S21_6

Bone mass in systemic lupus erythematosus

L. Sinigaglia, M. Varenna, L. Binelli, F. Zucchi, D. Ghiringhelli, F. Fantini

Chair and Department of Rheumatology, Gaetano Pini Institute, University of Milan, Milan, Italy

ABSTRACT
As a consequence of the chronic course of the disease, osteoporosis can be a further clinical challenge in patients with systemic lupus erythematosus (SLE). Most studies have reported that mean bone mineral density is significantly reduced in premenopausal SLE patients as compared to controls and 12 - 25% of premenopausal SLE patients are considered to have osteoporosis. SLE patients have a 5-fold probability of sustaining a fracture as compared to the normal population. Causes of bone loss in SLE include the deleterious effects of long-term glucocorticoids and immunosuppressive drugs on the skeleton, but there is good evidence that the disease per se can lead to reduced bone mass through several mechanisms such as reduced motility, renal impairment, endocrine dysfunctions and the systemic effect of bone-resorbing cytokines. Strategies to counteract bone loss in these patients must be applied soon after the disease onset and include effective treatment of the underlying disease, use of the lowest steroid dosages possible, and the prevention and treatment of glucocorticoid-induced osteoporosis. Available data suggest that postmenopausal women at risk for osteoporosis may benefit from hormone replacement therapy without experiencing further disease flares.

Key words
Systemic lupus erythematosus, osteoporosis, bone mineral density.

Please address correspondence and reprint requests to: Luigi Sinigaglia, MD, Department of Rheumatology, Gaetano Pini Orthopedic Institute, Piazza Cardinal Ferrari 1, 20123 Milan, Italy.
E-mail:Sinigaglia@g-pini.unimi.it