title: Bone mineral density in rheumatoid arthritis patients 1 year after adalimumab therapy: arrest of bone loss.
abstract: OBJECTIVE
  To explore the effects of anti-tumour necrosis factor (TNF)alpha antibody therapy on bone mineral density (BMD) of the lumbar spine and femur neck in patients with rheumatoid arthritis (RA).
  
  
  METHODS
  A total of 50 patients with active RA (DAS28> or =3.2) who started adalimumab (40 mg subcutaneously/2 weeks) were included in an open label prospective study. All patients used stable methotrexate and were allowed to use prednisone (< or =10 mg/day). The BMD of the lumbar spine and femur neck was measured before and 1 year after start of treatment.
  
  
  RESULTS
  Disease activity at baseline (28-joint Disease Activity Score (DAS28)) and disease duration were inversely correlated with femoral neck BMD and lumbar spine BMD (p<0.05). Mean BMD of lumbar spine and femur neck remained unchanged after 1 year of adalimumab therapy (+0.3% and +0.3%, respectively). Of interest, a beneficial effect of prednisone on change in femur neck BMD was observed with a relative increase with prednisone use (+2.5%) compared to no concomitant prednisone use (-0.7%), (p = 0.015).
  
  
  CONCLUSIONS
  In contrast to the progressive bone loss observed after conventional disease-modifying antirheumatic drug therapy, TNF blockade may result in an arrest of general bone loss. Consistent with previous observations, the data also suggest that the net effect of low-dose corticosteroids on BMD in RA may be beneficial, possibly resulting from their anti-inflammatory effects.
authors.affiliation: Division of Clinical Immunology and Rheumatology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: C A
authors.initials: CA
authors.lastname: Wijbrandts
authors.forename: R
authors.initials: R
authors.lastname: Klaasen
authors.forename: M G W
authors.initials: MG
authors.lastname: Dijkgraaf
authors.forename: D M
authors.initials: DM
authors.lastname: Gerlag
authors.forename: B L F
authors.initials: BL
authors.lastname: van Eck-Smit
authors.forename: P P
authors.initials: PP
authors.lastname: Tak
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000494:pharmacology* / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D015519:Bone Density / Q000187:drug effects*; D002097:C-Reactive Protein / Q000378:metabolism; D004359:Drug Therapy, Combination; D005260:Female; D005272:Femur Neck / Q000187:drug effects / Q000503:physiopathology; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D008159:Lumbar Vertebrae / Q000187:drug effects / Q000503:physiopathology; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D010024:Osteoporosis / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D011241:Prednisone / Q000627:therapeutic use; D011446:Prospective Studies; D012720:Severity of Illness Index; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D005938:Glucocorticoids; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000068879:Adalimumab; D011241:Prednisone; D008727:Methotrexate