Glucocorticoid-induced osteoporosis: pathophysiological data and recent treatments.
Long-term glucocorticoid therapy promptly induces osteoporosis, whose severity depends on the dose and duration of the treatment. Recent data suggest that there is no safety threshold for adverse effects on bone. Glucocorticoid therapy impairs calcium intestinal absorption, dramatically suppresses osteoblastic formation, and stimulates osteocyte apoptosis. In contrast, the contribution of secondary hyperparathyroidism and increased bone resorption, although frequently mentioned, is now a focus of controversy. Beneficial effects on bone have been obtained with calcium and vitamin D supplementation, as well as with hormone replacement therapy (HRT) in postmenopausal women. Bisphosphonates are clearly effective in preventing and treating glucocorticoid-induced osteoporosis, although their mechanism of action in this condition remains poorly understood. Parathyroid hormone (PTH) is being evaluated as a potential therapeutic agent for glucocorticoid-induced osteoporosis.
Lafage-Proust
Marie Hélène
MH
Laboratory for the biology of bony tissue, Faculté de médecine, Equipe Inserm 9901, 15, rue A-Paré, 42023 Saint-Etienne cedex 2, France. lafagemh@univ-st-etienne.fr
Boudignon
Benjamin
B
Thomas
Thierry
T
D000818:Animals; D001862:Bone Resorption / Q000503:physiopathology; D002118:Calcium / Q000627:therapeutic use; D004164:Diphosphonates / Q000627:therapeutic use; D005938:Glucocorticoids / Q000009:adverse effects* / Q000494:pharmacology; D006801:Humans; D007408:Intestinal Absorption / Q000187:drug effects; D010006:Osteoblasts / Q000187:drug effects; D010010:Osteoclasts / Q000187:drug effects; D010024:Osteoporosis / Q000139:chemically induced / Q000503:physiopathology* / Q000628:therapy*; D014807:Vitamin D / Q000502:physiology
D004164:Diphosphonates; D005938:Glucocorticoids; D014807:Vitamin D; D002118:Calcium