John Fitton1,2, Andrew R Melville1,2, Paul Emery1,2, Jacqueline L Nam1,2, Maya H Buch1,3. 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.
OBJECTIVES: To evaluate real world efficacy of approved JAK inhibitors (JAKi) tofacitinib and baricitinib in a large, single-centre cohort of RApatients across the treatment pathway, including those refractory to multiple biologic drugs. METHODS: All RApatients, 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 RApatients, including in a subset of patients refractory to multiple previous bDMARDs.
Authors: John Fitton; Andrew Melville; Kamran Naraghi; Jacqueline Nam; Shouvik Dass; Paul Emery; Maya H Buch Journal: Rheumatol Adv Pract Date: 2022-08-01