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Arthritis Res Ther. 2019 Jul 22;21(1):177. doi: 10.1186/s13075-019-1958-z.

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

Author information

1
Musculoskeletal Biology I, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK.
2
Department of Academic Rheumatology, Aintree University Hospital, Liverpool, UK.
3
Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA, USA.
4
Departments of Epidemiology and Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
5
Epidemiology Group, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK.
6
Aberdeen Centre for Arthritis and Musculoskeletal Health, University of Aberdeen, Aberdeen, UK.
7
Department of Biostatistics, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
8
Department of Medicine, Harvard Medical School, Boston, MA, USA.
9
Department of Orthopaedics, General Hospital of Chinese PLA, Beijing, China.
10
Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
11
Musculoskeletal Biology I, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK. ngoodson@liverpool.ac.uk.
12
Department of Academic Rheumatology, Aintree University Hospital, Liverpool, UK. ngoodson@liverpool.ac.uk.

Abstract

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.

KEYWORDS:

Ankylosing spondylitis; Axial spondyloarthritis; Biologic DMARDs; Discontinuation; Effectiveness; Marginal structural model; Persistence; Response; TNF inhibitor

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