Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis

Kenneth G. Saag, Ronald Emkey, Thomas J. Schnitzer, Jacques P. Brown, Federico Hawkins, Stefan Goemaere, Gorm Thamsborg, Uri A. Liberman, Pierre D. Delmas, Marie Pierre Malice, Michelle Czachur, Anastasia G. Daifotis, Nancy E Lane, Ricardo Correa-Rotter, Melissa Yanover, Rene Westhovens, Sol Epstein, Jonathan D. Adachi, Patrice Poubelle, Jose Melo-GomesJose A. Rodriguez-Portales

Research output: Contribution to journalArticle

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Abstract

Background: Osteoporosis is a common complication of long-term glucocorticoid therapy for which there is no well-proved preventive or restorative treatment. Methods: We carried out two 48-week, randomized, placebo-controlled studies of two doses of alendronate in 477 men and women, 17 to 83 years of age, who were receiving glucocorticoid therapy. The primary end point was the difference in the mean percent change in lumbar-spine bone density from base line to week 48 between the groups. Secondary outcomes included changes in bone density of the hip, biochemical markers of bone turnover, and the incidence of new vertebral fractures. Results: The mean (±SE) bone density of the lumbar spine increased by 2.1±0.3 percent and 2.9±0.3 percent, respectively, in the groups that received 5 and 10 mg of alendronate per day (P<0.001) and decreased by 0.4±0.3 percent in the placebo group. The femoral-neck bone density increased by 1.2±0.4 percent and 1.0±0.4 percent in the respective alendronate groups (P<0.01) and decreased by 1.2±0.4 percent in the placebo group (P<0.01). The bone density of the trochanter and total body also increased significantly in the patients treated with alendronate. There were proportionally fewer new vertebral fractures in the alendronate groups (overall incidence, 2.3 percent) than in the placebo group (3.7 percent) (relative risk, 0.6; 95 percent confidence interval, 0.1 to 4.4). Markers of bone turnover decreased significantly in the alendronate groups (P<0.001). There were no differences in serious adverse effects among the three groups, but there was a small increase in nonserious upper gastrointestinal effects in the group receiving 10 mg of alendronate. Conclusions: Alendronate increases bone density in patients receiving glucocorticoid therapy.

Original languageEnglish (US)
Pages (from-to)292-299
Number of pages8
JournalNew England Journal of Medicine
Volume339
Issue number5
DOIs
StatePublished - Jul 30 1998
Externally publishedYes

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Alendronate
Glucocorticoids
Osteoporosis
Bone Density
Placebos
Bone Remodeling
Therapeutics
Spine
Femur Neck
Incidence
Femur
Hip
Biomarkers
Confidence Intervals

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Saag, K. G., Emkey, R., Schnitzer, T. J., Brown, J. P., Hawkins, F., Goemaere, S., ... Rodriguez-Portales, J. A. (1998). Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis. New England Journal of Medicine, 339(5), 292-299. https://doi.org/10.1056/NEJM199807303390502

Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis. / Saag, Kenneth G.; Emkey, Ronald; Schnitzer, Thomas J.; Brown, Jacques P.; Hawkins, Federico; Goemaere, Stefan; Thamsborg, Gorm; Liberman, Uri A.; Delmas, Pierre D.; Malice, Marie Pierre; Czachur, Michelle; Daifotis, Anastasia G.; Lane, Nancy E; Correa-Rotter, Ricardo; Yanover, Melissa; Westhovens, Rene; Epstein, Sol; Adachi, Jonathan D.; Poubelle, Patrice; Melo-Gomes, Jose; Rodriguez-Portales, Jose A.

In: New England Journal of Medicine, Vol. 339, No. 5, 30.07.1998, p. 292-299.

