title: Enhancement of bone mass in osteoporotic women with parathyroid hormone followed by alendronate.
abstract: Treatment of osteoporosis with PTH causes a marked increase in vertebral bone mineral density (BMD). However, this effect is rapidly reversed when the treatment is stopped. The purpose of the present study was to determine whether the bisphosphonate alendronate could preserve or enhance bone density in patients previously treated with PTH. Sixty-six postmenopausal osteoporotic women were treated for 1 yr with 50, 75, or 100 microg recombinant human PTH-(1-84) or placebo, and then were given 10 mg alendronate daily for an additional year. BMD was measured in the femoral neck, lumbar spine, and whole body. Markers of bone turnover included skeletal alkaline phosphatase, osteocalcin, and N-telopeptide. During the first year, changes in BMD (mean +/- SD) in women receiving PTH (all doses combined) were 7.1 +/- 5.6% (spine), 0.3 +/- 6.2% (femoral neck), and -2.3 +/- 3.3% (total body). After switching to alendronate for 1 yr in women who previously had received PTH, mean changes in BMD were 13.4 +/- 6.4% (spine), 4.4 +/- 7.2% (femoral neck), and 2.6 +/- 3.1% (whole body). In the subgroup of patients who had received the highest dose of PTH, the mean increase in vertebral BMD was 14.6 +/- 7.9%. All markers of bone turnover increased during treatment with PTH and decreased to below baseline after 1 yr of alendronate. In conclusion, sequential treatment of osteoporosis with PTH and alendronate results in an increase in vertebral bone density that is considerably more than has been reported with alendronate or estrogens alone. This combination of drugs may be a useful approach to maximizing bone density in women with vertebral osteoporosis.
authors.affiliation: Department of Medicine and the Queen Elizabeth II Health Sciences Center, Dalhousie University, Halifax, Nova Scotia, Canada. rsr89794@glaxowellcome.com
authors.forename: R S
authors.initials: RS
authors.lastname: Rittmaster
authors.forename: M
authors.initials: M
authors.lastname: Bolognese
authors.forename: M P
authors.initials: MP
authors.lastname: Ettinger
authors.forename: D A
authors.initials: DA
authors.lastname: Hanley
authors.forename: A B
authors.initials: AB
authors.lastname: Hodsman
authors.forename: D L
authors.initials: DL
authors.lastname: Kendler
authors.forename: C J
authors.initials: CJ
authors.lastname: Rosen
mesh_terms: D000368:Aged; D019386:Alendronate / Q000627:therapeutic use*; D000469:Alkaline Phosphatase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D015519:Bone Density / Q000187:drug effects*; D003094:Collagen / Q000097:blood; D024042:Collagen Type I; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D005269:Femur; D005500:Follow-Up Studies; D006801:Humans; D008159:Lumbar Vertebrae; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D015663:Osteoporosis, Postmenopausal / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D010281:Parathyroid Hormone / Q000627:therapeutic use*; D010455:Peptides / Q000097:blood; D019379:Teriparatide / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D010281:Parathyroid Hormone; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D015675:Osteocalcin; D019379:Teriparatide; D003094:Collagen; D000469:Alkaline Phosphatase; D019386:Alendronate