i n f o
Article history: Received 1 August 2013 Received in revised form 11 October 2013 Accepted 25 October 2013 Keywords: Primary hypertension Body composition 25(OH)D level Vitamin D Left ventricular hypertrophy Carotid intima-media thickness
a b s t r a c t Overweight/obesity and high blood pressure during growth period are important risk factors of cardiovascular disease later in life. Cardiovascular system, fat and muscles are among target tissues for vitamin D and low 25(OH)D levels are likely to attenuate potential benefits of its action. The study was aimed to evaluate vitamin D status and body composition in children and adolescents with primary hypertension (PH). The study population comprised 78 patients aged 15.4 ± 2.3 yrs (9–18 yrs; 15 girls) with diagnosed PH. Total 25(OH)D and parathyroid hormone (PTH) were assayed by Cobas e411 machine (Roche Diagnostics). DXA (Prodigy, GE Lunar) was used to assess total body bone mineral content (TBBMC; g), total body bone mineral density (TBBMD; g/cm2 ), lean body mass (LBM; g), % lean body mass (%LBM), fat mass (FM; g), % fat mass (% FM), Android %Fat, Gynoid %Fat and Trunk fat mass (Trunk FM; g). Hypertensive cases (BMI = 25.6 ± 4.2 kg/m2 ), compared to reference, had slightly increased TBBMD and TBBMC Z-scores (+0.40 ± 0.91 and +0.59 ± 0.96; both p < 0.001), and had markedly increased FM and FM/body weight ratio Z-scores of ±1.83 ± 1.63 (p < 0.0001) and +1.43 ± 1.05 (p < 0.0001). LBM Z-scores were slightly increased as well (+0.34 ± 1.08, p < 0.001). In contrast, markedly reduced LBM/body weight ratio Z-scores of −1.47 ± 0.90 (p < 0.0001) and disturbed relationship between FM and LBM as assessed by FM/LBM ratio Z-score of +1.53 ± 1.29 (p < 0.0001) were noted. The average serum levels of 25(OH)D of 17.8 ± 6.9 ng/mL and PTH of 34.8 ± 16.8 pg/mL were noted in PH group. 91% PH cases showed 25(OH)D levels lower than 30 ng/mL. 71% of PH subjects revealed vitamin D deficiency (25(OH)D < 20 ng/ml). 10% of PH cases showed 25(OH)D levels lower than 10 ng/mL. 25(OH)D levels negatively correlated with PTH showing r = −0.24 (p = 0.03). Absolute LBM/body weight ratio values positively correlated with 25(OH)D levels (r = 0.31; p = 0.01). In contrast, absolute FM/body weight ratio values correlated negatively with 25(OH)D levels (r = −0.32; p < 0.01). Moreover, 25(OH)D levels negatively correlated with absolute Trunk FM (r = −0.29; p < 0.05), Android %Fat (r = −0.32; p < 0.01) and with Gynoid %Fat (r = −0.28; p < 0.05). PTH and 25(OH)D concentrations did not differ when severity of hypertension, left ventricular mass and carotid intimamedia thickness were controlled for. Concluding, higher muscle mass stores in body weight coincided with higher 25(OH)D levels. Higher fat mass stores coincided with lower 25(OH)D levels in PH group. Whether vitamin D insufficiency/deficiency in PH group should be considered as a cause of disease or epiphenomenon remains unknown. This article is part of a Special Issue entitled ‘16th Vitamin D Workshop’. © 2013 Published by Elsevier Ltd.
Contents 1. 2.
