Effects of 1,25-dihydroxyvitamin D3 and growth hormone therapy on serum osteocalcin levels in children with growth hormone deficiency

Antoniazzi, Franco; Radetti, Giorgio; Zamboni, Giorgio; Gambaro, G.; Adami, Silvano; Tatò, Luciano

doi:10.1016/s0169-6009(08)80017-7

Cited by 9 publications

(3 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Renal 1␣hydroxylase activity is enhanced through IGF-1 (45), which agrees with the correlation we observed between ⌬ in IGF-1 SDS and ⌬ in 1,25 dihydroxyvitamin D. The synthesis of osteocalcin is induced by the action of 1,25 dihydroxyvitamin D (46). Administration of 1,25 dihydroxyvitamin D to GHD children increased serum osteocalcin levels (47). Part of the stimulatory action on osteoblastic activity of GH might be mediated by 1,25 dihydroxyvitamin D. This is supported by our finding of a correlation between the increase of 1,25 dihydroxyvitamin D and the increase in BMD.…”

Section: Discussionsupporting

confidence: 89%

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

View full text Add to dashboard Cite

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

show abstract

Section: Discussionsupporting

confidence: 89%

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

View full text Add to dashboard Cite

show abstract

“…Our results, however, indicate that there is not a complete GH deficiency. We previously found low basal levels and a significant response of osteocalcin to stimulation with calcitriol before hGH treatment in GH deficiency, with no response following hGH treatment (20). In the present study there was no response of osteocalcin serum levels to calcitriol load, either before or after treatment.…”

Section: Discussioncontrasting

confidence: 65%

Bone mineral metabolism in girls with precocious puberty during gonadotrophin-releasing hormone agonist treatment

Antoniazzi

Bertoldo

Zamboni

et al. 1995

European Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

Bone mineral metabolism and mineralization before and during treatment were studied in 10 girls aged 6.9-8.4 years affected by central precocious puberty and treated with gonadotrophin-releasing hormone agonist (GnRHa) leuprolide acetate depot, in order to understand better the consequences of oestrogen deficiency and the reduction of growth hormone (GH)-insulin-like growth factor I (IGF-I) axis activity. Before and after 12 months of therapy, the patients underwent a clonidine stimulation test and a 4-day calcitriol osteoblast stimulation test. On day 0, day 5 and at 3-month intervals thereafter, serum calcium, phosphate, alkaline phosphatase, IGF-I, IGF binding protein 3 (IGFBP-3), GH, GH binding protein and osteocalcin levels were measured; urinary calcium, phosphate and hydroxyproline levels were evaluated in fasting spot samples. Trabecular and cortical bone mass variations, measured by dual X-ray absorptiometry in the lumbar spine and by dual photon absorptiometry in the radius, respectively were evaluated before the start and after 12 months of therapy. During treatment, a decrease of serum oestradiol levels from pubertal to prepubertal levels was observed. The GH peak following clonidine diminished significantly after 1 year. Growth hormone binding protein showed a slight increase, and IGF-I and IGFBP-3 decreased, although not significantly. Osteocalcin levels decreased significantly after 9 and 12 months of treatment, but they did not change significantly after calcitriol load, either before or after GnRHa therapy. Urinary hydroxyproline decreased significantly after 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…It is known that 1,25‐dihydroxyvitamin D stimulates intestinal calcium transport and promotes the mineralization of osteoid laid down by osteoblasts by maintaining the calcium and phosphorus concentrations within the normal range ( Holick, 1996). Furthermore, 1,25‐dihydroxyvitamin D enhances the synthesis of osteocalcin by osteoblasts indicating direct stimulatory effects on these cells ( Antoniazzi et al ., 1993 ; Fraser, 1995). 1,25‐dihydroxyvitamin D is primarily synthesized in the kidney.…”

Section: Discussionmentioning

confidence: 99%

Bone mineral density, bone metabolism and body composition of children with chronic renal failure, with and without growth hormone treatment

Boot¹,

Nauta

Jong

et al. 1998

Clinical Endocrinology

View full text Add to dashboard Cite

show abstract

Effects of 1,25-dihydroxyvitamin D3 and growth hormone therapy on serum osteocalcin levels in children with growth hormone deficiency

Cited by 9 publications

References 17 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

Bone mineral metabolism in girls with precocious puberty during gonadotrophin-releasing hormone agonist treatment

Bone mineral density, bone metabolism and body composition of children with chronic renal failure, with and without growth hormone treatment

Contact Info

Product

Resources

About