Increase in bone density in patients with spondyloarthritis during anti-tumor necrosis factor therapy: 6-year followup study.
OBJECTIVE
To assess the effects on bone mineral density (BMD) of prolonged anti-tumor necrosis factor (anti-TNF) therapy in patients with spondyloarthritis (SpA); to compare the BMD changes to those observed in SpA patients not treated with anti-TNF; and to identify the predictors of these changes.


METHODS
Fifty-nine patients with SpA according to the European Spondylarthropathy Study Group criteria who were treated with anti-TNF therapy for at least 4 years were included. Thirty-four patients with SpA from an international longitudinal observational study (OASIS cohort) were used as a control group. Lumbar spine and hip BMD were measured by dual-energy x-ray absorptiometry at baseline, after 1 year, and after at least 4 years.


RESULTS
Over an average 6.5 years' followup, the increase in BMD was 11.8% (± 12.8%) at the lumbar spine (p < 0.0001) and 3.6% (± 9.3%) at the great trochanter (p = 0.0001) in patients treated with anti-TNF. At the lumbar spine, the increase was similar in patients with and those without syndesmophytes. BMD changes were significantly higher in the anti-TNF group than in the control group at lumbar spine (p < 0.0001), at femoral neck (p = 0.002), and at trochanter (p = 0.011), but not at total hip (p = 0.062). Multivariate analysis showed that the predictors of lumbar spine BMD changes in the total population were the use of anti-TNF (p < 0.0001) and, in the anti-TNF therapy group, the 1-year lumbar spine BMD change (p = 0.007).


CONCLUSIONS
This study shows that prolonged anti-TNF therapy increases lumbar spine and trochanter BMD. This effect should be taken into account before introducing antiosteoporotic treatment in these patients.
From Paris Descartes University, Rheumatology Department, Cochin Hospital, Paris, France; Rheumatology Department, AZ Groeninge, Kortrijk, Belgium; and the University of Amsterdam, Amsterdam, and Atrium Medical Center, Heerlen, The Netherlands.
Anne
A
Durnez
Simon
S
Paternotte
Jacques
J
Fechtenbaum
Robert B M
RB
Landewé
Maxime
M
Dougados
Christian
C
Roux
Karine
K
Briot
D000068879:Adalimumab; D000328:Adult; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000494:pharmacology / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D015519:Bone Density / Q000187:drug effects*; D004359:Drug Therapy, Combination; D000068800:Etanercept; D005260:Female; D005500:Follow-Up Studies; D006621:Hip Joint / Q000000981:diagnostic imaging / Q000187:drug effects*; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology / Q000627:therapeutic use; D000069285:Infliximab; D008159:Lumbar Vertebrae / Q000000981:diagnostic imaging / Q000187:drug effects*; D008297:Male; D008727:Methotrexate / Q000494:pharmacology / Q000627:therapeutic use; D008875:Middle Aged; D011859:Radiography; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D025241:Spondylarthritis / Q000000981:diagnostic imaging / Q000188:drug therapy*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept; D008727:Methotrexate
ANTI-TUMOR NECROSIS FACTOR; BONE MINERAL DENSITY; OSTEOPOROSIS; SPONDYLOARTHRITIS