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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is believed that GER can trigger asthma by the stimulation of acid-sensitive receptors in the esophagus. The aim of this study was to determine whether esophageal acid stimulation in asthmatic patients can provoke clinically detectable bronchospasm and if a possible response is correlated to bronchial reactivity. Eight patients with chronic asthma and GER disease were investigated on three occasions with a histamine challenge test followed by acid provocation of the esophagus. Assessment of bronchial function was made by FEV1, chest auscultation, and respiratory symptoms. While symptoms and signs of bronchoconstriction induced by esophageal acid stimulation were not detected clinically on any occasion, there was a significant correlation between histamine reactivity and the subclinical bronchospasm following acid provocation. It is concluded that esophageal acid stimulation during daytime in the majority of asthmatic patients is not a strong and immediate trigger of asthma.
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PMID:Esophageal acid perfusion, airway function, and symptoms in asthmatic patients with marked bronchial hyperreactivity. 280 72

Gastroesophageal reflux may predispose patients to pulmonary complications such as bronchospasm and aspiration pneumonitis. This is especially true in patients who are critically ill, those with reflux-induced asthma and those undergoing general anesthesia. Decreasing the amount of acid reflux reduces the potential for respiratory complications. In patients at risk, administration of H2-receptor antagonists minimizes the risk of acid aspiration and resolves asthma symptoms.
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PMID:Respiratory complications of gastroesophageal reflux. 289 46

A possible role of methylxanthines in the high incidence of gastroesophageal reflux (GER) in patients with asthma has been suggested. Therefore, we used a randomized, double-blind, crossover design to compare the effects of a 1-week conventional theophylline treatment and a 1-week placebo treatment in 16 adult patients with asthma. No oral or parenteral glucocorticoids were administered, but seven patients were taking inhaled corticoids. All patients needed inhaled adrenergic drugs. At the end of each period of theophylline or placebo treatment, the patients were carefully questioned with respect to respiratory and digestive symptoms, forced expiratory flows were measured, and GER was assessed by prolonged nocturnal intraesophageal pH monitoring. Peak expiratory flow was measured three times a day throughout the study. No significant increase in GER was found with theophylline compared to placebo, and forced expiratory flows improved with theophylline (p less than 0.05 for FEV1 and p less than 0.01 for peak expiratory flow rate). There was no correlation between GER, the duration of asthma, and forced expiratory flows. Thus, our study failed to demonstrate any adverse effect of a slow-release theophylline preparation on GER in patients with asthma. These results further suggest that the presence of GER is not a contraindication to the use of a slow-release theophylline in subjects with asthma.
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PMID:Effect of theophylline on gastroesophageal reflux in patients with asthma. 260 84

During attacks of asthma, changes in the transdiaphragmatic pressure gradient may impair the antireflux barrier and provoke gastroesophageal reflux (GER). If GER triggers asthma and asthma causes GER, a vicious circle could arise with an increase in the severity of asthma symptoms. The aim of this investigation was to determine whether postprandial reflux in asthmatics with GER disease is increased during histamine-induced bronchospasm and also if theophylline increases GER during provoked episodes of bronchospasm. Ten patients with chronic asthma and pathologic GER were challenged with either histamine or saline in randomized order with and without their regular dose of oral slow-release theophylline. FEV1 was recorded at regular intervals during the hour of provocation, and acid reflux (pH less than 4) was monitored by antimony pH electrodes in the esophagus. GER was not more pronounced during the provoked bronchospasm period irrespective of theophylline treatment or not. It seems unlikely that mild bronchospasm provokes reflux in patients with asthma and GER. It would appear that mild bronchospasm is rather protective against gastroesophageal reflux.
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PMID:Can mild bronchospasm reduce gastroesophageal reflux? 291 56

Intrinsic asthma, defined as asthma which is not from allergy to pneumo-allergens, of cause unknown, may show several etiologies. Allergics, remembering that there in some subjects there may be small amounts of IgE on the mastocytes, with specific RAST IgE negative, skin tests only weakly positive, but with a positive provocation test to pneumo-allergens. Food allergy, isolated and associated, may also contribute a not-negligible cause. Non-allergics, responding to the frequent triggering factors: Gastro-oesophageal reflux; Neuro-endocrine origin; Infections; Physical origin (exercise). In our study, we quote two types of extremely severe asthma, linked to intolerance to aspirin and metabisulfites with others that are associated.
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PMID:[Must the concept of intrinsic asthma be supported?]. 307 65

