Alendronate prevents steroid-induced osteoporosis in patients with rheumatic diseases
Wang, Q-hong.; Wu, H-xiang.; Huang, Y-lu.; Xue, J.; Yang, X-yan.; Zhu, L.; Wen, L-hong.
Zhonghua Yi Xue Za Zhi 88(27): 1888-1891
2008
ISSN/ISBN: 0376-2491 PMID: 19040000 Document Number: 618862
To investigate the effects of alendronate (Alen) on the prevention of systemic glucocorticoid-induced osteoporosis in patients with rheumatic diseases. 140 patients suffering from rheumatic diseases, including systemic lupus erythematosus, polymyositis, dermatomyositis, and Sjögren's syndrome, with normal bone mineral density (BMD) and treated with oral glucocorticoids were randomly divided into 2 groups: Alen + calcium group (n = 74) receiving Alen 10 mg once a day and castrate D 600 0.6 g once a day for 24 weeks and control group (n = 66) receiving castrate D 600 0.6 g once a day for 24 weeks. The BMD and biomarkers of bone turnover were measured at baseline and 24 weeks after initiating glucocorticoid therapy. After 24 weeks, the BMD values at lumbar spine, femoral neck, major trochanter, and Ward' s triangle increased by 6.1%, 6.3%, 3.3%, and 2.2% respectively compared with those at baseline (all P<0.05), however, those of the control group decreased by 8.7%, 9.1%, 7.7%, and 6.4% respectively (P<0.01, P<0.05), and the BMD levels at lumbar spine and femoral neck 24 weeks later of the Alen + calcium group were both higher than those of the control group (P<0.01, P<0.05). 24 weeks later the level of urine cross linked N-telopeptides of type I collagen (NTX) of the Alen + calcium group decreased (P<0.05), and the blood osteocalcin (BGP) of the Alen + calcium group increased, however, not significantly (P>0.05). There were no significant differences in serum AKP and BGP and urine NTX 24 weeks later between these 2 groups. Improving BMD, alendronate plays an important role in the prevention of glucocorticoid-induced osteoporosis. However, calcium treatment alone fails to prevent the loss of bone.