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SAT0350 Bone mineral density in lupus erythematosus women 1 year after rituximab therapy
  1. M. Garcia-Carrasco1,2,
  2. C. Mendoza-Pinto1,3,
  3. I. Etchegaray-Morales4,5,
  4. C. Jimenez-Hernandez4,
  5. A.B. Rodriguez-Gallego6,
  6. R. Briones-Rojas7,
  7. E. Ordoñez-Andrade4,
  8. S. Mendez-Martinez4,
  9. J.E. Aguilar-Cuenca8,
  10. R. Cervera3
  1. 1Systemic Autoimmunity Disease Research Unit, Hgr 36-Cibior, IMSS
  2. 2Department of Rheumatology, School of Medicine, BUAP, Puebla, Mexico
  3. 3Department of Autoimmune Diseases, Institut Clínic de Medicina i Dermatologia, Hospital Clinic, Barcelona, Spain
  4. 4Systemic Autoimmunity Disease Research Unit, Hgr 36, IMSS
  5. 5Department of Physiotherapy, School of Medicine, BUAP
  6. 6Laboratorios Clinicos de Puebla, Clinica Ruiz
  7. 7Department of Epidemiology, School of Medicine
  8. 8Systemic Autoimmunity Disease Research Unit, Hgr 36, BUAP, Puebla, Mexico

Abstract

Background Patients with systemic lupus erythematosus (SLE) have a higher prevalence of osteoporosis and low bone mineral density (BMD) compared with the general population. Rituximab, a CD20 depleting antibody, has been administrated in patients with refractory SLE. However, to date, its influence on bone mineral density (BMD) in women with SLE is unknown.

Objectives The aim of this prospective study was to assess the effects of rituximab treatment on BMD of the lumbar and femoral neck in women with SLE.

Methods Thirty active female SLE patients treated with rituximab were compared with control SLE women not treated with rituximab. BMD of the femoral neck and lumbar spine was measured using dual energy x-ray absorptiometry (Hologic, Inc.) before initiating biologic therapy and after one year. The Student’s t test was used to detect differences in BMD in the rituximab and control groups. Analysis of covariance was used to examine for confounders including disease duration, disease activity and age.

Results 76 patients were studied. 30 patients received rituximab and 46 controls received conventional treatment. In the rituximab group, the mexSLEDAI score was 3.4±1.8 at baseline and 0.8±1.5 (p=0.001) after one year of rituximab. There were 5 non-responders. Patients receiving rituximab were significantly younger and had significantly higher activity scores (mexSLEDAI) than controls. Baseline BMD measurements were higher in the rituximab group but the only significant difference was at the lumbar spine. BMD was reduced from 0.980±0.130 g/cm2to 0.809±0.139 g/cm2 (-17.4%; p=0.001) at the femoral neck and from 1.062±0.137g/cm2 to 0.893±0.194 g/cm2 (-15.8%; p=0.001) at the lumbar spine in the rituximab group after 12 months of rituximab. BMD was reduced from 0.914±0.193 g/cm2 to 0.790±0.135 g/cm2 (-13.6%; p=0.001) at the femoral neck and 0.926±0.128 g/cm2 to 0.867±0.139 g/cm2 (-6.2%; p=0.09) at the lumbar spine in controls after 12 months of treatment. Variables associated with a low BMD included age, menopausal status and steroid dose. A logistic regression model was used to analyze the specific effect of rituximab within the context of these possible confounding factors and showed that only postmenopausal status was associated with BMD loss (p=0.03). However, BMD loss was higher in postmenopausal rituximab patients than in postmenopausal controls (0.324±0.128 g/cm2 vs 0.138±0.099 g/cm2).

Conclusions After one year of follow up, patients had lower BMD at both the femoral neck and lumbar spine, but the loss was greater in patients receiving rituximab than in patients receiving conventional treatment, and in postmenopausal women. Although further studies are required to confirm this relationship, postmenopausal candidates for rituximab should be evaluated closely to prevent further BMD loss.

Disclosure of Interest None Declared

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