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Abstract
Objectives Extra-articular manifestations (EAMs) are important systemic features of axial spondyloarthritis (axSpA), which may influence the choice of tumour necrosis factor-inhibitor (TNFi). We examined the cumulative incidence and predictors of EAMs and the influence of these on first TNFi choice in a ‘real-world’ cohort of patients with axSpA.
Methods Clinical and patient-reported outcomes of 2420 patients with axSpA from 83 centres were collected by the British Society for Rheumatology Biologics Register in Ankylosing Spondylitis. Lifestyle factors for EAMs (acute anterior uveitis (AAU), inflammatory bowel diseases (IBD), psoriasis) were compared with those without EAMs. Also, the association between pretreatment EAMs and choice of first TNFi (adalimumab, etanercept, certolizumab) was analysed.
Results AAU was directly associated with human leukocyte antigen (HLA)-B27 (incidence rate ratio (IRR) 1.95, 95% CI 1.40 to 2.73) and inversely associated with ever-smoking (IRR=0.71, 95% CI 0.55 to 0.92). For both psoriasis and IBD, there was an inverse relationship with HLA-B27 (IRR 0.54, 95% CI 0.36 to 0.79 and IRR 0.63, 95% CI 0.43 to 0.91, respectively). A diagnosis of either AAU (OR 3.79, 95% CI 2.11 to 6.80) or IBD (OR 5.50, 95% CI 2.09 to 14.46) was associated with preference for adalimumab versus others. In contrast, a diagnosis of either AAU (OR 0.14, 95% CI 0.06 to 0.33) or IBD (OR 0.17, 95% CI 0.05 to 0.57) was associated with less preference for etanercept over other TNFi.
Conclusion The higher occurrence of AAU and lower occurrence of psoriasis and IBD in HLA-B27-positive patients with axSpA are consistent with current pathophysiology. Patients with previous AAU and IBD are more likely to be prescribed adalimumab and less likely to receive etanercept, consistent with the superior efficacy of monoclonal TNFi for these indications. Future work will determine whether EAMs influence TNFi survival, or effectiveness, and whether this varies between agents.
- Spondyloarthritis
- Anti-TNF
- Epidemiology
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Contributors Study concept and design: MHD, SS, KG. Analysis and interpretation of data: all authors. Drafting the manuscript: MHD, SS, KG. Critical revision of the manuscript for important intellectual content: all authors.
Funding This work was supported by the British Society for Rheumatology (BSR) who have funded the BSRBR-AS. The BSR received funding for this from Pfizer, AbbVie and UCB. These companies receive advance copies of manuscripts for comments but have no input into the topics for analysis in the register nor the work involved in undertaking analysis. Original analysis of data was supported by the Versus Arthritis/Medical Research Council Centre for Musculoskeletal Health and Work (grant number 20665). The current analyses were funded by the British Society of Spondyloarthritis (BritSpA).
Competing interests GTJ reports grants from AbbVie, Pfizer and UCB during the conduct of the study; grants from Amgen and GlaxoSmithKline, outside the submitted work. SS has received research grants, speaker or consultancy fees from AbbVie, Amgen (previously Celgene), BMS, Boehringer-Ingelheim, GlaxoSmithKline, Janssen, Novartis, Pfizer and UCB. KG has received research grants, speaker or consultancy fees from AbbVie, Celgene, Biogen, MSD, Novartis, Pfizer and UCB Pharma. Other authors have no relevant interests to declare.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data are available upon reasonable request.