title: [Glucocorticoid-induced osteoporosis: recent findings].
abstract: The clinical features, pathogenesis and management of bone involvement in Cushing's syndrome are briefly reviewed. Personal data on bone mineral density and markers of bone turnover in Cushing's syndrome and adrenal incidentalomas are also reported. As long ago as 1932, Harvey Cushing recognized osteoporosis as a serious consequence of endogenous hypercortisolism. The introduction of cortisone in the therapy of autoimmune, rheumatic, allergic or dermatologic disorders was followed by several reports of detrimental effects on bone of patients who had undergone prolonged glucocorticoid treatment. Due to the rarity of Cushing's syndrome, most of the studies in the literature on glucocorticoid-induced osteoporosis refer to exogenous over-exposure to cortisone and its synthetic derivatives. Only a small number of works concern endogenous hypercortisolism, even if the characteristics of bone damage seem qualitatively the same. Finally, very few data are reported on the hypothetical detrimental effect on bone in the condition of the silent hypercortisolism of adrenal incidentalomas. Glucocorticoid-induced osteoporosis in Cushing's syndrome often results in vertebral fractures, and bone loss is more evident in trabecular than in cortical bone. Notwithstanding some distinctive features in osteoporosis induced by endogenous and exogenous glucocorticoid excess, the common eventual picture is notable bone damage that involves mainly the trabecular bone. Prompt and effective therapy is mandatory to reduce the risk of fractures. The present options include calcium and vitamin D supplementation, estrogen replacement therapy, bisphosphonates, either oral or parenteral. A novel approach to the clinical problem of glucocorticoid-induced osteoporosis might, in the future, be based on studies on selective glucocorticoid receptor modulators, a new class of synthetic glucocorticoids that exhibit significant anti-inflammatory and immunosuppressive activities, with reduced side effects on bone.
authors.affiliation: Dipartimento di Scienze Cliniche e Biologiche, Università degli Studi di Torino. angeli@pasteur.sluigi.unito.it
authors.forename: A
authors.initials: A
authors.lastname: Angeli
authors.forename: G
authors.initials: G
authors.lastname: Osella
authors.forename: G
authors.initials: G
authors.lastname: Reimondo
authors.forename: M
authors.initials: M
authors.lastname: Terzolo
mesh_terms: D000306:Adrenal Cortex Neoplasms / Q000150:complications / Q000378:metabolism; D000308:Adrenocortical Hyperfunction / Q000150:complications / Q000378:metabolism; D015519:Bone Density / Q000187:drug effects; D003480:Cushing Syndrome / Q000150:complications / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D010024:Osteoporosis / Q000139:chemically induced* / Q000378:metabolism
chemical_list: D005938:Glucocorticoids