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Abstract Number: 2558

Etanercept Increases Bone Mineral Density in Ankylosing Spondylitis, but Does Not Prevent Vertebral Fractures

M.a.C. van der Weijden1,2, J.C. van Denderen2, W.F. Lems1, M.T. Nurmohamed1,2, B.a.C Dijkmans1,2 and I.E. van der Horst-Bruinsma1, 1Rheumatology, VU University Medical Center, Amsterdam, Netherlands, 2Rheumatology, Jan van Breemen Research Institute | Reade, Amsterdam, Netherlands

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: anti-TNF therapy, axial spondyloarthritis, Bone density, etanercept and fractures

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Session Information

Title: Spondyloarthropathies and Psoriatic Arthritis - Clinical Aspects and Treatment III

Session Type: Abstract Submissions (ACR)

Background/Purpose

Ankylosing spondylitis (AS) is characterized by chronic inflammation often leading to ankylosis of the spine, but also by a decrease of bone mineral density (BMD) and high prevalence of vertebral fractures (VF). Treatment with TNF blocking agents decreases inflammation and has shown to be effective in increasing BMD. We studied the effects of etanercept on BMD and VF in AS patients after two years of treatment. Furthermore we studies changes in bonemarkers (CTXI, CTXII, RANKL, OPG, Osteocalcin) and radiological damage.

Methods

Patients with active AS, treated with etanercept for two years, were included. BMD lumbar spine and hips was measured at baseline and after two years, as well as the radiological damage (mSASSS, including thoracic spine), VF (Genant method) and change in bone-markers.

Results

Forty-nine AS patients were included (Table). After two years of etanercept, hip BMD raised with 2.2% (p=0.014) and lumbar spine BMD with 7.0% (p<0.001). The BASDAI decreased significantly (p<0.001) as well as CRP and ESR (p<0.001). Despite etanercept therapy, the number of patients with vertebral fractures more than doubled (from 6 to 15 patients, p=0.004) as well as the severity. Also the radiological damage mSASSS+ThSpine increased significantly over time (from 12.1 to 18.5, p<0.001). No significant change in bone-markers was found.

Clinical characteristics N=49

baseline

after 2 years etanercept

  Mena

40 (81.6)

 

  Ageb, years

41.8 (9.2)

 

  Disease durationb, years

12.2 (9.1)

 

  ESRc, (mm/hr) [<20]

20.0 (6.0-39.0)

6.5 (3.0-16.0)*

  CRPc, (mg/l) [<10]

14.0 (3.0-39.0)

2.5 (1.0-9.8)*

  BASDAIb, (0-10)

5.7 (1.6)

2.9 (2.1)*

  BASFIb, (0-10)

5.7 (2.1)

3.5 (2.9)*

  BASMIb, (0-10)

4.4 (2.3)

4.0 (2.4)

  Total mSASSSc, (0-72)

10.0 (3.8-35.5)

15.5 (5.5-42.5)*

  Total mSASSS+ThSpinec, (0-90)

12.1 (6.8-42.7)

18.5 (8.7-52.0)*

  sBMD hipb

0.903 (0.152)

0.921 (0.146)*

  sBMD L2-L4b

1.141 (0.203)

0.213 (0.200)*

  number vertebral fracturesa

8 (16.3)

21 (42.9)*

  patients with vertebral fracturesa

6 (12.2)

15 (30.6)*

anumber (%), bmean (SD), cmedian (IQR), *significant change p <0.05

Conclusion

This prospective longitudinal observational cohort study in AS patients showed that after two years etanercept treatment, BMD of the hip and spine increased significantly. However, the number and severity of vertebral fractures increased, as well as the radiological progression, including the thoracic spine. Thus, the favourable effect of etanercept on BMD in AS is accompanied by unfavourable outcomes on vertebral fractures and radiological damage


Disclosure:

M. A. C. van der Weijden,
None;

J. C. van Denderen,
None;

W. F. Lems,
None;

M. T. Nurmohamed,
None;

B. A. C. Dijkmans,
None;

I. E. van der Horst-Bruinsma,
None.

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