Gastroesophageal reflux: a potential asthma trigger

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Gastroesophageal reflux prevalence and epidemiologic considerations in asthmatics

GER symptoms are common in adults and children with asthma. Field et al [4] examined 109 asthmatics and 135 subjects in two control groups and found that heartburn was present in 77% of asthmatics compared with 50% of subjects in the control groups. Furthermore, 41% of asthmatics noted GER-associated respiratory symptoms, and 28% used their inhalers while experiencing GER symptoms. These data verify that GER symptoms are more prevalent in asthmatics compared with control populations and that

Predisposing factors to gastroesophageal reflux development in asthmatics

Under normal conditions in the stomach, the angle of His acts as a flap valve to prevent material from leaving the stomach. The lower esophageal sphincter (LES) is the major anti-reflux barrier and has an intrinsic basal tone along with augmentation by crural diaphragm contractions [20]. If GER occurs, a swallow initiates peristalsis that clears gastric contents from the esophagus. Saliva neutralizes the acid pH and rinses the refluxate from the esophageal mucosa. GER disease is a

Potential mechanisms of gastroesophageal reflux–triggered asthma

There are many mechanisms whereby the esophagus and lung can interact and result in esophageal acid–induced bronchoconstriction. Neurogenic inflammation plays a role in many of these mechanisms. Mechanisms include a vagally mediated reflex (whereby acid in the esophagus triggers airway responses), a direct axonal reflex (whereby the central nervous system [CNS] is not required to complete a reflex arc), heightened bronchial reactivity, and microaspiration [26]. Esophageal acid also causes

Medical therapy

If GER is a potential asthma trigger, then aggressive GER therapy should improve asthma outcomes. Multiple studies have evaluated asthma outcomes, and most show an improvement in asthma symptoms. In reviewing the combined results of 12 studies examining medical therapy in 326 treated asthmatics with GER, asthma symptoms improved in 69%, medication use was reduced in 62%, and evening PEF rates improved in 26% of patients; however, pulmonary function did not improve [45]. Most trials used H2

Potential predictors of gastroesophageal reflux–responsive asthma

Despite the numerous design flaws in many of the studies, some studies have identified potential predictors for asthma response either by the use of selected patient populations or by evaluation of predictive variables in the responders (Box 1). These predictors need to be verified in independent patient populations. Irwin et al [8] noted that difficult-to-control asthma is a potential predictor, whereas Ekström et al [58] noted that a history of reflux-associated respiratory symptoms predicted

Diagnosis

Making the diagnosis of GER in asthmatics is similar to making the diagnosis in people without asthma. GER symptoms may be intermittent, or continuous and progressive. Classic esophageal symptoms include heartburn, regurgitation, retrosternal and epigastric pain, dysphagia, cervical discomfort (globus), and belching [62]. GER symptoms may be temporally associated with chest tightness, wheezing or other asthma symptoms, and inhaler use [4], [6]. GER may cause arousals from sleep. It may also be

Potential management strategy of gastroesophageal reflux–triggered asthma

Because anti-reflux therapy has the potential to improve asthma outcome in selected patients, all asthmatics should be assessed for GER. If GER symptoms are present, then an empiric trial of acid suppressive therapy should be considered. A PPI should be used because of its superior effectiveness and should be given at high doses, twice daily, for at least 3 months. Asthma symptoms, PEF rates, and asthma medication use should be monitored before and during the empiric trial [78]. Also, an

Summary

GER is a potential asthma trigger. Further research is needed to elucidate the role of esophageal acid in perpetuating airway inflammation and for validating potential predictors for asthma response with anti-reflux therapy.

Acknowledgments

I thank Arren Graf for editorial assistance in the preparation of this manuscript.

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    This work was supported by NHLBI grant no. HL75614-01 from the National Institutes of Health. Dr. Harding has received grant funding and is a consultant for AstraZeneca LP.

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