Rapid cardiovascular effects of growth hormone treatment in short prepubertal children: impact of treatment duration
Article first published online: 9 NOV 2012
© 2012 Blackwell Publishing Ltd
Volume 77, Issue 6, pages 877–884, December 2012
How to Cite
Nygren, A., Sunnegårdh, J., Teien, D., Jonzon, A., Björkhem, G., Lindell, S., Albertsson-Wikland, K. and Kriström, B. (2012), Rapid cardiovascular effects of growth hormone treatment in short prepubertal children: impact of treatment duration. Clinical Endocrinology, 77: 877–884. doi: 10.1111/j.1365-2265.2012.04456.x
- Issue published online: 9 NOV 2012
- Article first published online: 9 NOV 2012
- Accepted manuscript online: 31 MAY 2012 11:54AM EST
- Manuscript Accepted: 28 MAY 2012
- Manuscript Revised: 8 MAY 2012
- Manuscript Revised: 18 MAR 2012
- Manuscript Received: 9 FEB 2012
- Swedish Research Council. Grant Number: 7509
- Sahlgrenska University Hospital
- West Sweden Region
Previous studies show that growth hormone (GH) treatment increases cardiac dimensions in short children with GH deficiency (GHD) and has diverse cardiac effects in children with idiopathic short stature (ISS). This study was performed to assess the effect of GH on the cardiovascular system in short children with a broad range of GH secretion and GH sensitivity/responsiveness.
Design and patients
In this prospective, multicentre study, short prepubertal children diagnosed with isolated GHD (89) or ISS (38) were followed during 2 years of GH treatment. They were randomized to receive either a standard (43 μg/kg/day) or an individualized GH dose (range 17–100 μg/kg/day) based on GH responsiveness estimated by a prediction model and distance to target height. Echocardiography, blood pressure and electrocardiography were performed at baseline, 3, 12 and 24 months.
Left ventricular mass (LVM) indexed to body surface area increased significantly during 2 years of GH treatment in both GHD and ISS irrespective of randomized dose. This change was already apparent at 3 months, when standard deviation scores (SDS) of wall thickness and diameter were increased. At 24 months, left ventricular diameter SDS remained increased, whereas myocardial thickness SDS returned to baseline values. There was no impairment of systolic or diastolic function. There was no correlation with treatment dose and LVM SDS at 24 months.
Irrespective of GH status, there was a rapid increase in LVM during GH treatment in short children. At 3 months, wall thickness and diameter were increased, whereas only diameter remained increased at 24 months.