scholarly journals 145. OPPORTUNISTIC INFECTIONS IN RHEUMATOID ARTHRITIS PATIENTS EXPOSED TO BIOLOGIC THERAPY: UPDATED RESULTS FROM THE BRITISH SOCIETY FOR RHEUMATOLOGY BIOLOGICS REGISTER

Rheumatology ◽  
2017 ◽  
Vol 56 (suppl_2) ◽  
Author(s):  
Andrew I. Rutherford ◽  
Eunice Patarata ◽  
Sujith Subesinghe ◽  
Kimme L. Hyrich ◽  
James B. Galloway
2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 177.2-178
Author(s):  
E. Burn ◽  
L. Kearsley-Fleet ◽  
K. Hyrich ◽  
M. Schaefer ◽  
D. Huschek ◽  
...  

Background:The Observational and Medical Outcomes Partnerships (OMOP) common data model (CDM) provides a framework for standardising health data.Objectives:To map national biologic registry data collected from different European countries to the OMOP CDM.Methods:Five biologic registries are currently being mapped to the OMOP CDM: 1) the Czech biologics register (ATTRA), 2) Registro Español de Acontecimientos Adversos de Terapias Biológicas en Enfermedades Reumáticas (BIOBADASER), 3) British Society for Rheumatology Biologics Register for Rheumatoid Arthritis (BSRBR-RA), 4) German biologics register ‘Rheumatoid arthritis observation of biologic therapy’ (RABBIT), and 5) Swiss register ’Swiss Clinical Quality Management in Rheumatic Diseases’ (SCQM).Data collected at baseline are being mapped first. Details that uniquely identify individuals are mapped to the person table, with the observation_period table defining the time a person may have had clinical events recorded. Baseline comorbidities are mapped to the condition_occurrence CDM table, while baseline medications are mapped to the drug_exposure CDM table. This mapping is summarised in Figure 1.Figure 1.Overview of initial mappingResults:A total of 64,901 individuals are included in the 5 registries being mapped to the OMOP CDM, see table 1. The number of unique baseline conditions being mapped range from 17 in BSRBR-RA to 108 in RABBIT, while the number of baseline medications range from 26 in ATTRA to 802 in BSRBR-RA. Those registries which captured more comorbidities or medications generally allowed for these to be inputted as free text.Table 1.Summary of initial code mappingRegistryNumber of individualsNumber of mapped baseline conditionsNumber of mapped baseline medicationsATTRA5,3262626BIOBADASER6,4963051BSRBR-RA21,69517802RABBIT13,06210878SCQM18,3222633Conclusion:Due to differences in study design and data capture, the baseline information captured on comorbidities and drugs across registries varies greatly. However, these data have been mapped and mapping biologic registry data to the OMOP CDM is feasible. The adoption of the OMOP CDM will facilitate collaboration across registries and allow for multi-database studies which include data from both biologic registries and other sources of health data which have been mapped to the CDM.Disclosure of Interests:Edward Burn: None declared, Lianne Kearsley-Fleet: None declared, Kimme Hyrich Grant/research support from: Pfizer, UCB, BMS, Speakers bureau: Abbvie, Martin Schaefer: None declared, Doreen Huschek: None declared, Anja Strangfeld Speakers bureau: AbbVie, BMS, Pfizer, Roche, Sanofi-Aventis, Jakub Zavada Speakers bureau: Abbvie, UCB, Sanofi, Elli-Lilly, Novartis, Zentiva, Accord, Markéta Lagová: None declared, Delphine Courvoisier: None declared, Christoph Tellenbach: None declared, Kim Lauper: None declared, Carlos Sánchez-Piedra: None declared, Nuria Montero: None declared, Jesús-Tomás Sanchez-Costa: None declared, Daniel Prieto-Alhambra Grant/research support from: Professor Prieto-Alhambra has received research Grants from AMGEN, UCB Biopharma and Les Laboratoires Servier, Consultant of: DPA’s department has received fees for consultancy services from UCB Biopharma, Speakers bureau: DPA’s department has received fees for speaker and advisory board membership services from Amgen


Rheumatology ◽  
2011 ◽  
Vol 50 (Supplement 3) ◽  
pp. iii31-iii34 ◽  
Author(s):  
M. M. Soliman ◽  
D. M. Ashcroft ◽  
K. D. Watson ◽  
M. Lunt ◽  
D. Symmons ◽  
...  

2014 ◽  
Vol 74 (6) ◽  
pp. 1087-1093 ◽  
Author(s):  
Louise K Mercer ◽  
Mark Lunt ◽  
Audrey L S Low ◽  
William G Dixon ◽  
Kath D Watson ◽  
...  

