Gastroesophageal reflux disease and asthma.

Gastroesophageal reflux (GER) and asthma occur together frequently. The relationship has been recognized for more than 2,000 years but has not been appreciated until recently. Attempts to determine the number of asthmatics that currently have GER (prevalence) have shown a higher-than-expected prevalence. Of the approximately 200 published studies on the relationship between GER and asthma, the true prevalence of GER in asthmatics, however, can be estimated from fewer than 20 of the studies. These studies, which comprise highly selected referred populations, are unlikely to reflect the overall population of patients with asthma. Nevertheless, the estimated prevalence of GER in asthmatics is between 60-80% in adults and 50-60% in children. No attempts have been made to determine the incidence of GER in asthmatics. To identify asthmatics who develop GER over time would be a formidable task, requiring decades of close follow-up of asthmatics who do not now have GER. Despite the lack of data on the incidence of GER, data on the prevalence raise an important issue: If the prevalence of GER in adult asthmatics is similar to the prevalence of GER in child asthmatics, what is the true incidence of GER? There are two potential answers: (1) all of the child asthmatics with GER grow up to become the adult asthmatics with GER (GER incidence = 0%); and (2) some child asthmatics with GER outgrow either the GER or the asthma; some adults with asthma develop GER while others with GER develop asthma (low, medium, or high incidence depending on the numbers). It is not unreasonable to suspect that some child asthmatics with GER become adult asthmatics with GER, and that children with GER who apparently "outgrow" their asthma surface later as adults with both asthma and GER. Because most children leave their pediatricians after adolescence, the information required to demonstrate continued asthma or GER is lost. As a result, the medical community sees two completely different populations, each with very similar conditions: childhood asthma with GER and adult asthma with GER. If the high prevalence of GER in asthmatics is clinically relevant, it should be readily explainable. We suggest that the GER/asthma relationship consists of a self-propagating situation whereby reflux aggravates asthma, which in turn induces further reflux. In the early course of the disease, asthma may not be apparent, as aspiration-induced pulmonary symptoms may occur very infrequently-perhaps once or twice a year. With time, however, aspiration may become more frequent, and the pulmonary tree may become hypersensitive. The individual may be diagnosed as having asthma. The pulmonary tree becomes increasingly hypersensitive, to a variety of stimuli. In such a scenario, the initial contribution of acid aspiration is no longer apparent, as the primary focus is on the asthma. In any individual patient, the emphasis may be placed on the GER if reflux symptoms predominate or on asthma if pulmonary symptoms predominate. The result is confusion over whether a patient with GER has asthma or whether a patient with asthma has GER. The unending debate about whether GER is a cause of the asthma or a result of the asthma becomes the focus of attention. At such a point, the question of whether GER exists in asthmatics or whether pulmonary symptoms exist in refluxers is irrelevant. For the individual patient, gastric contents refluxed into the pulmonary tree is an undesirable event, whether cause or effect, and it is up to the physician to determine how such events can be stopped.