Effects of Growth Hormone Treatment for Short Stature on Calcium Homeostasis, Bone Mineralisation, and Body Composition

Rosenberg, Andrew R.; Calligeros, Danny; Kainer, Gad

doi:10.1159/000183871

Cited by 33 publications

(22 citation statements)

References 15 publications

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“…GHRx had a short-term lipolytic effect during the first 6 months of treatment, while the anabolic effect continued. Similar results have been reported in other studies in adults and children with GHD and short stature children during GHRx (1,(42)(43)(44).…”

Section: Discussionsupporting

confidence: 91%

Changes in Bone Mineral Density, Body Composition, and Lipid Metabolism during Growth Hormone (GH) Treatment in Children with GH Deficiency

Boot¹

1997

Journal of Clinical Endocrinology & Metabolism

115

142

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Adults with childhood onset GH deficiency (GHD) have reduced bone mass, increased fat mass, and disorders of lipid metabolism. The aim of the present study was to evaluate bone mineral density (BMD), bone metabolism, body composition, and lipid metabolism in GHD children before and during 2-3 yr of GH treatment (GHRx). Forty children with GHD, mean age 7.9 yr, participated in the study of bone metabolism and body composition; and an additional group of 17 GHD children, in the study of lipid metabolism. Lumbar spine BMD, total body BMD, and body composition were measured with dual-energy x-ray absorptiometry. Volumetric BMD (bone mineral apparent density, BMAD) was calculated to correct for bone size. BMD, BMAD, lean tissue mass, bone mineral content, fat mass, and percentage body fat were expressed as SD scores (SDS), in comparison with normative data of the same population. Lumbar spine BMD and BMAD and total body BMD were all decreased at baseline. All BMD variables increased significantly during GHRx, lumbar spine BMD SDS, already after 6 months of treatment. Lean tissue mass SDS increased continuously. Bone mineral content SDS started to increase after 6 months GHRx. Fat mass SDS decreased during the first 6 months of GHRx and remained stable thereafter. Biochemical parameters of bone formation and bone resorption did not differ from normal at baseline and increased during the first 6 months of GHRx. Serum 1,25 dihydroxyvitamin D increased continuously during GHRx, whereas PTH and serum calcium remained stable. Lipid profile was normal at baseline. Atherogenic index had decreased and apolipoprotein A1 (Apo-A1) had increased after 3 yr of treatment.In conclusion, children with GHD have decreased bone mass. BMD, together with height and lean tissue mass, increased during GHRx. GHRx had a beneficial effect on lipid metabolism. (J Clin Endocrinol

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Section: Discussionsupporting

confidence: 91%

Changes in Bone Mineral Density, Body Composition, and Lipid Metabolism during Growth Hormone (GH) Treatment in Children with GH Deficiency

Boot¹

1997

Journal of Clinical Endocrinology & Metabolism

115

142

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“…This absence of change in total body BMD SDS and the decrease in total body BMAD after 1 year of GH treatment may reflect a faster rate of bone expansion than of mineral acquisition. Similar changes in BMD during GH treatment have been reported in previous studies in children with GHD (21) and short stature children without GHD (27).…”

Section: Discussionsupporting

confidence: 88%

Changes in body composition and leptin levels during growth hormone (GH) treatment in short children with various GH secretory capacities

Matsuoka

Fors

Bosæus

et al. 1999

European Journal of Endocrinology

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Objective: The aim of this study was to follow changes in body composition, estimated by dual-energy Xray absorptiometry (DXA), in relation to changes in leptin during the first year of GH therapy in order to test the hypothesis that leptin is a metabolic signal involved in the regulation of GH secretion in children. Design and Methods: In total, 33 prepubertal children were investigated. Their mean (S.D.) chronological age at the start of GH treatment was 11.5 (1.6) years, and their mean height was ¹ 2.33 (0.38) S.D. scores (SDS). GH was administered subcutaneously at a daily dose of 0.1 (n ¼ 26) or 0.2 (n ¼ 7) IU/kg body weight. Ten children were in the Swedish National Registry for children with GH deficiency, and twenty-three children were involved in trials of GH treatment for idiopathic short stature. Spontaneous 24-h GH secretion was studied in 32 of the children. In the 24-h GH profiles, the maximum level of GH was determined and the secretion rate estimated by deconvolution analysis (GH t ). Serum leptin levels were measured at the start of GH treatment and after 10 and 30 days and 3, 6 and 12 months of treatment. Body composition measurements, by DXA, were performed at baseline and 12 months after the onset of GH treatment. Results: After 12 months of GH treatment, mean height increased from ¹ 2.33 to ¹ 1.73 SDS and total body fat decreased significantly by 3.0 (3.3)%. Serum leptin levels were decreased significantly at all time points studied compared with baseline. There was a significant correlation between the change in total body fat and the change in serum leptin levels during the 12 months of GH treatment, whereas the leptin concentration per unit fat mass did not change. In a multiple stepwise linear regression analysis with 12 month change in leptin levels as the dependent variable, the percentage change in fat over 12 months, the baseline fat mass (%) of body mass and GH t accounted for 24.0%, 11.5% and 12.2% of the variability respectively. Conclusions: There are significant correlations between changes in leptin and fat and endogenous GH secretion in short children with various GH secretory capacities. Leptin may be the messenger by which the adipose tissue affects hypothalamic regulation of GH secretion.

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“…Therefore, it is remarkable that GH induces sustained metabolic effects in PWS. Moreover, data on the metabolic effects of GH in children are scarce and changes in body composition seem to be independent of prior endogenous GH secretion or the dose of GH administered [40, 81], in contrast to the effects of GH administration on longitudinal growth. Hence, it should be emphasized that the dose dependency of the effects of GH on muscular and fat tissue has not yet been investigated in children.…”

Section: Are Changes In Body Composition Under Gh Therapy An Argumentmentioning

confidence: 99%

Is There Growth Hormone Deficiency in Prader-Willi Syndrome?

Eiholzer¹,

Bachmann²,

l’Allemand³

2000

Horm Res Paediatr

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Prader-Labhart-Willi syndrome (PWS) is the most frequent form of syndromal obesity. Its main features are associated with hypothalamic dysfunction, which has not yet been comprehensively described. The aim of this review is to present arguments to define the presence of genuine growth hormone (GH) deficiency (GHD) in these patients. Decreasing growth velocity despite the onset of obesity, reduced lean body mass in the presence of adiposity, small hands and feet, relatively low insulin-like growth factor-I and low insulin levels, as well as the dramatic effect of GH treatment on growth, support the presence of hypothalamic GHD in PWS. Even though it might be difficult to ultimately prove GHD in PWS because of the obesity-induced counterregulation, the hormonal situation differs from that in simple obesity. The effects of long-term therapies with GH on body composition in these patients are summarized. GH therapy dramatically changes the phenotype of PWS in childhood: height and weight become normal and there is a sustained impact on the net loss of body fat. We conclude that GHD may account for several features of PWS.

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Effects of Growth Hormone Treatment for Short Stature on Calcium Homeostasis, Bone Mineralisation, and Body Composition

Cited by 33 publications

References 15 publications

Changes in Bone Mineral Density, Body Composition, and Lipid Metabolism during Growth Hormone (GH) Treatment in Children with GH Deficiency

Changes in Bone Mineral Density, Body Composition, and Lipid Metabolism during Growth Hormone (GH) Treatment in Children with GH Deficiency

Changes in body composition and leptin levels during growth hormone (GH) treatment in short children with various GH secretory capacities

Is There Growth Hormone Deficiency in Prader-Willi Syndrome?

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