The effect of DPP-4 inhibitors on asthma control: an administrative database study to evaluate a potential pathophysiological relationship
Received 14 June 2017
Accepted for publication 13 October 2017
Published 1 December 2017 Volume 2017:8 Pages 231—240
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Professor Amanda Lee
Gene Colice,1 David Price,2,3 Maria Gerhardsson de Verdier,4 Karma Rabon-Stith,5 Christopher Ambrose,5 Katherine Cappell,6 Debra E Irwin,7 Paul Juneau,7 Anna Vlahiotis7
In collaboration with Respiratory Effectiveness Group (REG)
1Global Medicines Development, AstraZeneca, Gaithersburg, MD, USA; 2Observational & Pragmatic Research Institute, Singapore; 3Centre of Academic Primary Care, University of Aberdeen, Aberdeen, UK; 4Global Medical Affairs, AstraZeneca, Mölndal, Sweden; 5Global Medical Affairs, AstraZeneca, Gaithersburg, MD, USA; 6Custom Data Analytics, Life Sciences, Truven Health Analytics, an IBM Watson Health Company, Ann Arbor, MI, USA; 7Outcomes Research, Life Sciences, Truven Health Analytics, an IBM Watson Health Company, Bethesda, MD, USA
Rationale: DPP-4 may regulate immunological pathways implicated in asthma. Assessing whether DPP-4 inhibitor (DPP-4i) use might affect asthma control is clinically important because DPP-4i use in type 2 diabetes mellitus management (T2DM) is increasing. This study evaluated associations between DPP-4i use and asthma control.
Methods: This was a retrospective, observational, matched cohort study using administrative claims in the MarketScan® Commercial Claims and Encounters (Commercial) and Medicare Supplemental and Coordination of Benefits (Medicare Supplemental) databases. Adult asthma patients initiating an oral DPP-4i or a non-DPP-4i between November 1, 2006 and March 31, 2014 were included. Patients were followed for asthma-related outcomes for 12 months after initiation of the antidiabetes medication. Outcomes included risk-domain asthma control (RDAC), defined as no asthma hospitalizations, no lower respiratory tract infections, and no oral corticosteroid (OCS) prescriptions; overall asthma control (RDAC criteria plus limited short-acting beta agonist use); treatment stability (RDAC criteria plus no increase of ≥50% in inhaled corticosteroid dose or addition of other asthma therapy); and severe asthma exacerbation rates (asthma-related hospitalizations, emergency room visits, or acute treatments with OCS). Comparisons were made between two matched cohorts (DPP-4i vs. non-DPP-4i initiators) using multivariable logistic regression and generalized linear modeling. Covariates included baseline demographic and clinical characteristics related to asthma and T2DM.
Results: The adjusted odds of achieving RDAC (odds ratio [OR]: 1.05; 95% CI: 0.964 to 1.147), overall asthma control (OR: 1.04; 95% CI: 0.956 to 1.135), and treatment stability (OR: 1.04; 95% CI: 0.949 to 1.115) did not differ between the DPP-4i and non-DPP-4i cohorts. A difference was not found between cohorts in severe asthma exacerbation rates during the 12 months following initiation of antidiabetes treatment (mean = 0.32 vs. 0.34 exacerbations per subject-year, respectively; p=0.064).
Conclusion: Asthma control was similar between patients initiating DPP-4i and non-DPP-4i antidiabetes medications, suggesting no association between DPP-4i use and asthma control.
Keywords: asthma control, DPP-4i, type 2 diabetes
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