Parathyroid hormone treatment can reverse corticosteroid-induced osteoporosis. Results of a randomized controlled clinical trial.

Corticosteroid-induced osteoporosis is the most common secondary cause of osteoporosis. We conducted a 12-mo, randomized clinical trial of human parathyroid hormone 1-34 (hPTH 1-34) in postmenopausal women (mean age was 63 yr) with osteoporosis who were taking corticosteroids 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 (+/-SE) changes in BMD of the lumbar spine by QCT and DXA in the PTH group were 35+/-5.5% and 11+/-1.4%, respectively, compared with a relatively small change of 1.7+/-1.8% and 0+/-0.9% in the estrogen-only group. The differences in mean percentage between the groups at 1 yr were 33.5% for the lumbar spine by QCT (P < 0.001) and 9.8% for the lumbar spine by DXA (P < 0.001). The changes in the hip and forearm were not significantly different between or within the groups. During the first 3 mo of PTH treatment, markers of bone formation increased to nearly 150%, whereas markers of bone resorption increased only 100%, suggesting an early uncoupling of bone turnover in favor of formation. These results suggest that parathyroid hormone dramatically increases bone mass in the central skeleton of postmenopausal women with corticosteroid- induced osteoporosis who are taking hormone replacement.

[1]  S. Ikuyama,et al.  Glucocorticoid-induced osteoporosis: pathogenesis and management , 2000, Journal of Bone and Mineral Metabolism.

[2]  Jacques P. Brown,et al.  Alendronate for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis , 1998 .

[3]  R. Lindsay,et al.  Randomised controlled study of effect of parathyroid hormone on vertebral-bone mass and fracture incidence among postmenopausal women on oestrogen with osteoporosis , 1997, The Lancet.

[4]  Jacques P. Brown,et al.  Intermittent etidronate therapy to prevent corticosteroid-induced osteoporosis. , 1997, The New England journal of medicine.

[5]  S. Cummings,et al.  Randomised trial of effect of alendronate on risk of fracture in women with existing vertebral fractures , 1996, The Lancet.

[6]  R. Lindsay,et al.  Temporal expression of the anabolic action of PTH in cancellous bone of ovariectomized rats , 1996, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[7]  J. Adachi Corticosteroid-induced osteoporosis. , 1996, Drug and therapeutics bulletin.

[8]  J. Kinney,et al.  Intermittent treatment with human parathyroid hormone (hPTH[1‐34]) increased trabecular bone volume but not connectivity in osteopenic rats , 1995, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[9]  W. Sietsema Animal models of cortical porosity. , 1995, Bone.

[10]  Robert Epstein,et al.  Comparison of methods for defining prevalent vertebral deformities: The study of osteoporotic fractures , 1995, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[11]  F. Melsen,et al.  Reconstruction of cortical bone remodeling in untreated primary hyperparathyroidism and following surgery. , 1995, Bone.

[12]  T. Spector,et al.  Effect of hormone replacement therapy on bone mass in rheumatoid arthritis patients treated with and without steroids. , 1994, Arthritis and rheumatism.

[13]  L. Mosekilde,et al.  The effect on vertebral bone mass and strength of long term treatment with antiresorptive agents (estrogen and calcitonin), human parathyroid hormone-(1-38), and combination therapy, assessed in aged ovariectomized rats. , 1994, Endocrinology.

[14]  G. Segre,et al.  Parathyroid hormone induces sequential c-fos expression in bone cells in vivo: in situ localization of its receptor and c-fos messenger ribonucleic acids. , 1994, Endocrinology.

[15]  J. Eisman,et al.  Prevention of corticosteroid osteoporosis. A comparison of calcium, calcitriol, and calcitonin. , 1993, The New England journal of medicine.

[16]  S. Cummings,et al.  Bone density at various sites for prediction of hip fractures , 1993, The Lancet.

[17]  R. Robinson,et al.  Estrogen and progesterone replacement therapy reduces glucocorticoid‐induced bone loss , 1992, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[18]  W M O'Fallon,et al.  Effect of fluoride treatment on the fracture rate in postmenopausal women with osteoporosis. , 1990, The New England journal of medicine.

[19]  C C Glueer,et al.  Quantitative computed tomography in assessment of osteoporosis. , 1987, Seminars in nuclear medicine.

[20]  R M Neer,et al.  Restoration of spinal bone in osteoporotic men by treatment with human parathyroid hormone (1–34) and 1,25‐dihydroxyvitamin D , 1986, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[21]  A. Jones,et al.  Parathyroid hormone receptor in intact embryonic chicken bone: characterization and cellular localization , 1982, The Journal of cell biology.

[22]  J. Heersche,et al.  Parathyroid hormone stimulates the bone apposition rate independently of its resorptive action: differential effects of intermittent and continuous administration. , 1982, Endocrinology.

[23]  S. Krane,et al.  An evaluation of antibodies and clinical resistance to salmon calcitonin. , 1972, The Journal of clinical investigation.