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Original Research: Signs and Symptoms of Chest Diseases |

Response of Chronic Cough to Acid-Suppressive Therapy in Patients With Gastroesophageal Reflux DiseaseResponse of Cough to Acid-Suppressive Therapy

Peter J. Kahrilas, MD; Colin W. Howden, MD; Nesta Hughes, PhD; Michael Molloy-Bland, DPhil
Author and Funding Information

From the Division of Gastroenterology and Hepatology (Drs Kahrilas and Howden), Northwestern University Feinberg School of Medicine, Chicago, IL; and the Research Evaluation Unit (Drs Hughes and Molloy-Bland), Oxford PharmaGenesis Ltd, Oxford, England.

Correspondence to: Peter J. Kahrilas, MD, Northwestern University, Feinberg School of Medicine, Division of Gastroenterology and Hepatology, Department of Medicine, 676 N St. Clair St, 14th Floor, Chicago, IL 60611; e-mail: p-kahrilas@northwestern.edu


Funding/Support: This study was supported by funding from AstraZeneca R&D Mölndal, Sweden. Dr Kahrilas is supported by Public Health Service [Grant R01 DK56033].

For editorial comment see page 587

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(3):605-612. doi:10.1378/chest.12-1788
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Background:  Epidemiologic and physiologic studies suggest an association between gastroesophageal reflux disease (GERD) and chronic cough. However, the benefit of antireflux therapy for chronic cough remains unclear, with most relevant trials reporting negative findings. This systematic review aimed to reevaluate the response of chronic cough to antireflux therapy in trials that allowed us to distinguish patients with or without objective evidence of GERD.

Methods:  PubMed and Embase systematic searches identified clinical trials reporting cough response to antireflux therapy. Datasets were derived from trials that used pH-metry to characterize patients with chronic cough.

Results:  Nine randomized controlled trials of varied design that treated patients with acid suppression were identified (eight used proton pump inhibitors [PPIs], one used ranitidine). Datasets from two crossover studies showed that PPIs significantly improved cough relative to placebo, albeit only in the arm receiving placebo first. Therapeutic gain in seven datasets was greater in patients with pathologic esophageal acid exposure (range, 12.5%-35.8%) than in those without (range, 0.0%-8.6%), with no overlap between groups.

Conclusions:  A therapeutic benefit for acid-suppressive therapy in patients with chronic cough cannot be dismissed. However, evidence suggests that rigorous patient selection is necessary to identify patient populations likely to be responsive, using physiologically timed cough events during reflux testing, minimal patient exclusion because of presumptive alternative diagnoses, and appropriate power to detect a modest therapeutic gain. Only then can we hope to resolve this vexing clinical management problem.

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