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THU0271 Emergence of severe spondyloarthropathy related entheseal pathology following vedolizumab therapy for inflammatory bowel disease
  1. S. Dubash1,2,
  2. T. Marianayagam3,
  3. T. Al-Araimi4,
  4. C. Pagnoux4,
  5. A. Weizman4,
  6. M.-L. Tran Minh5,
  7. M. Allez5,
  8. P. Richette5,
  9. H. Marzo-Ortega1,2,
  10. D. McGonagle1,2
  1. 1NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals
  2. 2Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds
  3. 3Rheumatology, East and North Hertfordshire NHS Trust, Stevenage, UK
  4. 4Division of Rheumatology, Mount Sinai Hospital, Toronto, Canada
  5. 5Hopital Lariboisiere, University Hospitals Group, Paris, France

Abstract

Background The Spondyloarthritides (SpA) and inflammatory bowel disease (IBD) share common aetiopathogenetic and clinical manifestations. Vedolizumab, a humanised IgG1 monoclonal antibody to α4β7 integrin, has been approved for the treatment of inflammatory bowel disease (IBD) and inhibits α4β7 integrin at the gut level. Vedolizumab therapy for IBD has been associated with mild SpA related features including sacroiliitis and synovitis. Herein, we report the emergence of severe SpA under therapy with Vedolizumab.

Objectives We conducted a clinical evaluation of 7 vedolizumab treated patients with IBD that developed severe active SpA and/or enthesopathy with the aim of characterising the vedolizumab associated SpA/entheseal flares.


Methods Vedolizumab treated IBD patients with SpA/enthesopathy were identified across four hospitals. We identified clinical, biochemical and imaging characteristics within routine case records as part of a clinical evaluation.

Results We identified 6/7 subjects that developed de novo SpA/enthesopathy and 1/7 (subject 1) with a severe flare of pre-existing SpA. There were 3/7 patients hospitalised due to the severity of skeletal disease. The median time from vedolizumab initiation to flare was 10 weeks (table 1 below). Subject 4 developed new-onset SpA with severe spinal vertebral end-plate oedema (T6–12) and inflammatory Romanus lesions (L3–4) (image below). Acute sacroiliitis was identified on MRI in 3 subjects, one of which showed evidence of radiographic bilateral grade 2 sacroiliitis. In at least 4 cases the IBD disease activity was considered to be low or well controlled. Following vedolizumab discontinuation, so far 3 patients have switched to alternative biologic therapies including certolizumab pegol, golimumab, and 1 subject to sulphasalazine.

cpd=cigarettes per day, MTX=methotrexate, AZA=azathioprine, OC=oral corticosteroid, Pred=prednisolone, nr=non radiographic, MRI+ve= MRI positive, XR +ve = radiograph positive, NA=not available.

Conclusions This case series demonstrates severe vedolizumab associated SpA/enthesopathy that resulted in hospitalised cases. The severity of vedolizumab related SpA flares is relatively severe disease in comparison to the literature. We recognise that vedolizumab is efficacious in IBD, however our observations highlight the need to monitor symptoms to identify patients that develop axial or peripheral SpA several weeks from commencing vedolizumab.

Disclosure of Interest None declared

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