Carolyn Crandall1. 1. Department of Medicine, David Geffen School of Medicine at University of California, Iris Cantor-UCLA Women's Health Center, UCLA School of Medicine, 100 UCLA Medical Plaza, Suite 250, Los Angeles, CA 90095-7023, USA. ccrandall@mednet.ucla.edu
Abstract
BACKGROUND: Osteoporosis is a common condition associated with multiple deleterious consequences. No therapy entirely abolishes fracture risk. METHODS: A MEDLINE database (1966 to the present) search was performed for randomized controlled trials in humans using the keywords osteoporosis and parathyroid hormone (PTH) or parathyroid hormone and fracture. The Cochrane database was searched using the search terms osteoporosis and parathyroid hormone. RESULTS: Parathyroid hormone (usually subcutaneous) dosages varied markedly across the 20 randomized controlled trial studies retrieved. In the range of 50 to 100 micro g/d, effects may be dose-related. Results of larger trials (up to 1637 patients) were conflicting as to whether effects were limited to the spine and suggested detrimental effects on radius bone mineral density. Little data analyzed the effects of PTH in older vs younger subjects or directly compared the effects by sex. Increases in spine bone mineral density are induced by PTH in postmenopausal osteoporosis, glucocorticoid-induced osteoporosis, and idiopathic osteoporosis. Parathyroid hormone may protect against gonadotropin-releasing hormone agonist-related bone loss. Effects are less clear at nonspine sites when PTH is used as part of combination or sequential therapies or for treatment of glucocorticoid-induced osteoporosis. Parathyroid hormone decreased the incidence of radiographically detected spinal fractures. The numbers of nonvertebral fractures were too low to be broken down by individual site. Parathyroid hormone injections were difficult for some patients to comply with. Occasionally, PTH-associated hypercalcemia may be dose-dependent, often manifesting early in treatment. An increase in cancer risk from PTH is not reported in humans. CONCLUSIONS: Parathyroid hormone decreases vertebral fractures and increases spinal bone density in postmenopausal osteoporosis and glucocorticoid-induced osteoporosis, but at the expense of a decrease in radius bone density. The long-term safety and nonvertebral fracture efficacy are unknown.
BACKGROUND:Osteoporosis is a common condition associated with multiple deleterious consequences. No therapy entirely abolishes fracture risk. METHODS: A MEDLINE database (1966 to the present) search was performed for randomized controlled trials in humans using the keywords osteoporosis and parathyroid hormone (PTH) or parathyroid hormone and fracture. The Cochrane database was searched using the search terms osteoporosis and parathyroid hormone. RESULTS:Parathyroid hormone (usually subcutaneous) dosages varied markedly across the 20 randomized controlled trial studies retrieved. In the range of 50 to 100 micro g/d, effects may be dose-related. Results of larger trials (up to 1637 patients) were conflicting as to whether effects were limited to the spine and suggested detrimental effects on radius bone mineral density. Little data analyzed the effects of PTH in older vs younger subjects or directly compared the effects by sex. Increases in spine bone mineral density are induced by PTH in postmenopausal osteoporosis, glucocorticoid-induced osteoporosis, and idiopathic osteoporosis. Parathyroid hormone may protect against gonadotropin-releasing hormone agonist-related bone loss. Effects are less clear at nonspine sites when PTH is used as part of combination or sequential therapies or for treatment of glucocorticoid-induced osteoporosis. Parathyroid hormone decreased the incidence of radiographically detected spinal fractures. The numbers of nonvertebral fractures were too low to be broken down by individual site. Parathyroid hormone injections were difficult for some patients to comply with. Occasionally, PTH-associated hypercalcemia may be dose-dependent, often manifesting early in treatment. An increase in cancer risk from PTH is not reported in humans. CONCLUSIONS:Parathyroid hormonedecreases vertebral fractures and increases spinal bone density in postmenopausal osteoporosis and glucocorticoid-induced osteoporosis, but at the expense of a decrease in radius bone density. The long-term safety and nonvertebral fracture efficacy are unknown.
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