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Patients and methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
00 00
∗ Corresponding author at: The Children’s Memorial Health Institute, Department of Biochemistry, Radioimmunology and Experimental Medicine, Aleja Dzieci Polskich 20, 04-730 Warsaw, Poland. Tel.: +48 22 8151776; fax: +48 22 8151789. E-mail address: [email protected] (P. Pludowski). 0960-0760/$ – see front matter © 2013 Published by Elsevier Ltd. http://dx.doi.org/10.1016/j.jsbmb.2013.10.026
Please cite this article in press as: P. Pludowski, et al., Vitamin D status, body composition and hypertensive target organ damage in primary hypertension, J. Steroid Biochem. Mol. Biol. (2013), http://dx.doi.org/10.1016/j.jsbmb.2013.10.026
G Model SBMB-4089; No. of Pages 5
ARTICLE IN PRESS P. Pludowski et al. / Journal of Steroid Biochemistry & Molecular Biology xxx (2013) xxx–xxx
2
2.1. Assessment of skeletal status and body composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2. Laboratory investigations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1. Blood pressure status and body composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2. 25(OH)D and parathyroid hormone (PTH) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.3. 25(OH)D and in relation to body composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.4. PTH and 25(OH)D in relation to severity of hypertension, LVMi and cIMT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Funding sources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1. Introduction Vitamin D has been postulated to prevent a wide range of health problems, including cancer, diabetes and other autoimmune diseases, infections, depressive disorders, osteoporotic fracture, etc. [1]. The cardiovascular system is another target tissue for vitamin D since its receptors (VDRs) and vitamin D metabolizing enzymes are expressed in arterial vessels, heart and vascular smooth muscle cells, endothelial cells, and other cells that affect systemic BP [2,3]. Adequate vitamin D levels can prevent vascular smooth muscle contraction and increase arterial compliance, acting as a possible vasodilator on blood vessels. It has also been shown to improve endothelial function. These protective or beneficial mechanisms can be potentially compromised with lower vitamin D levels. Analysis of data from NHANES 2001–2006 study of US children and adolescents based on assay-adjusted serum 25-hydroxyvitamin D (25(OH)D) revealed an inverse association between serum 25(OH)D and waist circumference (p = 0.001), systolic blood pressure (p = 0.01), and HOMA-IR score (p = 0.002) and a positive association between serum 25(OH)D and HDL cholesterol (p = 0.001) [4]. Elevated blood pressure recognized as early as during growth period is the risk factor of CVD later in life. Our study was aimed to evaluate vitamin D status and body composition in children and adolescents with primary hypertension (PH) and relations between vitamin D status and severity of hypertension and hypertensive target organ damage. 2. Patients and methods The study population comprised 78 patients (9–18 yrs; 15 girls) consecutively referred because of elevated blood pressure and in whom ultimately primary hypertension (PH) or prehypertension was diagnosed. All patients parents and all patients older than 12 yrs gave informed consent. PH was diagnosed after thorough examination excluding known causes of secondary hypertension according to the fourth Task Force Report guidelines [5]. In all subjects, hypertension was confirmed by 24-h ambulatory blood pressure monitoring (ABPM). Blood pressure status and hypertension severity were defined according to recently published classification based on ABPM results [6]. Hypertensive target organ damage was assessed as left ventricular hypertrophy (LVH) determined by echocardiography and expressed as left ventricular mass indexed to height in meters (2.7) and as increased carotid artery intima-media thickness (cIMT). LVH was defined as left ventricular mass index (LVMi) greater than 95th percentile specific for age and sex [7]. cIMT was assessed by ultrasonography according to procedure described previously. Sex and age specific normative data were used as referential values [8]. 2.1. Assessment of skeletal status and body composition DXA (Prodigy, GE Lunar) was used to assess body composition. PH patients were measured at the time of diagnosis of PH. BH (in
00 00 00 00 00 00 00 00 00 00 00 00
