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  • Title: Short-term changes in magnetic resonance imaging and disease activity in response to infliximab.
    Author: Bonel HM, Boller C, Saar B, Tanner S, Srivastav S, Villiger PM.
    Journal: Ann Rheum Dis; 2010 Jan; 69(1):120-5. PubMed ID: 19329424.
    Abstract:
    OBJECTIVES: To characterise and quantify short-term changes in local inflammation using magnetic resonance imaging (MRI), and to correlate the findings with clinical disease activity in response to infliximab in patients with spondyloarthritis. METHODS: 28 consecutive patients with established spondyloarthritis under successful long-term treatment with infliximab underwent MRI immediately before and one week after re-administration of the TNF blocker. C-reactive protein and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) were assessed at both time points. The MRI protocol included coronal and sagittal turbo-short T1 inversion recovery (STIR) images as well as contrast-enhanced sagittal T1-weighted, fat-suppressed images. Images were assessed in independent sessions using the ASspiMRI-a score, the signal-difference-to-noise ratios (SDNR) and volumetry to assess oedematous and inflamed tissues. RESULTS: BASDAI values were expectedly low at study entry (3.3, SD 2.3). One week after administration of infliximab, 46% of patients reached a BASDAI 20, 39% a BASDAI 50. Kappa values for qualitative assessments and all measurements were excellent (range between 0.83 and 1.0) The ASspiMRI-a dropped most in the thoracic (3.3 points), less in the lumbar (1.21 points) and least in the cervical spine (0.38 points). The decrease of the ASspiMRI-a, the SDNR and the inflamed volumes in response to infliximab re-treatment was significant (p<0.01). The BASDAI showed a weak correlation with the ASspiMRI-a (r = 0.41). CONCLUSIONS: MRI proves to be a valid method to assess and quantify short-term effects of therapy in spondyloarthritis. Comparison between MRI and BASDAI changes show that the BASDAI may underestimate local inflammation. It suggests an explanation for the structural disease progression despite clinical remission.
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