The underlying gastro-esophageal reflux disease predisposes the patient to have repetitive episodes of acid aspiration, which subsequently causes repeated airway inflammation and results in irritant-induced asthma.[1][2] The incidence of GERD in patients with asthma is approximately 38%. Asthmatics resistant to therapy are commonly associated with GERD, but identification and treatment of GERD has not shown to relate to the improvement in asthmatic control.[3]
There are three mechanisms proposed to explain the pathophysiology of development of asthma in patients with GERD:
Vagal reflex: Both the esophagus and the bronchial tree, as they share a common embryonic origin, are innervated by the vagus nerve. Therefore, when there is reflux of acid contents from the stomach into the esophagus, the receptors in the esophagus are stimulated causing the vagus nerve to fire, which results in a bronchospasm. This phenomenon was demonstrated by Mansfield and Stein by the intraesophageal acid provocation test, which resulted in an increased resistance to airflow.[4] It was further strengthened by another series involving 136 subjects.[5] However, many studies failed to demonstrate a significant relationship between acid reflux and pulmonary function.[6][7]
Heightened Bronchial Reactivity: Acid reflux into the esophagus increases the bronchial response to other stimuli. This was demonstrated by increased bronchial response to methacholine challenge test.[8]
Microaspiration: Microaspiration of acidic contents from stomach into the upper airways and bronchial tree was shown to stimulate bronchial receptors resulting in broncho-constriction in asthmatic patients.[9] A murine study demonstrated that microaspiration of gastric contents caused an immune response similar to that observed in asthma.[10] However, a prospective single blinded study failed to demonstrate any significant bronchoconstriction with acid reflux into the airways.[11]
The chest x-ray in asthmatics is often normal. It is done to exclude other causes of wheeze and aid in the diagnosis of complications such as atelectasis and pneumonia.
Esophageal pH testing: Presence of symptoms of GERD, which is refractory to proton pump inhibitors, should undergo esophageal pH testing. This helps in correlating the symptoms of asthma with gastro-esophageal reflux.[17]
Upper GI endoscopy: Endoscopy, though not indicated in diagnosis of asthma in GERD, may be done to exclude the presence of Barrett's esophagus.
Treatment of asthma in GERD mainly pertains to treatment of GERD. Therefore, patients with poorly controlled asthma should be evaluated for GERD even in the absence of gastric reflux symptoms.
Proton pump inhibitors:Omeprazole demonstrates an improvement in the symptoms of asthma and peak expiratory flow rates in asthmatics with GERD symptoms.[19] Dosage of 40mg/day is recommended.[20]
Lansoprazole has shown to decrease the number of episodes of asthma exacerbations though it does not improve the asthmatic symptoms.[21]Esomeprazole improves peak expiratory flow in subjects with asthma who presents with both GERD and nocturnal symptoms.[22]
The role of fundoplication in patients with asthma and GERD has not yet been established. A meta-analysis of 24 studies concluded that the surgery improved asthma symptoms by 79% but had little effect on expiratory flow rate.[23] Surgical therapy has been found superior to the H2 antagonist. However, the benefit from surgery was not found to be different from those treated with proton pump inhibitors.[24]
↑Field SK (1999). "A critical review of the studies of the effects of simulated or real gastroesophageal reflux on pulmonary function in asthmatic adults". Chest. 115 (3): 848–56. PMID10084501.
↑Tan WC, Martin RJ, Pandey R, Ballard RD (1990). "Effects of spontaneous and simulated gastroesophageal reflux on sleeping asthmatics". Am Rev Respir Dis. 141 (6): 1394–9. PMID2350084.CS1 maint: Multiple names: authors list (link)
↑Herve P, Denjean A, Jian R, Simonneau G, Duroux P (1986). "Intraesophageal perfusion of acid increases the bronchomotor response to methacholine and to isocapnic hyperventilation in asthmatic subjects". Am Rev Respir Dis. 134 (5): 986–9. PMID3096180.CS1 maint: Multiple names: authors list (link)
↑Kiljander TO, Salomaa ER, Hietanen EK, Terho EO (1999). "Gastroesophageal reflux in asthmatics: A double-blind, placebo-controlled crossover study with omeprazole". Chest. 116 (5): 1257–64. PMID10559084.CS1 maint: Multiple names: authors list (link)
↑Field SK, Gelfand GA, McFadden SD (1999). "The effects of antireflux surgery on asthmatics with gastroesophageal reflux". Chest. 116 (3): 766–74. PMID10492285.CS1 maint: Multiple names: authors list (link)
↑Williams DB, Schade RR. Gastroesophageal reflux disease. In: DiPiro JT, Talbert RL, Yee GC, et al.Pharmacotherapy: A Pathophysiologic Approach. 6th ed. New York, NY: McGraw-Hill; 2005:613-628.