centimeter) and body weight (BW; in kilogram) were assessed on the day of the DXA scan. Total body bone mineral content (TBBMC; in grams), total body bone mineral density (TBBMD; in grams per centimeter squared), lean body mass (LBM; in grams), % lean body mass (%LBM), fat mass (FM; in grams), % fat mass (%FM), Android %Fat, Gynoid %Fat and Trunk fat mass (Trunk FM; in g) were evaluated on the basis of total body scan data. Absolute DXA data were compared to previously established age- and sex-matched reference values [9]. To ensure high accuracy of DXA measures, a daily quality control procedure and anthropometric spine phantom (Hologic) scans were performed. The coefficient of variation for BMC measurements of the Hologic spine phantom (L1–L4) was 0.56%. The coefficient of variation percentage for repeated DXA measures in 30 children and adolescents was
ARTICLE IN PRESS Journal of Steroid Biochemistry & Molecular Biology xxx (2013) xxx–xxx
Contents lists available at ScienceDirect
Journal of Steroid Biochemistry and Molecular Biology journal homepage: www.elsevier.com/locate/jsbmb
Review
Vitamin D status, body composition and hypertensive target organ damage in primary hypertension Pawel Pludowski a,∗ , Maciej Jaworski a , Anna Niemirska b , Mieczyslaw Litwin b , ˙ Mieczyslaw Szalecki c,d , Elzbieta Karczmarewicz a , Jacek Michalkiewicz e,f a
Department of Biochemistry, Radioimmunology and Experimental Medicine, The Children’s Memorial Health Institute, Warsaw, Poland Department of Nephrology and Arterial Hypertension, The Children’s Memorial Health Institute, Warsaw, Poland c Department of Endocrinology, The Children’s Memorial Health Institute, Warsaw, Poland d Department of Health Sciences, Jan Kochanowski University, Kielce, Poland e Department of Microbiology and Immunology, The Children’s Memorial Health Institute, Warsaw, Poland f Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, Poland b
a r t i c l e
i n f o
Article history: Received 1 August 2013 Received in revised form 11 October 2013 Accepted 25 October 2013 Keywords: Primary hypertension Body composition 25(OH)D level Vitamin D Left ventricular hypertrophy Carotid intima-media thickness
a b s t r a c t Overweight/obesity and high blood pressure during growth period are important risk factors of cardiovascular disease later in life. Cardiovascular system, fat and muscles are among target tissues for vitamin D and low 25(OH)D levels are likely to attenuate potential benefits of its action. The study was aimed to evaluate vitamin D status and body composition in children and adolescents with primary hypertension (PH). The study population comprised 78 patients aged 15.4 ± 2.3 yrs (9–18 yrs; 15 girls) with diagnosed PH. Total 25(OH)D and parathyroid hormone (PTH) were assayed by Cobas e411 machine (Roche Diagnostics). DXA (Prodigy, GE Lunar) was used to assess total body bone mineral content (TBBMC; g), total body bone mineral density (TBBMD; g/cm2 ), lean body mass (LBM; g), % lean body mass (%LBM), fat mass (FM; g), % fat mass (% FM), Android %Fat, Gynoid %Fat and Trunk fat mass (Trunk FM; g). Hypertensive cases (BMI = 25.6 ± 4.2 kg/m2 ), compared to reference, had slightly increased TBBMD and TBBMC Z-scores (+0.40 ± 0.91 and +0.59 ± 0.96; both p < 0.001), and had markedly increased FM and FM/body weight ratio Z-scores of ±1.83 ± 1.63 (p < 0.0001) and +1.43 ± 1.05 (p < 0.0001). LBM Z-scores were slightly increased as well (+0.34 ± 1.08, p < 0.001). In contrast, markedly reduced LBM/body weight ratio Z-scores of −1.47 ± 0.90 (p < 0.0001) and disturbed relationship between FM and LBM as assessed by FM/LBM ratio Z-score of +1.53 ± 1.29 (p < 0.0001) were noted. The average serum levels of 25(OH)D of 17.8 ± 6.9 ng/mL and PTH of 34.8 ± 16.8 pg/mL were noted in PH group. 91% PH cases showed 25(OH)D levels lower than 30 ng/mL. 71% of PH subjects revealed vitamin D deficiency (25(OH)D < 20 ng/ml). 10% of PH cases showed 25(OH)D levels lower than 10 ng/mL. 25(OH)D levels negatively correlated with PTH showing r = −0.24 (p = 0.03). Absolute LBM/body weight ratio values positively correlated with 25(OH)D levels (r = 0.31; p = 0.01). In contrast, absolute FM/body weight ratio values correlated negatively with 25(OH)D levels (r = −0.32; p < 0.01). Moreover, 25(OH)D levels negatively correlated with absolute Trunk FM (r = −0.29; p < 0.05), Android %Fat (r = −0.32; p < 0.01) and with Gynoid %Fat (r = −0.28; p < 0.05). PTH and 25(OH)D concentrations did not differ when severity of hypertension, left ventricular mass and carotid intimamedia thickness were controlled for. Concluding, higher muscle mass stores in body weight coincided with higher 25(OH)D levels. Higher fat mass stores coincided with lower 25(OH)D levels in PH group. Whether vitamin D insufficiency/deficiency in PH group should be considered as a cause of disease or epiphenomenon remains unknown. This article is part of a Special Issue entitled ‘16th Vitamin D Workshop’. © 2013 Published by Elsevier Ltd.
Contents 1. 2.
