Adults with childhood-onset growth hormone deficiency: effects fo growth harmone treatment on cardiac structure
Article first published online: 31 AUG 2007
Journal of Internal Medicine
Volume 241, Issue 6, pages 515–520, June 1997
How to Cite
SARTORIO, A., FERRERO, S., CONTI, A., BRAGATO, R., MALFATTO, G., LEONETTI, G. and FAGLIA, G. (1997), Adults with childhood-onset growth hormone deficiency: effects fo growth harmone treatment on cardiac structure. Journal of Internal Medicine, 241: 515–520. doi: 10.1111/j.1365-2796.1997.tb00010.x
- Issue published online: 31 AUG 2007
- Article first published online: 31 AUG 2007
- Received 23 July 1996; accepted 21 January 1997.
- cardiac structure;
Abstract. Sartorio A, Perrero S, Conti A, Bragato R, Malfatto G, Leonetti G, Faglia G. (Laboratorio Sperimentale di Ricerche Endocrinologiche, Istituto AuxoIogico Italiano, Milano, Italy). Adults with childhood-onset growth hormone deficiency: effects of growth hormone treatment on cardiac structure.
Objectives: To evaluate the effects of growth hormone deficiency (GHD) and of growth hormone (GH) therapy on cardiac structure in adults with child-hood-onset GHD.
Settiig: Out-patient clinic in the Italian Institute for Auxology, Milan.
Subjects: Eight adults with childhood-onset GHD and eight healthy controls, matched for sex, age, exercise and body mass index.
Interventions: Recombinant GH (Saizen Serono, Italy), administered in a conventional dose of 0.5 IU kg-1 week-1 for 6 months.
Main outcome measures: Cardiac structure parameters, evaluated by two-dimensional, M-mode and Doppler echocardiograms, and stress test, by means of a modified Bruce protocol with a bicycle ergometer, were determined before and after 6 months GH therapy.
Results: Before treatment, mean (±SE) intraventricular septal thickness (IVST: 7.1 ± 0.2 mm), LV posterior wall thickness (LVPT: 5.2± 0.1 mm), LV mass(LVM: 94.6 ± 5.0 g), LV massindex (LVM/body surface area, LVMI: 65.1 ± 3.0 g m-2) and left ventricular end-diastolic diameter (LVED 41.4 ± 0.6 mm) of patients were significantly lower (P< < 0.01) than in controls, whilst LV end-systolic diameter (LVES) of patients (25.5 ± 0.7 mm) was similar to controls (27.5 ± 0.7). GH treatment significantly (P < 0.01) increased LWT (6.8 ± 0.2 mm), LVM (111.6 ± 4.6 g) and LVMI (80.5 ± 3.5 gm-2): no sigdcant changes were observed in LVED, LVES and IVST values. The stress test showed a significant improvement of cardiac performance, as demonstrated by the reduction of blood pressure x heart rate product at the same workload (basal: 32722.5 ± 897.4 vs. after: 25574.6 ± 439.7).
Conclusions: GH plays a role in the maintenance of a normal cardiac structure in adulthood. The present study suggests that GH treatment might be able to improve the cardiac structure of patients with childhood-onset GHD.