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Normal osteoclastic and osteoblastic responses to exogenous growth hormone in patients with postmenopausal spinal osteoporosis.
J Bone Miner Res 1994; 9(9):1365-70JB

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+Show Affiliations

Aarhus Bone and Mineral Research Group, Department of Endocrinology and Metabolism, Aarhus University Hospital, Denmark.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Comparative Study
Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

7817819

Citation

Kassem, M, et al. "Normal Osteoclastic and Osteoblastic Responses to Exogenous Growth Hormone in Patients With Postmenopausal Spinal Osteoporosis." Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research, vol. 9, no. 9, 1994, pp. 1365-70.
Kassem M, Brixen K, Blum WF, et al. Normal osteoclastic and osteoblastic responses to exogenous growth hormone in patients with postmenopausal spinal osteoporosis. J Bone Miner Res. 1994;9(9):1365-70.
Kassem, M., Brixen, K., Blum, W. F., Mosekilde, L., & Eriksen, E. F. (1994). Normal osteoclastic and osteoblastic responses to exogenous growth hormone in patients with postmenopausal spinal osteoporosis. Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research, 9(9), pp. 1365-70.
Kassem M, et al. Normal Osteoclastic and Osteoblastic Responses to Exogenous Growth Hormone in Patients With Postmenopausal Spinal Osteoporosis. J Bone Miner Res. 1994;9(9):1365-70. PubMed PMID: 7817819.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Normal osteoclastic and osteoblastic responses to exogenous growth hormone in patients with postmenopausal spinal osteoporosis. AU - Kassem,M, AU - Brixen,K, AU - Blum,W F, AU - Mosekilde,L, AU - Eriksen,E F, PY - 1994/9/1/pubmed PY - 1994/9/1/medline PY - 1994/9/1/entrez SP - 1365 EP - 70 JF - Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research JO - J. Bone Miner. Res. VL - 9 IS - 9 N2 - 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. SN - 0884-0431 UR - https://www.unboundmedicine.com/medline/citation/7817819/Normal_osteoclastic_and_osteoblastic_responses_to_exogenous_growth_hormone_in_patients_with_postmenopausal_spinal_osteoporosis_ L2 - https://doi.org/10.1002/jbmr.5650090907 DB - PRIME DP - Unbound Medicine ER -