Parathyroid hormone and teriparatide for the treatment of osteoporosis: a review of the evidence and suggested guidelines for its use.
All therapies currently recommended for the management of osteoporosis act mainly to inhibit bone resorption and reduce bone remodeling. PTH and its analog, teriparatide [recombinant human PTH(1-34)], represent a new class of anabolic therapies for the treatment of severe osteoporosis, having the potential to improve skeletal microarchitecture. Significant reductions in both vertebral and appendicular fracture rates have been demonstrated in the phase III trial of teriparatide, involving elderly women with at least one prevalent vertebral fracture before the onset of therapy. However, there is as yet no evidence that the antifracture efficacy of PTH will be superior to the bisphosphonates, whereas cost-utility estimates suggest that teriparatide is significantly more expensive. Teriparatide should be considered as treatment for postmenopausal women and men with severe osteoporosis, as well as for patients with established glucocorticoid-induced osteoporosis who require long-term steroid treatment. Teriparatide should also be considered for the management of individuals at particularly high risk for fractures, including subjects who are younger than age 65 and who have particularly low bone mineral density measurements (T scores < or = 3.5). Teriparatide therapy is not recommended for more than 2 yr, based, in part, on the induction of osteosarcoma in a rat model of carcinogenicity. Total daily calcium intake from both supplements and dietary sources should be limited to 1500 mg together with adequate vitamin D intake (< or =1000 U/d). Monitoring of serum calcium may be safely limited to measurement after 1 month of treatment; mild hypercalcemia may be treated by withdrawing dietary calcium supplements, reducing the dosing frequency of PTH, or both. At present, concurrent therapy with antiresorptive therapy, particularly bisphosphonates, should be avoided, although sequential therapy with such agents may consolidate the beneficial effects upon the skeleton after PTH is discontinued.
Hodsman
Anthony B
AB
University of Western Ontario, St. Joseph's Health Care, Room 2F-15, 268, Grosvenor Street, London, Ontario N6A 4V2, Canada. anthony.hodsman@sjhc.london.on.ca
Bauer
Douglas C
DC
Dempster
David W
DW
Dian
Larry
L
Hanley
David A
DA
Harris
Steven T
ST
Kendler
David L
DL
McClung
Michael R
MR
Miller
Paul D
PD
Olszynski
Wojciech P
WP
Orwoll
Eric
E
Yuen
Chui Kin
CK
D000368:Aged; D015519:Bone Density / Q000187:drug effects; D016723:Bone Remodeling / Q000187:drug effects; D002986:Clinical Trials as Topic; D004164:Diphosphonates / Q000627:therapeutic use; D005260:Female; D006801:Humans; D008297:Male; D010024:Osteoporosis / Q000188:drug therapy*; D010281:Parathyroid Hormone / Q000627:therapeutic use*; D017410:Practice Guidelines as Topic; D019379:Teriparatide / Q000627:therapeutic use*
D004164:Diphosphonates; D010281:Parathyroid Hormone; D019379:Teriparatide