Bone Mass Continues to Increase at the Hip After Parathyroid Hormone Treatment Is Discontinued in Glucocorticoid-Induced Osteoporosis: Results of a Randomized Controlled Clinical Trial
- 1 May 2000
- journal article
- clinical trial
- Published by Oxford University Press (OUP) in Journal of Bone and Mineral Research
- Vol. 15 (5) , 944-951
- https://doi.org/10.1359/jbmr.2000.15.5.944
Abstract
Glucocorticoid-induced osteoporosis is the most common secondary cause of osteoporosis. In this 24-month study, we report changes in bone turnover and bone mass after 12 months of daily injections of human parathyroid hormone 1–34 [hPTH(1–34)] and 12 months off treatment in postmenopausal women (mean age, 63 years) with osteoporosis treated with glucocorticoid and hormone replacement therapy. Response to the treatment was assessed with bone mineral density (BMD) measurements of the lumbar spine by quantitative computed tomography (QCT); BMD measurements of the lumbar spine, hip, and forearm by dual-energy X-ray absorptiometry (DXA); and biochemical markers of bone turnover. The mean (± SEM) change in BMD of the lumbar spine by QCT and DXA in the PTH group at 24 months was 45.9 ± 6.4% and 12.6 ± 2.2% (p < 0.001). The change in total hip and femoral neck BMD was not significant at 12 months but increased to 4.7 ± 0.9% (p < 0.01) and 5.2 ± 1.3% at 24 months, respectively, as compared with a relatively small change of 1.3 ± 0.9% and 2.6 ± 1.7% in the estrogen-only group. The mean percent differences in BMD of the lumbar spine by QCT and DXA between the groups at 24 months were 43.1% and 11.9%, respectively (p < 0.001). The mean percent differences over the estrogen-only group in hip BMD were 3.4% for total hip (p < 0.01) and 2.6% for femoral neck at 24 months. Biochemical markers of bone turnover increased to more than 150% during the first 6 months of therapy, remained elevated throughout the 12-month treatment period, and returned to baseline values within 6 months of discontinuing the PTH treatment. These results suggest that PTH dramatically increases bone mass in the lumbar spine and hip in postmenopausal women with glucocorticoid-induced osteoporosis who are taking hormone replacement therapy. However, the maximum effect of this anabolic agent on bone mass at the hip after 12 months of treatment requires at least 6–12 months after the PTH treatment is discontinued (J Bone Miner Res 2000;15:944–951)Keywords
This publication has 21 references indexed in Scilit:
- Parathyroid hormone treatment can reverse corticosteroid-induced osteoporosis. Results of a randomized controlled clinical trial.Journal of Clinical Investigation, 1998
- Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone.Journal of Clinical Investigation, 1998
- Randomised controlled study of effect of parathyroid hormone on vertebral-bone mass and fracture incidence among postmenopausal women on oestrogen with osteoporosisPublished by Elsevier ,1997
- Comparison of methods for defining prevalent vertebral deformities: The study of osteoporotic fracturesJournal of Bone and Mineral Research, 1995
- Effect of hormone replacement therapy on bone mass in rheumatoid arthritis patients treated with and without steroidsArthritis & Rheumatism, 1994
- Prevention of Corticosteroid Osteoporosis -- A Comparison of Calcium, Calcitriol, and CalcitoninNew England Journal of Medicine, 1993
- Estrogen and progesterone replacement therapy reduces glucocorticoid-induced bone lossJournal of Bone and Mineral Research, 1992
- Restoration of spinal bone in osteoporotic men by treatment with human parathyroid hormone (1–34) and 1,25-dihydroxyvitamin DJournal of Bone and Mineral Research, 1986
- A Bioassay for Parathyroid Hormone using ChicksEndocrinology, 1973
- An evaluation of antibodies and clinical resistance to salmon calcitoninJournal of Clinical Investigation, 1972