title: Effects of 12 months of growth hormone (GH) treatment on calciotropic hormones, calcium homeostasis, and bone metabolism in adults with acquired GH deficiency: a double blind, randomized, placebo-controlled study.
abstract: The effects of GH substitution on skeletal mass, bone turnover, and calcium metabolism were investigated in 29 patients with GH deficiency who were randomized to sc injections with GH (2 IU/m2 day) or placebo for 12 months. During GH treatment, serum insulin-like growth factor I increased 263 +/- 98% (P < 0.001). Serum osteocalcin, bone a alkaline phosphatase, and procollagen type I C-terminal propeptide increased by 376 +/- 78% (P < 0.005), 128 +/- 17% (P < 0.005), and 100 +/- 17% (P < 0.005), respectively. Serum type I collagen telopeptide and urinary levels of pyridinoline, deoxypyridinoline, and hydroxyproline rose by 158 +/- 39% (P < 0.005), 170 +/- 48% (P < 0.005), 156 +/- 78% (P < 0.005), and 161 +/- 50% (P < 0.005), respectively. Serum ionized calcium rose by 1.7 +/- 0.6% (P < 0.05), whereas serum PTH decreased insignificantly. Vitamin D metabolites remained unaltered. Urinary calcium/creatinine increased and phosphate/creatinine decreased transiently, returning to baseline values at 9 months. When measured by dual energy x-ray absorptiometry, whole body bone mineral density (BMD) and (BMD) of the radius decreased 2.4 +/- 0.6% (P < 0.05) and 3.5 +/- 1.0% (P < 0.005), respectively, whereas no significant changes were observed in BMD of the femur or spine. Our results indicate that long term GH treatment activates bone remodeling in patients with GH deficiency. The observed slight decrease in BMD may be explained by expansion of the remodeling space and reduced mean age of bone tissue. IT remains unclear whether long term treatment with GH will lead to an increase in bone mass and improved skeletal biomechanical competence.
authors.affiliation: Department of Endocrinology, Odense University Hospital, Denmark.
authors.forename: T B
authors.initials: TB
authors.lastname: Hansen
authors.forename: K
authors.initials: K
authors.lastname: Brixen
authors.forename: N
authors.initials: N
authors.lastname: Vahl
authors.forename: J O
authors.initials: JO
authors.lastname: Jørgensen
authors.forename: J S
authors.initials: JS
authors.lastname: Christiansen
authors.forename: L
authors.initials: L
authors.lastname: Mosekilde
authors.forename: C
authors.initials: C
authors.lastname: Hagen
mesh_terms: D000328:Adult; D015519:Bone Density; D001862:Bone Resorption; D002118:Calcium / Q000378:metabolism* / Q000652:urine; D004311:Double-Blind Method; D005260:Female; D013006:Growth Hormone / Q000009:adverse effects / Q000172:deficiency* / Q000627:therapeutic use*; D006706:Homeostasis; D006801:Humans; D007231:Infant, Newborn; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010710:Phosphates / Q000097:blood / Q000652:urine; D010919:Placebos; D011347:Procollagen / Q000097:blood; D014807:Vitamin D / Q000378:metabolism
chemical_list: D010281:Parathyroid Hormone; D010446:Peptide Fragments; D010710:Phosphates; D010919:Placebos; D011347:Procollagen; C042813:procollagen type I carboxy terminal peptide; D014807:Vitamin D; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D002118:Calcium