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Patients and methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
00 00
∗ Corresponding author at: The Children’s Memorial Health Institute, Department of Biochemistry, Radioimmunology and Experimental Medicine, Aleja Dzieci Polskich 20, 04-730 Warsaw, Poland. Tel.: +48 22 8151776; fax: +48 22 8151789. E-mail address: [email protected] (P. Pludowski). 0960-0760/$ – see front matter © 2013 Published by Elsevier Ltd. http://dx.doi.org/10.1016/j.jsbmb.2013.10.026
Please cite this article in press as: P. Pludowski, et al., Vitamin D status, body composition and hypertensive target organ damage in primary hypertension, J. Steroid Biochem. Mol. Biol. (2013), http://dx.doi.org/10.1016/j.jsbmb.2013.10.026
G Model SBMB-4089; No. of Pages 5
ARTICLE IN PRESS P. Pludowski et al. / Journal of Steroid Biochemistry & Molecular Biology xxx (2013) xxx–xxx
2
2.1. Assessment of skeletal status and body composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2. Laboratory investigations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1. Blood pressure status and body composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2. 25(OH)D and parathyroid hormone (PTH) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.3. 25(OH)D and in relation to body composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.4. PTH and 25(OH)D in relation to severity of hypertension, LVMi and cIMT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Funding sources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1. Introduction Vitamin D has been postulated to prevent a wide range of health problems, including cancer, diabetes and other autoimmune diseases, infections, depressive disorders, osteoporotic fracture, etc. [1]. The cardiovascular system is another target tissue for vitamin D since its receptors (VDRs) and vitamin D metabolizing enzymes are expressed in arterial vessels, heart and vascular smooth muscle cells, endothelial cells, and other cells that affect systemic BP [2,3]. Adequate vitamin D levels can prevent vascular smooth muscle contraction and increase arterial compliance, acting as a possible vasodilator on blood vessels. It has also been shown to improve endothelial function. These protective or beneficial mechanisms can be potentially compromised with lower vitamin D levels. Analysis of data from NHANES 2001–2006 study of US children and adolescents based on assay-adjusted serum 25-hydroxyvitamin D (25(OH)D) revealed an inverse association between serum 25(OH)D and waist circumference (p = 0.001), systolic blood pressure (p = 0.01), and HOMA-IR score (p = 0.002) and a positive association between serum 25(OH)D and HDL cholesterol (p = 0.001) [4]. Elevated blood pressure recognized as early as during growth period is the risk factor of CVD later in life. Our study was aimed to evaluate vitamin D status and body composition in children and adolescents with primary hypertension (PH) and relations between vitamin D status and severity of hypertension and hypertensive target organ damage. 2. Patients and methods The study population comprised 78 patients (9–18 yrs; 15 girls) consecutively referred because of elevated blood pressure and in whom ultimately primary hypertension (PH) or prehypertension was diagnosed. All patients parents and all patients older than 12 yrs gave informed consent. PH was diagnosed after thorough examination excluding known causes of secondary hypertension according to the fourth Task Force Report guidelines [5]. In all subjects, hypertension was confirmed by 24-h ambulatory blood pressure monitoring (ABPM). Blood pressure status and hypertension severity were defined according to recently published classification based on ABPM results [6]. Hypertensive target organ damage was assessed as left ventricular hypertrophy (LVH) determined by echocardiography and expressed as left ventricular mass indexed to height in meters (2.7) and as increased carotid artery intima-media thickness (cIMT). LVH was defined as left ventricular mass index (LVMi) greater than 95th percentile specific for age and sex [7]. cIMT was assessed by ultrasonography according to procedure described previously. Sex and age specific normative data were used as referential values [8]. 2.1. Assessment of skeletal status and body composition DXA (Prodigy, GE Lunar) was used to assess body composition. PH patients were measured at the time of diagnosis of PH. BH (in
00 00 00 00 00 00 00 00 00 00 00 00
centimeter) and body weight (BW; in kilogram) were assessed on the day of the DXA scan. Total body bone mineral content (TBBMC; in grams), total body bone mineral density (TBBMD; in grams per centimeter squared), lean body mass (LBM; in grams), % lean body mass (%LBM), fat mass (FM; in grams), % fat mass (%FM), Android %Fat, Gynoid %Fat and Trunk fat mass (Trunk FM; in g) were evaluated on the basis of total body scan data. Absolute DXA data were compared to previously established age- and sex-matched reference values [9]. To ensure high accuracy of DXA measures, a daily quality control procedure and anthropometric spine phantom (Hologic) scans were performed. The coefficient of variation for BMC measurements of the Hologic spine phantom (L1–L4) was 0.56%. The coefficient of variation percentage for repeated DXA measures in 30 children and adolescents was
