It is believed that GER can trigger...

It is believed that GER can trigger asthma by the agency of the stimulation of acid-sensitive receptors in the esophagus. The aim of this consideration was to determine whether esophageal acid stimulation in asthmatic patients can produce clinically detectable bronchospasm and if a possible answer is correlated to bronchial reactivity. Eight patients with chronic asthma and GER disease were investigated forward three occasions with a histamine challenge proof followed by acid provocation of the esophagus. Assessment of bronchial function was made at [FEV.sub.1], chest auscultation, and respiratory symptoms. While symptoms and signs of broncho-constriction induced by way of esophageal acid stimulation were not discovered clinically on any occasion, there was a significant correlation between histamine reactivity and the subclinical bronchospasm following acid provocation. It is conclud that esophageal acid stimulation during daytime in the majority of asthmatic patients is not a solid and immediate trigger of asthma.

Gastroesophageal ebb has been suggested as a possible trigger of bronchospasm in asthmatic patients. near authors believe that bolus- or microaspiration of stomach make contenteds into the tracheobronchial tree is the greatest in number likely mechanism by which GER triggers asthma.[1,2] trial impression of aspiration, however, has been hard to obtain despite the use of sensitive radiolabeled isotopic scintigraphic techniques.[3] In a scarcely any studies aspiration has been demonstrated in a minority of asthmatic patients with GER[145]

Esophagobronchial reflexe triggered by way of acid stimulation of vagal receptors in the esophageal mucosa is another possible way by way of which GER may induce bronchospasm. In animals as well as in patients with asthma, acid perfusion of the esophagus has been shown to give offence [i]or[/i] umbrage to mild bronchoconstriction especially if esophagitis is present[5-12] However, patients rarely experience symptoms of bronchospasm and real attacks of asthma have not been seen[57-12] In a reflection by Davis et al[13] acid perfusion of the esophagus during nighttime, however, caused sharp bronchospasm in four children with asthma. A direct causal relationship between episodes of ebb and bronchial symptoms could not be demonstrated in the studies according to Hughes et al[14] or according to Ekstrom and Tibbling,[15] but Pellegrini and coworkers[1] reported a correlation between episodes of GER and attacks of asthma.

The contradictory rises obtained by different authors could be explained by the agency of a difference in the severity of asthma in various patients studied.

Like any other trigger of asthma, bronchial susceptibility to esophageal acid stimulation should be related to the severity of asthma and to the rank of underlying airway hyperresponsiveness. In asthmatic subdues the sensitivity of the airways to acid stimulation of the esophagus might vary considerably from time to time depending in succession whether the patient is being influenced through aggravating factors such as airway infections, bad weather, or mental stress

The aim of this research was to determine whether clinically significant bronchospasm and respiratory symptoms can generally be provok in patients with asthma and marked bronchial hyperreactivity during lengthened esophageal acid stimulation in the daytime. Further, we wanted to subject of attention whether a bronchial response to esophageal acid stimulation is correlated to the extent of bronchial reactivity.

PATIENTS AND METHODS

In this subject of attention eight patients with moderate to censorious intrinsic asthma and a history of airway hyperresponsiveness to various models of airborne irritants, emotional stres weather fluctuations, and exercise were evaluated. The diagnosis of asthma was based onward the criteria established by the American Thoracic Society.[16] All patients required daily medication of oral and inhaled [unkeyable.sub.2]-agonists, theophylline, and inhaled steroids. Six patients took oral steroids in addition. No patient had anticholinergic medication. All had a known GER disease, ie, a history of heartburn and regurgitation, pathologic GER with a 24-h pH-monitoring in the esophagus, ie, ebb in more than 1 percent during the day,[17] and a positive acid perfusion standard The 24-h pH-monitoring experiment and an acid perfusion exhibition were performed prior to the current study without changing regular asthma medication. Four patients had a history of RARS, ie, wheeziness, cough or a vague feeling of respiratory distress when having heartburn or symptoms of regurgitation. Patients with RARS had asthma of longer mean duration and more pronounced impairment of lung function than patients without RARS (Table 1) There was no difference as regards asthma medication, predominence of either daytime or nighttime attacks of asthma or severity of ebb disease between patients with and without RARS. Oral medication was withdrawn at least 12 h prior to each acid perfusion experiment and [Beta.sub.2]-inhalants were withdrawn at least 4 h prior to testing. Serum plains of theophylline and [Beta.sub.2]-agonists were not analyzed upon different study days. [TABULAR DATA OMITTED]