Sujith Subesinghe1,2, Andrew Ian Rutherford1,3, Rachel Byng-Maddick4, Kimme Leanne Hyrich5,6, James Benjamin Galloway1,3. 1. Academic Department of Rheumatology, Weston Education Centre, King's College London, London, UK. 2. Department of Rheumatology, Guy's and St Thomas' NHS Foundation Trust, Guy's Hospital, London, UK. 3. Department of Rheumatology, King's College Hospital NHS Foundation Trust, London, UK. 4. Department of Rheumatology, Homerton Hospital, London, UK. 5. Arthritis Research UK Centre for Epidemiology, Division of Musculoskeletal and Dermatological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK. 6. NIHR Manchester Musculoskeletal Biomedical Research Centre, Central Manchester University Hospitals NHS Foundation Trust and University of Manchester Partnership, Manchester, UK.
Abstract
Objectives: To establish whether the decision to stop, continue or switch TNF inhibitor (TNFi) therapy to a biologic drug with an alternative mode of action following a serious infection (SI) impacts upon the risk of recurrent SI in patients with RA. Methods: Patients recruited to the British Society for Rheumatology Biologics Register-RA with at least one episode of SI while on TNFi were included. The biologic treatment decision following SI was considered. A multivariable adjusted Cox proportional hazards model was used to identify predictors of recurrent SI and whether biologic treatment choices influenced future SI risk. Results: In total, 1583 patients suffered at least one SI while on TNFi. Most patients (73%) were recorded as continuing TNFi 60 days after an index SI. The rate of recurrent SI was 25.6% per annum (95% CI: 22.5, 29.2%). The rate of recurrent SI was highest in patients who stopped their TNFi (42.6% per annum, 95% CI: 32.5, 55.7%) and lowest in those who switched biologic drug class (12.1% per annum, 95% CI: 3.9, 37.4%). Compared with patients stopping biologic therapy, patients who continued or switched drug class had significantly lower risk of recurrent SI (drug continuation hazard ratio = 0.54, 95% CI: 0.40, 0.74; drug switch hazard ratio = 0.29, 95% CI: 0.09, 0.95). Conclusions: Patients who continued or switched their TNFi post-index SI had a lower risk of recurrent SI infection compared with those who stopped the drug. This may be explained by better control of disease activity with reintroduction of biologic therapy, a driving factor for SI or alternatively channelling fitter patients to restart biologic therapy.
Objectives: To establish whether the decision to stop, continue or switch TNF inhibitor (TNFi) therapy to a biologic drug with an alternative mode of action following a serious infection (SI) impacts upon the risk of recurrent SI in patients with RA. Methods:Patients recruited to the British Society for Rheumatology Biologics Register-RA with at least one episode of SI while on TNFi were included. The biologic treatment decision following SI was considered. A multivariable adjusted Cox proportional hazards model was used to identify predictors of recurrent SI and whether biologic treatment choices influenced future SI risk. Results: In total, 1583 patients suffered at least one SI while on TNFi. Most patients (73%) were recorded as continuing TNFi 60 days after an index SI. The rate of recurrent SI was 25.6% per annum (95% CI: 22.5, 29.2%). The rate of recurrent SI was highest in patients who stopped their TNFi (42.6% per annum, 95% CI: 32.5, 55.7%) and lowest in those who switched biologic drug class (12.1% per annum, 95% CI: 3.9, 37.4%). Compared with patients stopping biologic therapy, patients who continued or switched drug class had significantly lower risk of recurrent SI (drug continuation hazard ratio = 0.54, 95% CI: 0.40, 0.74; drug switch hazard ratio = 0.29, 95% CI: 0.09, 0.95). Conclusions: Patients who continued or switched their TNFi post-index SI had a lower risk of recurrent SI infection compared with those who stopped the drug. This may be explained by better control of disease activity with reintroduction of biologic therapy, a driving factor for SI or alternatively channelling fitter patients to restart biologic therapy.
Authors: Susan R Aungier; Alison J Cartwright; Anja Schwenzer; Jennifer L Marshall; Michael R Dyson; Peter Slavny; Kothai Parthiban; Aneesh Karatt-Vellatt; Ilfita Sahbudin; Eric Culbert; Patrick Hextall; Felix Il Clanchy; Richard Williams; Brian D Marsden; Karim Raza; Andrew Filer; Christopher Dominic Buckley; John McCafferty; Kim S Midwood Journal: Ann Rheum Dis Date: 2018-12-14 Impact factor: 19.103
Authors: Silvia Sánchez-Ramón; Lidia Fernández-Paredes; Paula Saz-Leal; Carmen M Diez-Rivero; Juliana Ochoa-Grullón; Concepción Morado; Pilar Macarrón; Cristina Martínez; Virginia Villaverde; Antonia Rodríguez de la Peña; Laura Conejero; Keyla Hernández-Llano; Gustavo Cordero; Miguel Fernández-Arquero; Benjamin Fernández- Gutierrez; Gloria Candelas Journal: Front Immunol Date: 2021-06-04 Impact factor: 7.561