Smoking status and cause-specific discontinuation of tumour necrosis factor inhibitors in axial spondyloarthritis

Sizheng Steven Zhao, Kazuki Yoshida, Gareth T. Jones, David M. Hughes, Stephen J. Duffield, Sara K. Tedeschi, Houchen Lyu, Robert J. Moots, Daniel H. Solomon, Nicola J. Goodson (Corresponding Author)

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BACKGROUND: The impact of smoking on TNF inhibition (TNFi) therapy is unclear. We examined the effect of smoking on all-cause and cause-specific TNFi discontinuation in axial spondyloarthritis (axSpA).

METHODS: We used longitudinal data from the British Society for Rheumatology Biologics Register for Ankylosing Spondylitis (BSRBR-AS). Patients fulfilling the ASAS criteria for axSpA, who started their first TNFi, were eligible for analysis. Inverse-probability weights were used to balance differences in baseline disease severity and other confounders. We used marginal structural Cox proportional hazard models to estimate hazard ratios (HR) for TNFi discontinuation according to smoking status. In analyses of cause-specific discontinuation, competing risk events were considered as censoring, using inverse-probability weights.

RESULTS: A total of 758 participants were included in the analysis (66% male, mean age 45 years), providing 954 patient-years of follow-up. TNFi was discontinued in 174 (23%) patients, among whom 26% stopped due to infections, 20% due to other adverse events and 44% due to inefficacy or other reasons. Thirty-four percent were current smokers and 30% ex-smokers. Compared to never smokers, current smokers' risk of TNFi discontinuation was HR 0.79 (95%CI 0.53 to 1.20) and ex-smokers HR 0.68 (95%CI 0.45 to 1.04). Our data did not show evidence that current smoking influenced discontinuation due to infections (HR 0.79, 95%CI 0.40 to 1.54), other adverse events (HR 0.86, 95%CI 0.41 to 1.78) or inefficacy/other causes (HR 1.44, 95%CI 0.86 to 2.41).

CONCLUSION: Baseline smoking status did not impact TNFi discontinuation in this UK cohort of axSpA participants.

Original languageEnglish
Article number177
Number of pages7
JournalArthritis Research & Therapy
Issue number1
Publication statusPublished - 22 Jul 2019

Bibliographical note

Availability of data and materials
BSRBR-AS data are held at the University of Aberdeen.

The BSRBR-AS is funded by the British Society for Rheumatology (BSR) who have received funding for this from Pfizer, AbbVie and UCB. These companies receive advance copies of manuscripts for comments. They have no input in determining the topics for analysis or work involved in undertaking it. SZ was supported by awards from the Royal College of Physicians (John Glyn bursary) and Royal Society of Medicine (Kovacs fellowship). KY received financial support for his doctoral study from the Pharmacoepidemiology Program at the Harvard T.H. Chan School of Public Health (partially supported by training grants from Pfizer, Takeda, Bayer and ASISA) and Honjo International Scholarship Foundation. DHS was supported by grants from the National Institute of Health (NIH-P30-AR072577 (VERITY) and NIH-K24AR055989) and has received funding from Abbvie and Amgen unrelated to this work.

We are grateful to Professor Gary Macfarlane (Chief Investigator of BSRBR-AS) and the staff of the BSRBR-AS register who are currently Claudia Zabke, Elizabeth Ferguson-Jones, Maureen Heddle, Nafeesa Nazlee and Barry Morris, and to the recruiting staff at the clinical centres, details of which are available at:


  • Axial spondyloarthritis
  • TNF inhibitor
  • Biologic DMARDs
  • Persistence
  • Effectiveness
  • Response
  • Discontinuation
  • Marginal structural model


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