DRUG-INDUCED DISORDERS OF BONE METABOLISM - INCIDENCE, MANAGEMENT AND AVOIDANCE

被引:28
作者
JONES, G [1 ]
SAMBROOK, PN [1 ]
机构
[1] ST VINCENTS HOSP,GARVAN INST MED RES,DIV BONE & MINERAL RES,384 VICTORIA ST,DARLINGHURST,NSW 2010,AUSTRALIA
关键词
D O I
10.2165/00002018-199410060-00006
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Calcium homeostasis depends upon the interplay of intestinal calcium absorption, renal excretion and skeletal mobilisation of calcium, mediated through bone formation and resorption, which are closely coupled in the adult skeleton. Serum calcium is extremely important for maintenance of normal cellular functions and is regulated by the major calciotropic hormones, parathyroid hormone (PTH), 1,25-dihydroxy-vitamin D and calcitonin. Certain drugs can interfere with calcium metabolism by effects at different stages in calcium metabolism, and a knowledge of the mechanism of drug action is generally helpful in understanding the various resultant clinical skeletal syndromes. Corticosteroids, for example, have profound effects at multiple stages of calcium metabolism, resulting in decreased bone formation and enhanced bone resorption leading to accelerated osteoporosis. Drugs such as aluminium and anticonvulsants impair mineralisation, leading to osteomalacia. Other drugs, such as fluoride, are employed for their known effects on bone, but in excess dosage can be harmful by producing mineralisation defects. Management of these conditions will be discussed in this review.
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收藏
页码:480 / 489
页数:10
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共 95 条
[21]  
Goodman W.G., Duarte M.E.L., Aluminium: effects on bone and role in the pathogenesis of renal osteodystrophy, Mineral and Electrolyte Metabolism, 17, pp. 221-232, (1991)
[22]  
Grecu E.O., Weinshelbaum A., Simmons R., Effective therapy of glucocorticoid-induced osteoporosis with medroxyprogesterone acetate, Calcified Tissue International, 46, pp. 294-299, (1990)
[23]  
Griffith G., Nichols G., Asher J.D., Flanaghan B., Heparin Osteoporosis, Journal of the American Medical Association, 193, pp. 85-88, (1965)
[24]  
Hahn T.J., Halstead L.R., Bran D.T., Effects of short term glucocorticoid administration on intestinal calcium absorption and circulating vitamin D metabolite concentrations in man, Journal of Clinical Endocrinology and Metabolism, 52, pp. 111-115, (1981)
[25]  
Hahn T.J., Hendin B.A., Scharp C.R., Boisseau V.C., Haddad J.G., Serum 25-hydroxycalciferol levels and bone mass in children on chronic anticonvulsant therapy, New England Journal of Medicine, 292, pp. 550-554, (1975)
[26]  
Hall G.M., Spector T.D., Griffin A.J., Et al., The effect of rheumatoid arthritis and steroid therapy on bone density in postmenopausal women, Arthritis and Rheumatism, 36, pp. 1510-1516, (1993)
[27]  
Haram K., Thordarson H., Hervig T., Calcium homeostasis in pregnancy and lactation, Acta Obstetricia et Gynecologica Scandi, 72 avica, pp. 509-513, (1993)
[28]  
Heaney R.P., Saville P.D., Etidronate disodium in postmenopausal osteoporosis, Clinical Pharmacology and Therapeutics, 20, pp. 593-604, (1976)
[29]  
Hunter J., Maxwell J.D., Steward D.A., Et al., Altered calcium metabolism in epileptic children on anticonvulsants, British Medical Journal, 14, pp. 202-204, (1971)
[30]  
Inkovaara J., Heikenheimo R., Jarvinen K., Et al., Prophylactic fluoride treatment and aged bones, British Medical Journal, 3, pp. 73-74, (1975)