PT - JOURNAL ARTICLE AU - Shingo Nakayamada AU - Yosuke Okada AU - Kazuyoshi Saito AU - Yoshiya Tanaka TI - Etidronate prevents high dose glucocorticoid induced bone loss in premenopausal individuals with systemic autoimmune diseases. DP - 2004 Jan 01 TA - The Journal of Rheumatology PG - 163--166 VI - 31 IP - 1 4099 - http://www.jrheum.org/content/31/1/163.short 4100 - http://www.jrheum.org/content/31/1/163.full SO - J Rheumatol2004 Jan 01; 31 AB - OBJECTIVE: To assess the efficacy of etidronate and alfacalcidol in preventing glucocorticoid induced bone loss in premenopausal women and men starting high dose glucocorticoid therapy. METHODS: Premenopausal women (n = 16) and men (n = 5) who had just developed autoimmune diseases, and who agreed to use high dose glucocorticoid therapy for the first time, were randomized to receive alfacalcidol (1 micro g/day) alone (alfacalcidol group, n = 11); or alfacalcidol (1 micro g/day) and intermittent cyclical etidronate (200 mg/day for 14 days), given for 4 cycles (combined group, n = 10). They were treated with these medications as well as high dose glucocorticoids for 12 months. RESULTS: In the alfacalcidol group the percentage changes in bone mineral density (BMD) of the lumbar spine after 6 and 12 mo of therapy were -9.6 +/- 0.6% and -10.3 +/- 1.0%, respectively. However, in the combined group the percentage changes in lumbar spine BMD after 6 and 12 mo were -3.8 +/- 1.3% and -4.5 +/- 2.1%. The percentage lumbar spine bone loss rate in the combined group was significantly lower than in the alfacalcidol group at both 6 and 12 mo. After 12 mo the percentage change in femoral neck BMD was increased 2.3 +/- 1.5% in the combined group and was decreased 2.5 +/- 2.4% in the alfacalcidol group; this difference was also statistically significant. There were no significant differences in metabolic bone markers between the groups during the study. CONCLUSION: The results suggest that etidronate could prevent high dose glucocorticoid induced bone loss in premenopausal individuals with systemic autoimmune diseases.