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Vertebral Fracture and Bone Mineral Density in Women Receiving High Dose Glucocorticoids for Treatment of Autoimmune Diseases
SHUNICHI KUMAGAI, SEIJI KAWANO, TATSUYA ATSUMI, SHIGEKO INOKUMA, YOSUKE OKADA, YOSHIKI KANAI, JUNICHI KABURAKI, HIDETO KAMEDA, AKIRA SUWA, HIROYUKI HAGIYAMA, SHUNSEI HIROHATA, HIROFUMI MAKINO, and HIROSHI HASHIMOTO
ABSTRACT.
Methods. A cross-sectional study was performed on women who had received at least 0.5 mg/kg of oral glucocorticoid for the treatment of autoimmune diseases for more than 1 month between 1998 and 2003. Logistic regression analysis and chi-square test were used to examine the effects of glucocorticoid dose and other factors on vertebral fractures. Receiver-operating characteristics curve (ROC) analysis was used to determine the bone mineral density (BMD) cutoff value for the risk of vertebral fracture. Results. The study population comprised 160 women, including 35 with vertebral fractures. In ROC analysis, the BMD threshold of the risk of fracture for postmenopausal women (0.787 g/cm2 , T score –2.1) was lower than that for premenopausal women (0.843 g/cm2 , T score –1.7). Among patients with fractures, 7 of 16 premenopausal patients had normal BMD values (T score > –1), whereas only one of 19 postmenopausal patients showed a comparable level of BMD. Additionally, vertebral fracture was more frequent for patients with high total cholesterol values (> 280 mg/dl) than for those with normal total cholesterol values (< 220 mg/dl). Moreover, patients with high total cholesterol values had lower BMD values than those with normal total cholesterol values. Conclusion. The fact that vertebral fracture frequently occurred in premenopausal patients with normal BMD and evidence that hyperlipidemia correlated with fracture suggest the pathology of vertebral fracture secondary to high dose glucocorticoid therapy is multifactorial and possibly involves lipid metabolism. (J Rheumatol 2005;32:863-9) Key Indexing Terms:
OSTEOPOROSIS
From the Department of Clinical Pathology and Immunology, Kobe University Graduate School of Medicine, Kobe; Department of Medicine II, Hokkaido University Graduate School of Medicine, Sapporo; Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital, Tokyo; First Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Fukuoka; Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo; Department of Internal Medicine, Tokyo Electric Power Company Hospital, Tokyo; Second Department of Internal Medicine, Saitama Medical Center, Saitama; Department of Internal Medicine, Keio University School of Medicine, Tokyo; Department of Medicine and Rheumatology, Graduate School, Tokyo Medical and Dental University, Tokyo; Department of Internal Medicine, Teikyo University School of Medicine, Tokyo; and Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan. The Research Committee for Glucocorticoid-Induced Osteoporosis was supported by Health and Labor Sciences Research Grants (14211301) from the Japanese Ministry of Health, Labor and Welfare. S. Kumagai, MD, PhD; S. Kawano, MD, PhD, Department of Clinical Pathology and Immunology, Kobe University Graduate School of Medicine; T. Atsumi, MD, PhD, Department of Medicine II, Hokkaido University Graduate School of Medicine; S. Inokuma, MD, PhD, Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital; Y. Okada, MD, PhD, First Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Fukuoka; Y. Kanai, MD, PhD; H. Hashimoto, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; J. Kaburaki, MD, PhD, Department of Internal Medicine, Tokyo Electric Power Company Hospital; H. Kameda, MD, PhD, Second Department of Internal Medicine, Saitama Medical Center; A. Suwa, MD, PhD, Department of Internal Medicine, Keio University School of Medicine; H. Hagiyama, MD, PhD, Department of Medicine and Rheumatology, Graduate School, Tokyo Medical and Dental University; S. Hirohata, MD, PhD, Department of Internal Medicine, Teikyo University School of Medicine; H. Makino, MD, PhD, Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry. Address reprint requests to Prof. S. Kumagai, Department of Clinical Pathology and Immunology, Kobe University Graduate School of Medicine, Kusunoki-Cho 7-5-2, Chuo-Ku, Kobe, Hyogo 650-17, Japan. E-mail: kumagais@kobe-u.ac.jp Accepted for publication December 20, 2004. |