title: Normal osteoclastic and osteoblastic responses to exogenous growth hormone in patients with postmenopausal spinal osteoporosis.
abstract: The cause of bone loss in patients with osteoporosis is not known, but both increased bone resorption and decreased bone formation have been reported. Theoretically, these effects may result from either increased activity of osteoclasts or decreased activity of osteoblasts, or both. In vivo, growth hormone (GH) administration leads to activation of osteoclasts and osteoblasts as evidenced by increased biochemical markers of bone resorption and bone formation. To test for disturbances in responsiveness of bone cells to exogenous hormonal stimuli in osteoporosis, we compared 15 patients with postmenopausal osteoporosis with 15 healthy age-matched postmenopausal women before and during a 3 day stimulation test with GH (0.2 IU/kg/day). Serum insulin-like growth factor I increased in both groups (p < 0.001). GH treatment increased biochemical markers of bone resorption (serum carboxyl-terminal telopeptide of type I collagen [ICTP] [p < 0.001] and, to a lesser extent, 24 h urinary hydroxyproline/creatinine) in the two groups. Similarly, biochemical markers for bone formation increased in both groups [osteocalcin (p < 0.01) and procollagen type I C-terminal propeptide, PICP (p < 0.001)]. GH treatment reduced alkaline phosphatase (ALP, p < 0.05) and its bone-specific isoenzyme (bone ALP, p < 0.01) in both groups. The maximal response, the area under the curve (AUC) of response curves for IGF-I, bone resorption markers, and bone formation markers were not different between groups. Our data do not support the hypothesis that osteoporotic patients display major disturbances in responsiveness to GH.
authors: Aarhus Bone and Mineral Research Group, Department of Endocrinology and Metabolism, Aarhus University Hospital, Denmark.
authors: M
authors: M
authors: Kassem
authors: K
authors: K
authors: Brixen
authors: W F
authors: WF
authors: Blum
authors: L
authors: L
authors: Mosekilde
authors: E F
authors: EF
authors: Eriksen
mesh_terms: D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001824:Body Constitution; D015519:Bone Density / Q000187:drug effects; D001846:Bone Development / Q000187:drug effects; D001862:Bone Resorption / Q000188:drug therapy; D002118:Calcium / Q000097:blood; D003094:Collagen / Q000097:blood; D024042:Collagen Type I; D005260:Female; D013006:Growth Hormone / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008875:Middle Aged; D010006:Osteoblasts / Q000187:drug effects* / Q000378:metabolism; D010010:Osteoclasts / Q000187:drug effects* / Q000378:metabolism; D015663:Osteoporosis, Postmenopausal / Q000188:drug therapy* / Q000378:metabolism; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D011347:Procollagen / Q000097:blood; D011863:Radioimmunoassay; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; D011994:Recombinant Proteins; C052929:collagen type I trimeric cross-linked peptide; C042813:procollagen type I carboxy terminal peptide; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D003094:Collagen; D000469:Alkaline Phosphatase; D002118:Calcium