The American Journal of Gastroenterology
Chapter 5Asthma and gastroesophageal reflux
Introduction
Asthma is an inflammatory disease with multiple triggers. Its prevalence continues to rise, and it is associated with continued morbidity and even mortality (1). Gastroesophageal reflux (GER) is a trigger of asthma 2, 3. The prevalence of GER is as high as 80% in asthma patients and may even be “clinically silent” 4, 5, 6. Mechanisms of bronchoconstriction include a vagally mediated reflex whereby acid in the distal esophagus results in bronchoconstriction, increased airway responsiveness, and/or microaspiration of esophageal contents into the upper airway (3). Medical and surgical therapy for GER may improve asthma symptoms in up to 70% of patients 7, 8, 9. This article reviews the current data on GER prevalence in asthma patients, mechanisms of bronchoconstriction, and asthma outcomes with antireflux therapy.
Section snippets
The prevalence of GER in asthmatics
Of the 222 articles published, we identified 18 articles (seven concerning children, 11 about adults) with sufficient information from which prevalence data could be extracted. For the most part, however, the definition of GER did reflect the presence of pathological reflux. The terms for prevalence and incidence were often confused and used interchangeably. We took the liberty of switching the terms when “incidence” was mistakenly used for “prevalence.”
Pathogenesis
Esophageal acid can cause respiratory symptoms by means of at least two mechanisms: by bronchoconstriction, and/or by increasing minute ventilation and respiratory rate, as shown in Figure 4. This section will discuss: 1) how esophageal acid induces bronchoconstriction through a vagally mediated reflex; 2) how esophageal acid augments airway hyper-responsiveness; 3) evidence of microaspiration causing bronchoconstriction; 4) evidence of airway inflammation with esophageal acid; and 5) how
The diagnosis of GER-related or GER-induced asthma
There are numerous methods that have been used in an attempt to document and to clarify the relationship between GER and asthma. These methods include a) inspection of sputum for lipid-laden alveolar macrophages 41, 42, b) scintigraphic technetium monitoring to document pulmonary aspiration of gastric contents 43, 44, 45, c) esophageal acid infusion to provoke vagally mediated bronchoconstriction 22, 46, 47, (d) ambulatory esophageal pH monitoring to document acid reflux into the esophagus, and
Asthma response to antireflux therapy
The association between asthma and GER is very complex. Because of the complexities of airway inflammation and the clinical heterogeneity of asthma, treatment effects may be difficult to show. Despite this, there are medical and surgical trials that show significant asthma improvement. Some recent trials evaluating asthma outcomes are reviewed below.
Conclusions
The prevalence of GER is more common in asthmatics compared to control populations, with 82% of consecutive asthmatics having abnormal esophageal acid contact times 4, 12. Gastroesophageal reflux may be clinically silent from an esophageal standpoint 5, 6. Not all asthmatics with GER have esophageal symptoms, with up to 65% of asthmatics without heartburn or regurgitation having abnormal esophageal pH study results. The mechanisms of esophageal acid-induced bronchoconstriction include a vagally
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