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

来源：

DRUG SAFETY | 1994年 / 10卷 / 06期

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.

引用

页码：480 / 489

页数：10

共 95 条

[1]

Adami S., Fossaluzza V., Rossini M., Fertoldo F., Gatti D., Et al., Prevention of corticosteroid-induced osteoporosis with nandrolone decanoate, Bone and Mineral, 15, pp. 72-81, (1991)

[2]

Adinoff A.D., Hollister J.R., Steroid-induced fractures and bone loss in patients with asthma, New England Journal of Medicine, 309, pp. 265-268, (1983)

[3]

Alexandre C., Chappard D., Intoxication fluoree par l’eau de Vichy St Yorre, un nouveau cas, Presse Medicale, 13, (1984)

[4]

Boyce B.F., Byars J., McWillia S., Et al., Histological and electron microprobe studies of mineralisation in aluminium-related osteomalacia, Journal of Clinical Pathology, 45, pp. 502-508, (1992)

[5]

Boyce B.F., Fell G.S., Elder H.Y., Et al., Hypercalcaemic osteomalacia due to aluminium toxicity, Lancet, 2, pp. 1009-1013, (1982)

[6]

Bressot C., Meunier P.J., Chapuy M.C., Et al., Histomorphometric profile, pathophysiology and reversibility of corticosteroid induced osteoporosis, Metabolic Bone Disease and Related Research, 1, pp. 303-319, (1979)

[7]

Butler R.C., Davie M.W.J., Worsfold M., Sharp C.A., Bone mineral content in patients with rheumatoid arthritis: relationship to low-dose steroid therapy, British Journal of Rheumatology, 30, pp. 86-90, (1991)

[8]

Christiansen C., Rodbro P., Lund M., Incidence of antoconvulsant osteomalacia and effect of vitamin D: controlled therapeutic trial, British Medical Journal, 4, pp. 695-701, (1973)

[9]

Dahlman T., Lindval N., Hellgren M., Osteopenia in pregnancy during long-term heparin treatment, British Journal of Obstetrics and Gynaecology, 97, pp. 221-228, (1990)

[10]

Dambacher M.A., Ittner J., Rueggsegger P., Fluoride therapy of postmenopausal osteoporosis, Bone, 7, pp. 199-205, (1986)

← 1 2 3 4 5 6 7 8 9 10 →