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Glucocorticoid induced osteoporosis

Glucocorticoid induced osteoporosis Carlo Gennari Institute of Internal Medicine, University of Siena, Italy The association between glucocorticoid excess and osteoporosis, first described by Cushing (1 932) in one case with adrenal hyperfunction secondary to a pituitary tumour, has become a significant problem since compound E (cortisone) was first administered to a patient with rheumatoid arthritis in 1948 (Hench et al., 1949). It soon appeared that patients with autoimmune, rheumatic, allergic or dermatological disorders receiving prolonged glucocorticoid therapy develop a clinically significant degree of bone loss and atraumatic fractures. The earliest attempts to establish the incidence of glucocorticoid induced bone loss were based on radiological signs of vertebral crush fractures reported in approximately 3-15% of cases studied (Nordin 1960). The past 20 years have seen the development of new techniques for quantitating bone mass with high precision and accuracy at axial, appendicular and total skeletal sites, including total body calcium by neutron activation analysis, photon or X-ray absorptiometry and computed tomography. As more precise methods for evaluating bone mass were utilized, the incidence of glucocorticoid induced osteoporosis, defined as number of patients suffering atraumatic fractures, was found to be of the order of 30-50% (Adinoff & Hollister, 1983). Using these methods, substantial http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Endocrinology Wiley

Glucocorticoid induced osteoporosis

Gennari, Carlo
Clinical Endocrinology , Volume 41 (3) – Sep 1, 1994
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References (20)

Publisher
Wiley
Copyright
Copyright © 1994 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0300-0664
eISSN
1365-2265
DOI
10.1111/j.1365-2265.1994.tb02544.x
Publisher site
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Abstract

Carlo Gennari Institute of Internal Medicine, University of Siena, Italy The association between glucocorticoid excess and osteoporosis, first described by Cushing (1 932) in one case with adrenal hyperfunction secondary to a pituitary tumour, has become a significant problem since compound E (cortisone) was first administered to a patient with rheumatoid arthritis in 1948 (Hench et al., 1949). It soon appeared that patients with autoimmune, rheumatic, allergic or dermatological disorders receiving prolonged glucocorticoid therapy develop a clinically significant degree of bone loss and atraumatic fractures. The earliest attempts to establish the incidence of glucocorticoid induced bone loss were based on radiological signs of vertebral crush fractures reported in approximately 3-15% of cases studied (Nordin 1960). The past 20 years have seen the development of new techniques for quantitating bone mass with high precision and accuracy at axial, appendicular and total skeletal sites, including total body calcium by neutron activation analysis, photon or X-ray absorptiometry and computed tomography. As more precise methods for evaluating bone mass were utilized, the incidence of glucocorticoid induced osteoporosis, defined as number of patients suffering atraumatic fractures, was found to be of the order of 30-50% (Adinoff & Hollister, 1983). Using these methods, substantial

Journal

Clinical Endocrinology – Wiley

Published: Sep 1, 1994

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