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Editorials |

Asthma and Gastroesophageal Reflux : Another Piece in the Puzzle?

Stephen K. Field, MD, CM, FCCP
Author and Funding Information

Affiliations: Calgary, AB, Canada
 ,  Dr. Field is Clinical Professor, Division of Respiratory Medicine, University of Calgary Medical School.

Correspondence to: Stephen K. Field, MD, CM, FCCP, Clinical Professor, University of Calgary Medical School, Foothills Hospital, 1403 29th St NW, Calgary, AB, Canada T2N 2T9



Chest. 2002;121(4):1024-1027. doi:10.1378/chest.121.4.1024
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Despite the strong association between the two conditions, few topics in medicine are as controversial as the nature of the relationship between asthma and gastroesophageal reflux (GER).1 The reported prevalence of GER in asthma patients ranges from 34 to 89%, depending on the criteria used to define GER and the population studied.2 Even asthma patients without GER symptoms are shown to frequently have abnormal pH monitoring findings.3 Although the strong association between GER and asthma has been reported repeatedly, the relationship between them remains unclear. Data have been published4 that both support and contradict the hypotheses that GER causes asthma, asthma causes GER, and bronchodilator medications cause GER. Despite the conflicting data, interest in the association between the two conditions is increasing. A PubMed search combining the terms asthma and gastroesophageal reflux reveals > 500 citations in the medical literature: an average of two citations per year between 1966 and 1980, 20 per year between 1991 and 1995, and 79 citations in the year 2000 alone. The strong association between GER and asthma, as well as reports that GER causes respiratory symptoms in asthma patients, led most investigators to assume that the relationship was due to GER causing asthma.5 One study6 demonstrated a temporal association between esophageal pH monitoring-confirmed acid reflux and worsening respiratory symptoms in asthma patients with GER. Moreover, animal data710 suggest that GER or acid perfusion of the esophagus (APE) may increase bronchial tone by several mechanisms, including vagally mediated esophagobronchial or laryngobronchial reflexes, repeated microaspiration, or neurally mediated bronchial inflammation.

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