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Nonsteroidal Anti-Inflammatory Drug Use is Not Associated With Reduced Risk of Barrett’s Esophagus

Thrift, Aaron P PhD1,2; Anderson, Lesley A PhD, MPH3; Murray, Liam J MD, MRCGP3; Cook, Michael B PhD4; Shaheen, Nicholas J MD, MPH5; Rubenstein, Joel H MD, MSc6,7; El-Serag, Hashem B MD, MPH1,8; Vaughan, Thomas L MD, MPH9; Schneider, Jennifer L MPH10; Whiteman, David C MBBS, PhD11; Corley, Douglas A MD, PhD10

American Journal of Gastroenterology: November 2016 - Volume 111 - Issue 11 - p 1528–1535
doi: 10.1038/ajg.2016.348

Objectives: Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced risk of esophageal adenocarcinoma. Epidemiological studies examining the association between NSAID use and the risk of the precursor lesion, Barrett’s esophagus, have been inconclusive.

Methods: We analyzed pooled individual-level participant data from six case–control studies of Barrett’s esophagus in the Barrett’s and Esophageal Adenocarcinoma Consortium (BEACON). We compared medication use from 1,474 patients with Barrett’s esophagus separately with two control groups: 2,256 population-based controls and 2,018 gastroesophageal reflux disease (GERD) controls. Study-specific odds ratio (OR) and 95% confidence intervals (CI) were estimated using multivariable logistic regression models and were combined using a random-effects meta-analytic model.

Results: Regular (at least once weekly) use of any NSAIDs was not associated with the risk of Barrett’s esophagus (vs. population-based controls, adjusted OR=1.00, 95% CI=0.76–1.32,I2=61%; vs. GERD controls, adjusted OR=0.99, 95% CI=0.82–1.19,I2=19%). Similar null findings were observed among individuals who took aspirin or non-aspirin NSAIDs. We also found no association with highest levels of frequency (at least daily use) and duration (≥5 years) of NSAID use. There was evidence of moderate between-study heterogeneity; however, associations with NSAID use remained non-significant in “leave-one-out” sensitivity analyses.

Conclusions: Use of NSAIDs was not associated with the risk of Barrett’s esophagus. The previously reported inverse association between NSAID use and esophageal adenocarcinoma may be through reducing the risk of neoplastic progression in patients with Barrett’s esophagus.

1Department of Medicine, Section of Gastroenterology and Hepatology, Baylor College of Medicine, Houston, Texas, USA

2Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, Texas, USA

3Centre for Public Health, Queen's University Belfast, Belfast, Northern Ireland

4Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA

5Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, University of North Carolina, Chapel Hill, North Carolina, USA

6Center for Clinical Management Research, Ann Arbor Veterans Affairs Medical Center, Ann Arbor, Michigan, USA

7Barrett’s Esophagus Program, Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA

8Department of Medicine, Houston VA HSR&D Center for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey VA Medical Center, Houston, Texas, USA

9Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA

10Kaiser Permanente Division of Research, Oakland, California and San Francisco Medical Center, USA

11QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia

Correspondence: Aaron P. Thrift, PhD, Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, One Baylor Plaza, MS: BCM305, Houston, Texas 77030-3498 USA. E-mail:

SUPPLEMENTARY MATERIAL accompanies this paper at

Received 19 May 2016; accepted 22 July 2016

Guarantor of the article: Aaron P. Thrift, PhD.

Specific author contributions: Contributed to data analysis, interpretation of data and drafting of the manuscript: Aaron P. Thrift; contributed to interpretation of data and drafting of the manuscript: Jennifer L. Schneider and Michael B. Cook; designed, obtained funding and collected data from individual case–control studies, contributed to the concept of the consortium, interpretation of data and refinement of the manuscript: Lesley A. Anderson, Liam J. Murray, Joel H. Rubenstein, Hashem B. El-Serag, Thomas L. Vaughan, David C. Whiteman, and Douglas A. Corley. All authors approved the final draft submitted.

Financial support: This work was supported by the National Institutes of Health RO1 DK63616 (D.A.C.); 1R21DK077742 (N.J.S. and D.A.C.); K23DK59311 (N.J.S.); R03 DK75842 (N.J.S.); K23DK079291 (J.H.R.); R01 CA116845 (H.B.E.-S.); K24–04–107 (H.B.E.-S.); the Intramural Program of the National Institutes of Health (M.B.C.); an Ireland–Northern Ireland cooperation research project grant sponsored by the Northern Ireland Research and Development Office and the Health Research Board, Ireland (FINBAR; L.J.M.: RES/1699/01N/S); the Study of Digestive Health, NCI RO1 CA 001833 (D.C.W.); the Study of Reflux Disease, NCI R01 CA72866 (T.L.V.), the Established Investigator Award in Cancer Prevention and Control, K05 CA124911 (T.L.V.), and the US Department of Veterans Affairs CSRD Merit I01-CX000899 (J.H.R.).

Potential competing interests: None.

© The American College of Gastroenterology 2016. All Rights Reserved.
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