[Glucocorticoid-induced osteopenia].
This article reviews the pathogenesis of glucocorticoid-induced osteopenia (GIO). GIO is a result of direct and indirect mechanisms leading to: 1) decreased intestinal calcium absorption, 2) decreased renal calcium reabsorption, 3) increased osteoclast activity with increased bone resorption, 4) decreased osteoclast activity with decreased bone formation. The mainly osteoclast activity is raised on the basis of secondary hyperparathyroidism. The different possible treatments in order to prevent GIO are reviewed on the basis of the results of the most important studies about the subject. We conclude that before a secure recommendation about prophylactic treatment can be made more prospective studies with fracture incidence as a measure should be made. However, on the basis of the studies that have already been made, it seems rational to give patients in longterm glucocorticoid treatment a calcium supplement of 0.5-1 g/day either in tablet form or by changing the diet, combined with a vitamin-D supply: either ergocalciferol 600-800 IU/day (e.g. in the form of 2 multivitamin tabs/day) or calcitriol 0.5 microgram/day.
Glerup
H
H
Arhus Kommunehospital, medicinsk afdeling V.
Eriksen
E F
EF
Mosekilde
L
L
D001851:Bone Diseases, Metabolic / Q000139:chemically induced* / Q000378:metabolism / Q000517:prevention & control; D001842:Bone and Bones / Q000378:metabolism / Q000473:pathology; D002118:Calcium / Q000008:administration & dosage / Q000378:metabolism; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D007408:Intestinal Absorption; D007668:Kidney / Q000378:metabolism; D014807:Vitamin D / Q000008:administration & dosage
D005938:Glucocorticoids; D014807:Vitamin D; D002118:Calcium
Glukokortikoidinduceret osteopeni.