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Real-world single centre use of JAK inhibitors across the rheumatoid arthritis pathway

Author

Rheumatology (Oxford)2020 Dec 17;keaa858. doi: 10.1093/rheumatology/keaa858.Online ahead of print.

John Fitton 1 2Andrew R Melville 1 2Paul Emery 1 2Jacqueline L Nam 1 2Maya H Buch 1 3

Author Information

1 Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Chapel Allerton Hospital, Leeds, UK.

2 NIHR Biomedical Research Centre, Leeds Teaching Hospitals NHS trust, Chapel Allerton Hospital, Leeds, UK.

3 Centre for Musculoskeletal Research, School of Biological Sciences, University of Manchester, Manchester, UK.

Abstract

Objectives: To evaluate real world efficacy of approved JAK inhibitors (JAKi) tofacitinib and baricitinib in a large, single-centre cohort of RA patients across the treatment pathway, including those refractory to multiple biologic drugs.

Methods: All RA patients, treated with tofacitinib (from time of compassionate access scheme) or baricitinib since approval in 2017 had DAS28-CRP scores and components recorded at baseline, 3 and 6 months (with retrospective data for compassionate access scheme). Efficacy was evaluated in the total cohort, each treatment group, and subgroups of number of prior biologic classes failed.

Results: One hundred and fifteen patients were treated with a JAKi (tofacitinib 54, baricitinib 69, 8 both); 76.4% female; mean (SD) age 57.3 (14.3) years. On average patients had received 3 previous bDMARDs; 11 (9.6%) were bDMARD naïve. Combined group baseline DAS28-CRP (SD) 5.62(1.14) improved by 1.49(1.44) and 1.67(1.61) at 3 and 6 months respectively, comparable in individual JAKi groups; with 24% in at least low disease activity at 3 months. The biggest improvement was observed in the biologic-naïve group (mean DAS28-CRP improved from 5.16-2.14 after 6 months); whilst those with prior exposure to minimum 3 bDMARD classes had DAS28-CRP improvement of > 1.2. 5/8 patients treated with both JAKi sequentially responded. Twelve patients previously unresponsive to IL-6 blockade responded to JAKi. No unexpected safety events were recorded. Two cases of venous thrombo-embolism were observed.

Conclusion: JAK inhibition is effective in a real world population of RA patients, including in a subset of patients refractory to multiple previous bDMARDs.