title: Sequential treatment of severe postmenopausal osteoporosis after teriparatide: final results of the randomized, controlled European Study of Forsteo (EUROFORS).
abstract: It is unclear which treatment should be given after stopping teriparatide therapy for severe osteoporosis. In a prospective, randomized, controlled, 2-yr study, we compared BMD effects and clinical safety of three follow-up treatments (anabolic with teriparatide, antiresorptive with raloxifene, or no active treatment) after 1 yr of teriparatide. Postmenopausal women with osteoporosis and a recent fragility fracture received open-label teriparatide (20 microg/d) for 12 mo before they were randomized (3:1:1) to continue teriparatide (n = 305), switch to raloxifene 60 mg/d (n = 100), or receive no active treatment for the second year (n = 102). All patients received calcium and vitamin D supplementation. Changes in areal BMD from baseline to 24 mo were analyzed using mixed-model repeated measures. Daily teriparatide treatment for 2 yr significantly increased spine BMD by 10.7%. Patients receiving raloxifene in year 2 had no further change in spine BMD from year 1 (change from baseline, 7.9%), whereas patients receiving no active treatment had a BMD decrease of 2.5% in year 2 (change from baseline, +3.8%). At the total hip, BMD increases from baseline at 2 yr were 2.5% with teriparatide, 2.3% with raloxifene, and 0.5% with no active treatment; the respective changes at the femoral neck were 3.5%, 3.1%, and 1.3%. The study had insufficient power to assess antifracture efficacy. In conclusion, BMD increases progressively over 2 yr of teriparatide therapy in women with severe osteoporosis. After discontinuation of teriparatide, raloxifene maintains spine BMD and increases hip BMD.
authors.affiliation: University of Sheffield, Sheffield, United Kingdom.
authors.forename: Richard
authors.initials: R
authors.lastname: Eastell
authors.forename: Thomas
authors.initials: T
authors.lastname: Nickelsen
authors.forename: Fernando
authors.initials: F
authors.lastname: Marin
authors.forename: Clare
authors.initials: C
authors.lastname: Barker
authors.forename: Peyman
authors.initials: P
authors.lastname: Hadji
authors.forename: Jordi
authors.initials: J
authors.lastname: Farrerons
authors.forename: Maurice
authors.initials: M
authors.lastname: Audran
authors.forename: Steven
authors.initials: S
authors.lastname: Boonen
authors.forename: Kim
authors.initials: K
authors.lastname: Brixen
authors.forename: Jose Melo
authors.initials: JM
authors.lastname: Gomes
authors.forename: Barbara
authors.initials: B
authors.lastname: Obermayer-Pietsch
authors.forename: Avraam
authors.initials: A
authors.lastname: Avramidis
authors.forename: Gunnar
authors.initials: G
authors.lastname: Sigurdsson
authors.forename: Claus C
authors.initials: CC
authors.lastname: Glüer
mesh_terms: D015519:Bone Density / Q000187:drug effects / Q000502:physiology; D050071:Bone Density Conservation Agents / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D015331:Cohort Studies; D004359:Drug Therapy, Combination; D005060:Europe; D005260:Female; D050723:Fractures, Bone / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D008875:Middle Aged; D015663:Osteoporosis, Postmenopausal / Q000139:chemically induced / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D019379:Teriparatide / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D050071:Bone Density Conservation Agents; D019379:Teriparatide