Role of the oesophagus in asthma induced by the ingestion of ice and acid.

Abstract

Twelve Asian patients with a history of asthma exacerbated by ingestion of ice and acidic drinks were selected for study. To determine the site of response to ingested ice and acid they were challenged with ice or dilute hydrochloric acid, which was orally retained on one day and swallowed on another. On a third day a placebo was given. The airway response was assessed by measuring FEV, and the provocative concentration of histamine that reduced the FEV1 by at least 20% (PC20). There was no significant change in FEV1 or histamine PC20 after placebo or the orally retained challenges for the group as a whole or for any individual. After the ice and hydrochloric acid had been swallowed there was a small but statistically significant mean fall in FEV,, increasing to a maximum 90 minutes after ingestion, together with a significant increase in bronchial responsiveness. As conditioning of the inspired air would have been similar after orally retained and after swallowed ice or acid, the response is likely to be due to oesophageal stimulation. The mechanism of the response to oesophageal stimulation is unclear, but the slow time course seems to preclude a simple neural reflex.Ingestion of ice' and of dilute hydrochloric acid2 have both been shown to increase bronchial responsiveness in some asthmatic individuals. As soft drinks (pH about 3) are frequently served iced this could be a potential hazard for many individuals with asthma, particularly children.The mechanism of this response is unclear but is likely to be due to stimulation of the upper gastrointestinal tract, although conditioning of the inspired air is a possibility. The

Gastro-Oesophageal Reflux in Patients with Bronchial Asthma

“…If a colloid labeled with 99m-Tc is instilled in the trachea, too rapid clearing of the isotope by the mucocil iary system is not a problem [ 12], A vagally mediated reflex, originating from acid-sensitive receptors in the oesopha geal mucosa, has been postulated originally by Mansfield and Stein [13]. In 15 asthmatic patients with a positive Bernstein test and a history of GER, they demonstrated a slight but significant increase in airway resistance during acid perfusion of the oesophagus [ 13], Other investigators confirmed this observa tion, but in most cases the bronchoconstrictive changes appeared to be modest, without clinically detectable bronchospasm [4,[14][15][16][17][18]. More recent reports have demonstrated a significant augmentation of bronchoconstriction, induced by isocapnic hyperventila tion, histamine or methacholine, after acid perfusion of the oesophagus [19], In the ani mal model vagal disruption abolished the reflex bronchoconstriction [20,21], How ever, a temporal relationship between acid reflux episodes and a decrease in peak respi ratory flow rate (PEFR) or respiratory symp toms, could not be demonstrated [22,23], The changes in intrathoracic pressures ac companying bronchoconstriction and the subsequent transdiaphragmatic pressure swings, have been postulated to promote GER in asthmatics [24,25].…”

High prevalence of gastroesophageal reflux symptoms in patients with both acute and nonacute cough

“…The intimate mechanisms of acid-induced airway obstruction are dependent on activation of capsaicin-sensitive sensory nerves, with the subsequent release of tachykinins, that modulate diverse aspects of airway dysfunction (Ricciardolo et al 2004). Wilson and colleagues (1987) demonstrated direct evidence that ingestion of 200 mL of 0.1 N Hcl increased bronchial activity. Field and colleagues (1988) reported increased minute ventilation due to sensations of discomfort during acid perfusion of the esophagus in patients with normal lung function.…”

Refractory Childhood Asthma

“…Reflux can cause symptoms either by direct contamination of the lower airway or indirectly by an esophagobronchial reflex; [17][18][19] respiratory disease can cause reflux, including via mechanisms secondary to abnormal pleural pressure swings or configuration of the diaphragm; and reflux may be an asymptomatic fellow-traveler. Reflux can cause symptoms either by direct contamination of the lower airway or indirectly by an esophagobronchial reflex; [17][18][19] respiratory disease can cause reflux, including via mechanisms secondary to abnormal pleural pressure swings or configuration of the diaphragm; and reflux may be an asymptomatic fellow-traveler.…”