Treatment Persistence and Clinical Outcomes of Tumor Necrosis Factor Inhibitor Cycling or Switching to a New Mechanism of Action Therapy: ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-07-03

AUTHORS

Wenhui Wei, Keith Knapp, Li Wang, Chieh-I Chen, Gary L. Craig, Karen Ferguson, Sergio Schwartzman

ABSTRACT

INTRODUCTION: To examine treatment persistence and clinical outcomes associated with switching from a tumor necrosis factor inhibitor (TNFi) to a medication with a new mechanism of action (MOA) (abatacept, anakinra, rituximab, tocilizumab, or tofacitinib) versus cycling to another TNFi (adalimumab, certolizumab pegol, etanercept, golimumab, or infliximab) among patients with rheumatoid arthritis. METHODS: This retrospective, longitudinal study included patients with rheumatoid arthritis in the JointMan® US clinical database who received a TNFi in April 2010 or later and either cycled to a TNFi or switched to a new MOA therapy by March 2015. Cox proportional hazards models were used for time to non-persistence (switching or discontinuing). An ordinary least squares regression model compared 1-year reduction from baseline for the Clinical Disease Activity Index (CDAI). RESULTS: There were 332 (54.2%) TNFi cyclers and 281 (45.8%) new MOA switchers. During a median follow-up of 29.9 months, treatment persistence was 36.7% overall. Compared with new MOA switchers, TNFi cyclers were 51% more likely to be non-persistent (adjusted hazard ratio, 1.511; 95% CI 1.196, 1.908), driven by a higher likelihood of switching again (adjusted hazard ratio, 2.016; 95% CI 1.428, 2.847). Clinical outcomes were evaluable for 239 (53.3%) TNFi cyclers and 209 (46.7%) new MOA switchers. One-year mean reduction in CDAI from baseline to end of follow-up was significantly higher for new MOA switchers than TNFi cyclers (-7.54 vs. -4.81; P = 0.037), but the difference was not statistically significant after adjustment for baseline CDAI (-6.39 vs. -5.83; P = 0.607). CONCLUSION: In this study, TNFi cycling was common in clinical practice, but switching to a new MOA DMARD was associated with significantly better treatment persistence and a trend toward greater CDAI reduction that was not significant after adjustment for baseline disease activity. FUNDING: Sanofi and Regeneron Pharmaceuticals. More... »

PAGES

1936-1952

References to SciGraph publications

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  • 2015-10-08. Non-adherence to disease-modifying antirheumatic drugs is associated with higher disease activity in early arthritis patients in the first year of the disease in ARTHRITIS RESEARCH & THERAPY
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  • 2014-01-28. Comparative effectiveness of cycling of tumor necrosis factor-α (TNF-α) inhibitors versus switching to non-TNF biologics in rheumatoid arthritis patients with inadequate response to TNF-α inhibitor using a Bayesian approach in ARCHIVES OF PHARMACAL RESEARCH
  • 2005-04-07. Acute phase reactants add little to composite disease activity indices for rheumatoid arthritis: validation of a clinical activity score in ARTHRITIS RESEARCH & THERAPY
  • 2014-09-23. Response to Biologic Disease-Modifying Anti-Rheumatic Drugs after Discontinuation of Anti-Tumor Necrosis Factor Alpha Agents for Rheumatoid Arthritis in RHEUMATOLOGY AND THERAPY
  • 2008-04. Rheumatoid Arthritis in DRUGS
  • 2015-09-07. Retention of the second-line biologic disease-modifying antirheumatic drugs in patients with rheumatoid arthritis failing one tumor necrosis factor alpha inhibitor: data from the BioRx.si registry in CLINICAL RHEUMATOLOGY
  • 2009-02-19. Medication persistence over 2 years of follow-up in a cohort of early rheumatoid arthritis patients: associated factors and relationship with disease activity and with disability in ARTHRITIS RESEARCH & THERAPY
  • 2015-07-11. Window of opportunity to achieve major outcomes in early rheumatoid arthritis patients: how persistence with therapy matters in ARTHRITIS RESEARCH & THERAPY
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s12325-017-0578-8

    DOI

    http://dx.doi.org/10.1007/s12325-017-0578-8

    DIMENSIONS

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    PUBMED

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    33 schema:description INTRODUCTION: To examine treatment persistence and clinical outcomes associated with switching from a tumor necrosis factor inhibitor (TNFi) to a medication with a new mechanism of action (MOA) (abatacept, anakinra, rituximab, tocilizumab, or tofacitinib) versus cycling to another TNFi (adalimumab, certolizumab pegol, etanercept, golimumab, or infliximab) among patients with rheumatoid arthritis. METHODS: This retrospective, longitudinal study included patients with rheumatoid arthritis in the JointMan<sup>®</sup> US clinical database who received a TNFi in April 2010 or later and either cycled to a TNFi or switched to a new MOA therapy by March 2015. Cox proportional hazards models were used for time to non-persistence (switching or discontinuing). An ordinary least squares regression model compared 1-year reduction from baseline for the Clinical Disease Activity Index (CDAI). RESULTS: There were 332 (54.2%) TNFi cyclers and 281 (45.8%) new MOA switchers. During a median follow-up of 29.9 months, treatment persistence was 36.7% overall. Compared with new MOA switchers, TNFi cyclers were 51% more likely to be non-persistent (adjusted hazard ratio, 1.511; 95% CI 1.196, 1.908), driven by a higher likelihood of switching again (adjusted hazard ratio, 2.016; 95% CI 1.428, 2.847). Clinical outcomes were evaluable for 239 (53.3%) TNFi cyclers and 209 (46.7%) new MOA switchers. One-year mean reduction in CDAI from baseline to end of follow-up was significantly higher for new MOA switchers than TNFi cyclers (-7.54 vs. -4.81; P = 0.037), but the difference was not statistically significant after adjustment for baseline CDAI (-6.39 vs. -5.83; P = 0.607). CONCLUSION: In this study, TNFi cycling was common in clinical practice, but switching to a new MOA DMARD was associated with significantly better treatment persistence and a trend toward greater CDAI reduction that was not significant after adjustment for baseline disease activity. FUNDING: Sanofi and Regeneron Pharmaceuticals.
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