Prevention of glucocorticoid-induced osteoporosis

被引:5
作者
van Brussel, M. S. [1 ]
Bultink, I. E. M. [1 ]
Lems, W. F. [1 ]
机构
[1] Vrije Univ Amsterdam, Med Ctr, Dept Rheumatol, NL-1081 HV Amsterdam, Netherlands
关键词
bone; fracture; glucocorticoids; osteoporosis; CORTICOSTEROID-INDUCED OSTEOPOROSIS; BONE-MINERAL DENSITY; STEROID-INDUCED OSTEOPOROSIS; LOW-DOSE PREDNISONE; VERTEBRAL FRACTURE; RHEUMATOID-ARTHRITIS; ORAL CORTICOSTEROIDS; DOUBLE-BLIND; CELL-DIFFERENTIATION; THERAPY;
D O I
10.1517/14656560902868225
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
Glucocorticoid-induced osteoporosis is the most common cause of secondary osteoporosis. The role of the Wnt signaling pathway in bone formation and the ratio of receptor activator for NF-kappa B ligand versus osteoprotegerin in bone resorption are exciting new insights. The absolute fracture risk helps both clinicians and patients to interpret the results of bone density measurement, which may have a positive influence on adherence to therapy. The bisphosphonates alendronate and risedronate are the first-line treatment in the prevention of glucocorticoid-induced osteoporosis, because both increase the bone mineral density of the spine and hips and reduce the vertebral fracture rate. Treatment with the anabolic agent parathyroid hormone (1 - 34) strongly stimulates bone turnover, and seems to be superior to treatment with alendronate. it might be attractive for glucocorticoid-treated patients with new vertebral fractures during treatment with bisphosphonates, and/or with severe fracture risk.
引用
收藏
页码:997 / 1005
页数:9
相关论文
共 71 条
[1]
Adachi JD, 2001, ARTHRITIS RHEUM-US, V44, P202, DOI 10.1002/1529-0131(200101)44:1<202::AID-ANR27>3.0.CO
[2]
2-W
[3]
THE ACUTE-PHASE RESPONSE AFTER BISPHOSPHONATE ADMINISTRATION [J].
ADAMI, S ;
BHALLA, AK ;
DORIZZI, R ;
MONTESANTI, F ;
ROSINI, S ;
SALVAGNO, G ;
LOCASCIO, V .
CALCIFIED TISSUE INTERNATIONAL, 1987, 41 (06) :326-331
[4]
Membrane glucocorticoid receptors (mGCR) are expressed in normal human peripheral blood mononuclear cells and up-regulated after in vitro stimulation and in patients with rheumatoid arthritis [J].
Bartholome, B ;
Spies, CM ;
Gaber, T ;
Schuchmann, S ;
Berki, T ;
Kunkel, D ;
Bienert, M ;
Radbruch, A ;
Burmester, GR ;
Lauster, R ;
Scheffold, A ;
Buttgereit, F .
FASEB JOURNAL, 2004, 18 (01) :70-80
[5]
Chronic elevation of parathyroid hormone in mice reduces expression of sclerostin by osteocytes: A novel mechanism for hormonal control of osteoblastogenesis [J].
Bellido, T ;
Ali, AA ;
Gubrij, I ;
Plotkin, LI ;
Fu, Q ;
O'Brien, CA ;
Manolagas, SC ;
Jilka, RL .
ENDOCRINOLOGY, 2005, 146 (11) :4577-4583
[6]
Buttgereit F, 1998, ARTHRITIS RHEUM, V41, P761, DOI 10.1002/1529-0131(199805)41:5<761::AID-ART2>3.0.CO
[7]
2-M
[8]
Glucocorticoid-induced osteoporosis: pathophysiology and therapy [J].
Canalis, E. ;
Mazziotti, G. ;
Giustina, A. ;
Bilezikian, J. P. .
OSTEOPOROSIS INTERNATIONAL, 2007, 18 (10) :1319-1328
[9]
Perspectives on glucocorticoid-induced osteoporosis [J].
Canalis, E ;
Bilezikian, JP ;
Angeli, A ;
Giustina, A .
BONE, 2004, 34 (04) :593-598
[10]
Mechanisms of anabolic therapies for osteoporosis [J].
Canalis, Ernesto ;
Giustina, Andrea ;
Bilezikian, John P. .
NEW ENGLAND JOURNAL OF MEDICINE, 2007, 357 (09) :905-916