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Homocysteine, Bone Mineral Density, and Fracture Risk Over 2 Years of Followup in Women with and without Systemic Lupus Erythematosus
ELISA Y. RHEW, CHIN LEE, POLIKSENI EKSARKO, ALAN R. DYER, HAJRA TILY, STEWART SPIES, RICHARD M. POPE, and ROSALIND RAMSEY-GOLDMAN
ABSTRACT. Methods. Women with SLE (n = 100) and without SLE (n = 100) were matched according to age (± 5 yrs), race, and menopausal status. Data were collected from 1997 to 2004, including hip, lumbar spine (L-spine), and distal forearm BMD, serum homocysteine levels, and a self-administered questionnaire on osteoporosis risk factors, medications and symptomatic fractures at baseline and 2-year followup. Analyses were performed to compare homocysteine levels, BMD, and incident fractures and to evaluate the relationship of homocysteine with BMD and incident fractures in both groups. Results. Mean homocysteine ± SD was higher (p < 0.001) in women with SLE (9.88 ± 3.8 µmol/l) than in women without SLE (7.98 ± 2.6 µmol/l). Women with SLE had significantly lower L-spine BMD Z-scores, while hip BMD Z-scores and distal forearm BMD T-scores were nonsignificantly lower than in women without SLE. No significant correlations were observed between homocysteine and BMD in either group. Thirteen women with SLE experienced new fractures, while 4 women without SLE had new fractures over 2 years (p = 0.035); however, there was no association between homocysteine levels and incident fractures in either group. Conclusion. Women with SLE had significantly greater baseline homocysteine, lower L-spine BMD, and more new fractures over 2 years, compared with women without SLE. Homocysteine levels were not significantly associated with BMD and did not predict new fractures in women with or without SLE over 2 years. (First Release Jan 15 2008; J Rheumatol 2008;35:230-6) Key Indexing Terms:
SYSTEMIC LUPUS ERYTHEMATOSUS
From the Department of Medicine, Division of Rheumatology; Department of Preventive Medicine; and Department of Radiology, Northwestern University, Feinberg School of Medicine; Department of Medicine, Michael Reece Medical Center, Chicago; and Abbott Laboratories, Abbott Park, Illinois, USA. Supported by grants from the National Institutes of Health F32-AR51681; Arthritis Foundation, Greater Chicago Chapter; Northwestern Memorial Foundation Young Investigator Award, and Mary Kirkland Center for Lupus Research and Rheuminations, Inc. (ER); National Institutes of Health K12-RR017707 (CL); K24-AR02318, P60-AR30692, P60-AR48098, NCRR/GCRC M01-RR00048, Arthritis Foundation Clinical Science Grant, The Lupus Foundation of Illinois, The Arthritis Foundation Greater Chicago Chapter, and unrestricted educational and research grants from Procter & Gamble Pharmaceuticals, Inc. and Merck Co., Inc. (RR-G). E.Y. Rhew, MD, MSCI, Instructor of Medicine; P. Eksarko, BS, Laboratory Technician; R.M. Pope, MD, Professor of Medicine; R. Ramsey-Goldman, MD, DrPH, Professor of Medicine, Division of Rheumatology, Department of Medicine; A.R. Dyer, PhD, Professor and Associate Chair, Department of Preventive Medicine; S.M. Spies, MD, Professor of Medicine, Department of Radiology, Northwestern University, Feinberg School of Medicine; C. Lee, MD, MPH, Assistant Medical Director, Abbott Laboratories, Adjunct Assistant Professor, Division of Rheumatology, Department of Medicine, Northwestern University; H. Tily, MD, Medical Resident, Michael Reece Medical Center. Address reprint requests to Dr. E.Y. Rhew, Northwestern University, Feinberg School of Medicine, Division of Rheumatology, 240 E. Huron, McGaw Pavilion, Suite M300, Chicago, IL 60611. E-mail: e-rhew@md.northwestern.edu Accepted for publication October 7, 2007. |
