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

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)

[1]  P. Sambrook Glucocorticoid osteoporosis. , 2002, Current pharmaceutical design.

[2]  J. Finkelstein,et al.  Increases in bone mineral density after discontinuation of daily human parathyroid hormone and gonadotropin-releasing hormone analog administration in women with endometriosis. , 1999, The Journal of clinical endocrinology and metabolism.

[3]  H. Genant,et al.  Parathyroid hormone treatment can reverse corticosteroid-induced osteoporosis. Results of a randomized controlled clinical trial. , 1998, The Journal of clinical investigation.

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

[5]  A. Parfitt,et al.  Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone. , 1998, The Journal of clinical investigation.

[6]  C. Moniz,et al.  A double blind placebo controlled study to determine the effects of intermittent cyclical etidronate on bone mineral density in patients on long term oral corticosteroid treatment , 1998, Thorax.

[7]  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.

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

[9]  E. Leib,et al.  Calcium and Vitamin D3 Supplementation Prevents Bone Loss in the Spine Secondary to Low-Dose Corticosteroids in Patients with Rheumatoid Arthritis , 1996, Annals of Internal Medicine.

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

[11]  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.

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

[14]  J. Adachi,et al.  Corticosteroid-induced osteoporosis. , 1993, Seminars in arthritis and rheumatism.

[15]  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.

[16]  L. Raisz,et al.  Glucocorticoid-induced osteoporosis: pathogenesis and management. , 1990, Annals of internal medicine.

[17]  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.

[18]  J. Parsons,et al.  A Bioassay for Parathyroid Hormone using Chicks , 1973 .

[19]  J. Parsons,et al.  A chick bioassay for parathyroid hormone. , 1973, Endocrinology.

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