Reflux may cause respiratory symptoms through different pathways, such as (micro-) aspiration or vagally mediated mechanisms. Many patients with chronic cough have gastrohypopharyngeal reflux.35 A consequence of pulmonary aspiration of refluxed material may be the presence of an increased number of lipid-laden macrophages. Although simply observing the presence of lipid-laden alveolar macrophages is likely to be nonspecific, it has been suggested that quantification would be a useful marker of silent aspiration.75 Data are lacking and are therefore needed on the diagnostic accuracy, sensitivity and specificity of the detection and quantification of other substances in tracheal aspirates, such as lactose, pepsin and intrinsic factor.
In some patients it may not be GER that is causing respiratory disease, but the reverse. Respiratory difficulties cause greater respiratory breathing efforts and thus more pronounced negative intrathoracic pressure, and thus respiratory symptoms may provoke GER. However, the incidence of a direct temporal relation between reflux and cough episodes is relatively low.76
The relation between respiratory disease and GER may also be neurogenic, in this case designated as 'gastric asthma'.77 The tracheobronchial tree and the esophagus have common embryonic foregut origins and share autonomic innervation through the vagus nerve.78 In other words, it can be speculated that GER increases the irritability of the vagal nerve endings in the esophagus, and that as a result these nerve endings hyper-react together with the nerve endings in the airways because they have the same embryonic origin.
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