Research output: Contribution to journalArticle

Saag, KG, Emkey, R, Schnitzer, TJ, Brown, JP, Hawkins, F, Goemaere, S, Thamsborg, G, Liberman, UA, Delmas, PD, Malice, MP, Czachur, M, Daifotis, AG, Lane, NE, Correa-Rotter, R, Yanover, M, Westhovens, R, Epstein, S, Adachi, JD, Poubelle, P, Melo-Gomes, J & Rodriguez-Portales, JA 1998, 'Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis', New England Journal of Medicine, vol. 339, no. 5, pp. 292-299. https://doi.org/10.1056/NEJM199807303390502
Saag, Kenneth G. ; Emkey, Ronald ; Schnitzer, Thomas J. ; Brown, Jacques P. ; Hawkins, Federico ; Goemaere, Stefan ; Thamsborg, Gorm ; Liberman, Uri A. ; Delmas, Pierre D. ; Malice, Marie Pierre ; Czachur, Michelle ; Daifotis, Anastasia G. ; Lane, Nancy E ; Correa-Rotter, Ricardo ; Yanover, Melissa ; Westhovens, Rene ; Epstein, Sol ; Adachi, Jonathan D. ; Poubelle, Patrice ; Melo-Gomes, Jose ; Rodriguez-Portales, Jose A. / Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis. In: New England Journal of Medicine. 1998 ; Vol. 339, No. 5. pp. 292-299.
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abstract = "Background: Osteoporosis is a common complication of long-term glucocorticoid therapy for which there is no well-proved preventive or restorative treatment. Methods: We carried out two 48-week, randomized, placebo-controlled studies of two doses of alendronate in 477 men and women, 17 to 83 years of age, who were receiving glucocorticoid therapy. The primary end point was the difference in the mean percent change in lumbar-spine bone density from base line to week 48 between the groups. Secondary outcomes included changes in bone density of the hip, biochemical markers of bone turnover, and the incidence of new vertebral fractures. Results: The mean (±SE) bone density of the lumbar spine increased by 2.1±0.3 percent and 2.9±0.3 percent, respectively, in the groups that received 5 and 10 mg of alendronate per day (P<0.001) and decreased by 0.4±0.3 percent in the placebo group. The femoral-neck bone density increased by 1.2±0.4 percent and 1.0±0.4 percent in the respective alendronate groups (P<0.01) and decreased by 1.2±0.4 percent in the placebo group (P<0.01). The bone density of the trochanter and total body also increased significantly in the patients treated with alendronate. There were proportionally fewer new vertebral fractures in the alendronate groups (overall incidence, 2.3 percent) than in the placebo group (3.7 percent) (relative risk, 0.6; 95 percent confidence interval, 0.1 to 4.4). Markers of bone turnover decreased significantly in the alendronate groups (P<0.001). There were no differences in serious adverse effects among the three groups, but there was a small increase in nonserious upper gastrointestinal effects in the group receiving 10 mg of alendronate. Conclusions: Alendronate increases bone density in patients receiving glucocorticoid therapy.",
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AU - Emkey, Ronald

AU - Schnitzer, Thomas J.

AU - Brown, Jacques P.

AU - Hawkins, Federico

AU - Goemaere, Stefan

AU - Thamsborg, Gorm

AU - Liberman, Uri A.

AU - Delmas, Pierre D.

AU - Malice, Marie Pierre

AU - Czachur, Michelle

AU - Daifotis, Anastasia G.

AU - Lane, Nancy E

AU - Correa-Rotter, Ricardo

AU - Yanover, Melissa

AU - Westhovens, Rene

AU - Epstein, Sol

AU - Adachi, Jonathan D.

AU - Poubelle, Patrice

AU - Melo-Gomes, Jose

AU - Rodriguez-Portales, Jose A.

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N2 - Background: Osteoporosis is a common complication of long-term glucocorticoid therapy for which there is no well-proved preventive or restorative treatment. Methods: We carried out two 48-week, randomized, placebo-controlled studies of two doses of alendronate in 477 men and women, 17 to 83 years of age, who were receiving glucocorticoid therapy. The primary end point was the difference in the mean percent change in lumbar-spine bone density from base line to week 48 between the groups. Secondary outcomes included changes in bone density of the hip, biochemical markers of bone turnover, and the incidence of new vertebral fractures. Results: The mean (±SE) bone density of the lumbar spine increased by 2.1±0.3 percent and 2.9±0.3 percent, respectively, in the groups that received 5 and 10 mg of alendronate per day (P<0.001) and decreased by 0.4±0.3 percent in the placebo group. The femoral-neck bone density increased by 1.2±0.4 percent and 1.0±0.4 percent in the respective alendronate groups (P<0.01) and decreased by 1.2±0.4 percent in the placebo group (P<0.01). The bone density of the trochanter and total body also increased significantly in the patients treated with alendronate. There were proportionally fewer new vertebral fractures in the alendronate groups (overall incidence, 2.3 percent) than in the placebo group (3.7 percent) (relative risk, 0.6; 95 percent confidence interval, 0.1 to 4.4). Markers of bone turnover decreased significantly in the alendronate groups (P<0.001). There were no differences in serious adverse effects among the three groups, but there was a small increase in nonserious upper gastrointestinal effects in the group receiving 10 mg of alendronate. Conclusions: Alendronate increases bone density in patients receiving glucocorticoid therapy.

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