BackgroundPatients with rheumatoid arthritis (RA) have an increased risk of certain solid cancers, in particular lung cancer, compared to the general population. Treatment with tumour necrosis factor (TNF) inhibitors (TNFi) may further enhance this risk.ObjectivesTo compare the risk of solid cancer in patients with RA treated with TNFi to that in patients treated with non-biologic (synthetic) disease modifying antirheumatic drugs (sDMARDs).MethodsPatients with a physician diagnosis of RA enrolled in the British Society for Rheumatology Biologics Register, a national prospective cohort study established in 2001 to monitor the long-term safety of TNFi, were followed via record linkage with the national cancer registries until first solid cancer, death, for 5 years, or until 2011. Rates of solid cancers in 11 767 patients without prior cancer who received TNFi were compared to those in 3249 patients without prior cancer treated with sDMARDs.Results427 solid cancers were reported in 52 549 patient-years follow-up for the TNFi group (81 (95% CI 74 to 89) per 10 000 patient-years) and 136 cancers were reported in 11 672 patient-years in the sDMARD cohort (117 (95% CI 98 to 138) per 10 000 patient-years). After adjusting for differences in baseline characteristics there was no difference in risk of solid cancer for TNFi compared to sDMARD treated patients: HR 0.83 (95% CI 0.64 to 1.07). There was no difference in the relative risk of cancer for any of the individual TNFi drugs.ConclusionsThe addition of TNFi to sDMARD does not alter the risk of cancer in RA patients selected for TNFi in the UK.


2018 ◽  
Vol 77 (10) ◽  
pp. 1405-1412 ◽  
Author(s):  
Lianne Kearsley-Fleet ◽  
Rebecca Davies ◽  
Diederik De Cock ◽  
Kath D Watson ◽  
Mark Lunt ◽  
...  

ObjectivesBiologic disease-modifying antirheumatic drugs (bDMARDs) have revolutionised treatment and outcomes for rheumatoid arthritis (RA). The expanding repertoire allows the option of switching bDMARD if current treatment is not effective. For some patients, even after switching, disease control remains elusive. This analysis aims to quantify the frequency of, and identify factors associated with, bDMARD refractory disease.MethodsPatients with RA starting first-line tumour necrosis factor inhibitor in the British Society for Rheumatology Biologics Register for RA from 2001 to 2014 were included. We defined patients as bDMARD refractory on the date they started their third class of bDMARD. Follow-up was censored at last follow-up date, 30 November 2016, or death, whichever came first. Switching patterns and stop reasons of bDMARDs were investigated. Cox regression identified baseline clinical factors associated with refractory disease. Multiple imputation of missing baseline data was used.Results867 of 13 502 (6%) patients were bDMARD refractory; median time to third bDMARD class of 8 years. In the multivariable analysis, baseline factors associated with bDMARD refractory disease included patients registered more recently, women, younger age, shorter disease duration, higher patient global assessment, higher Health Assessment Questionnaire score, current smokers, obesity and greater social deprivation.ConclusionsThis first national study has identified the frequency of bDMARD refractory disease to be at least 6% of patients who have ever received bDMARDs. As the choice of bDMARDs increases, patients are cycling through bDMARDs quicker. The aetiopathogenesis of bDMARD refractory disease requires further investigation. Focusing resources, such as nursing support, on these patients may help them achieve more stable, controlled disease.


Rheumatology ◽  
2020 ◽  
Vol 59 (Supplement_2) ◽  
Author(s):  
Katie Bechman ◽  
Kapil Halai ◽  
Sam Norton ◽  
Andrew P Cope ◽  
Kimme L Hyrich ◽  
...  

Abstract Background Patients with rheumatoid arthritis (RA) are at an increased risk of infection. Most attention has been given to serious infections, but these are the tip of the iceberg. Non-serious infections (NSI) are far more frequent, and although not life-threatening, have potential to impact treatment outcomes (drug survival) and quality of life. Our objective was to describe frequency of NSI and compare incidence of NSI by biologic drug within the British Society for Rheumatology Biologics Register (BSRBR-RA). Methods The BSRBR-RA is a prospective observational cohort study. NSI was identified as not requiring hospitalisation, intravenous therapy or leading to disability or death. Infections were captured from clinician questionnaires and patient diaries. Individuals were considered ‘at risk’ from the date of commencing biologic treatment for 3 years. Drug exposure was defined by agent; TNF inhibitor, IL-6 inhibitor, anti-CD20 or csDMARD only. To account for a high frequency of events, a multiple-failure Cox model was used. Multivariable adjustment included age, gender, DAS28-ESR, HAQ-DI, disease duration, smoking, steroid usage, year recruited to BSRBR-RA, line of biologic therapy and cumulative infection number. Results There were 17,304 NSI in 10,099 patients, with an event rate of 27.0 per year (95% CI 26.6 to 27.4). Increasing age, female gender, comorbidity burden, corticosteroid therapy, DAS28 and HAQ-DI were associated with an increased risk of NSI. The rate of NSI was numerically lowest with csDMARDs. Compared to TNFi, IL-6 inhibitor had a higher risk of NSI, whilst the csDMARD cohort had a lower risk. Between the TNFi agents, adalimumab had a higher risk than etanercept (Table 1). Conclusion These results confirm that NSI is a frequent occurrence for patients, which historically has received little attention in research literature. The data suggest biologics increase the risk of NSI, especially IL-6 inhibition. Whilst unmeasured confounding must be considered, the magnitude of effects are large and it seems likely that a causal link between targeted immunosuppression and NSI risk exists. Further research is needed to understand the impact of NSI on clinical outcomes including drug survival and quality of life. Disclosures K. Bechman: None. K. Halai: None. S. Norton: None. A.P. Cope: None. K.L. Hyrich: Honoraria; AbbVie paid to the institution and grant income from Pfizer and Bristol-Myers Squibb for activities outside of this work. J.B. Galloway: Honoraria; for speaking or attending conferences from AbbVie, Bristol-Myers Squibb, Celgene, Janssen, Pfizer and Union Chimique Belge.


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