Warren Fong1, Chris Holroyd2, Brian Davidson3, Ray Armstrong3, Nick Harvey2, Elaine Dennison2, Cyrus Cooper4, Christopher J Edwards5. 1. NIHR Wellcome Trust Clinical Research Facility, University Hospital Southampton NHS Foundation Trust, Southampton, UK Department of Rheumatology and Immunology, Singapore General Hospital, Singapore, Singapore. 2. Department of Rheumatology MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton, UK. 3. Department of Rheumatology. 4. Department of Rheumatology MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton, UK Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK. 5. NIHR Wellcome Trust Clinical Research Facility, University Hospital Southampton NHS Foundation Trust, Southampton, UK Department of Rheumatology cedwards@southampton.ac.uk.
Abstract
OBJECTIVE: To determine feasibility of TNF inhibitor (TNFi) dose reduction for severe AS and PsA patients. METHODS: A retrospective study in a real-world setting. Criteria for dose reduction of TNFi included BASDAI < 4 for ⩾6 months in AS; or DAS28-ESR ⩽ 3.2 for ⩾6 months in PsA. TNFi dose was reduced by one-third. Patients who flared (BASDAI > 4 in AS or DAS28-ESR > 3.2 in PsA) were re-escalated to standard treatment dose. RESULTS: Twenty-six per cent (33/125) of AS and 18% (15/83) of PsA patients fulfilled criteria and underwent TNFi dose reduction. Fifty-eight per cent (19/33) of AS and 60% (9/15) of PsA patients maintained TNFi dose reduction for mean (s.d) of 1.0 (0.8) years. Reinstating standard dose of TNFi recaptured low disease activity in all patients who failed dose reduction within 24 weeks, with no statistically significant difference in mean BASDAI compared with those maintaining TNFi dose reduction in AS at 24 weeks [mean (s.d) BASDAI 2.4 (1.1) vs 1.9 (1.5), respectively (P = 0.229)]; however in PsA, those who failed dose reduction had higher disease activity compared with patients maintained on TNFi dose reduction at 24 weeks [mean (s.d) DAS28-ESR 2.7 (0.6) vs 1.3 (0.5), respectively (P ⩽ 0.001)]. In PsA, a lower DAS28-ESR prior to dose reduction of TNFi was associated with more successful dose reduction. CONCLUSIONS: In a real-world setting, 60% of individuals with severe AS and PsA who achieve low disease activity can successfully reduce the dose of TNFi therapy by a third for a mean of 1 year.
OBJECTIVE: To determine feasibility of TNF inhibitor (TNFi) dose reduction for severe AS and PsA patients. METHODS: A retrospective study in a real-world setting. Criteria for dose reduction of TNFi included BASDAI < 4 for ⩾6 months in AS; or DAS28-ESR ⩽ 3.2 for ⩾6 months in PsA. TNFi dose was reduced by one-third. Patients who flared (BASDAI > 4 in AS or DAS28-ESR > 3.2 in PsA) were re-escalated to standard treatment dose. RESULTS: Twenty-six per cent (33/125) of AS and 18% (15/83) of PsA patients fulfilled criteria and underwent TNFi dose reduction. Fifty-eight per cent (19/33) of AS and 60% (9/15) of PsA patients maintained TNFi dose reduction for mean (s.d) of 1.0 (0.8) years. Reinstating standard dose of TNFi recaptured low disease activity in all patients who failed dose reduction within 24 weeks, with no statistically significant difference in mean BASDAI compared with those maintaining TNFi dose reduction in AS at 24 weeks [mean (s.d) BASDAI 2.4 (1.1) vs 1.9 (1.5), respectively (P = 0.229)]; however in PsA, those who failed dose reduction had higher disease activity compared with patients maintained on TNFi dose reduction at 24 weeks [mean (s.d) DAS28-ESR 2.7 (0.6) vs 1.3 (0.5), respectively (P ⩽ 0.001)]. In PsA, a lower DAS28-ESR prior to dose reduction of TNFi was associated with more successful dose reduction. CONCLUSIONS: In a real-world setting, 60% of individuals with severe AS and PsA who achieve low disease activity can successfully reduce the dose of TNFi therapy by a third for a mean of 1 year.
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