The authors review the now well-established data that concerns the relationship between asthma and gastro-oesophageal reflux (GER). These include the high frequency of the association in severe asthma, the diagnostic procedure of GER in asthmatics and the significance of reflux in these patients (reflux that causes asthma or reflux that is secondary to asthma). Then the mechanism of the action of GER on asthma are discussed. In the second part the authors summarise the following issues, that are only partly resolved. Evaluation of the possible worsening effect of GER on the symptoms of asthma. They insist in particular on the valuable contribution of clinical data and the results of the Bernstein acid infusion test. Therapeutic indications, particularly those for surgical correction. Recent results from a long term study of surgical treatment of 46 patients are presented.
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PMID:[Asthma and gastroesophageal reflux]. 307 67

Gastroesophageal reflux (GER) has been shown to be more frequent in people with asthma, but the mechanism by which it might aggravate asthmatic symptoms remains unclear. We compared the effects on maximal expiratory flow at 50% of VC (MEF50) of esophageal perfusion of hydrochloric acid (HCl) and of normal saline (NaCl) in 12 asthmatic subjects chosen at random. In all subjects, HCl perfusion did not change MEF50 but potentiated the bronchoconstriction induced by isocapnic hyperventilation of dry air (maximal decrease in MEF50 = 44 +/- 7% with HCl versus 22 +/- 5% with NaCl; p less than 0.001) or methacholine (provocative dose producing a 20% decrease in FEV1 = 349 +/- 99 micrograms with HCl versus 496 +/- 119 micrograms with NaCl; p less than 0.01). Seven of the asthmatic subjects were found to have GER on esophageal pH monitoring. In these subjects, HCl alone decreased MEF50 slightly but significantly (-17.5 +/- 5.5%; p less than 0.05), possibly reflecting the higher degree of basal bronchial hyperreactivity observed in this group. Thus, perfusion of acid into the distal esophagus caused slight but significant bronchoconstriction in asthmatic subjects with GER and increased the bronchoconstriction produced by isocapnic hyperventilation and by methacholine in asthmatic subjects without regard for the presence of GER.
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PMID:Intraesophageal perfusion of acid increases the bronchomotor response to methacholine and to isocapnic hyperventilation in asthmatic subjects. 309 80

A causal relation between gastro-oesophageal reflux and nocturnal asthma has been postulated. Forty four adult asthmatics underwent ambulatory monitoring of their oesophageal pH over 24 hours to find out if there was such a relation. Of these 21 showed significant "morning dipping" in which the peak expiratory flow falls during the night. Asthmatics with morning dipping had a history of nocturnal wheeze and a higher incidence of reflux symptoms, but measurement of oesophageal pH showed no significant difference in the amount or pattern of reflux when compared with "non-dippers." Overall, 15 asthmatics had gastro-oesophageal reflux, and these participated in a randomised, double blind crossover trial of ranitidine versus placebo. No significant difference was found in the peak expiratory flow rates or subjective evaluation of well being of the patients.
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PMID:Ambulatory pH monitoring of gastro-oesophageal reflux in "morning dipper" asthmatics. 314 69

A 25-yr-old man suffered from severe nocturnal asthma, which was shown to be provoked by pathological gastro-oesophageal reflux. A dramatic, immediate improvement of his pulmonary condition was achieved by treatment with omeprazole after failure of other therapeutic measures, including high doses of ranitidine.
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PMID:Beneficial effect of omeprazole in a patient with severe bronchial asthma and gastro-oesophageal reflux. 322 94

The assessment of cough starts with a search for possible causes, the commonest of which (acute or chronic inflammation of the upper airways, acute bronchial inflammation, smoking, asthma) are usually suggested by history and clinical examination. In chronic cases, where the chest X-ray is normal, the diagnosis must differentiate between ENT inflammation, asthma, post-infectious bronchial hyperresponsiveness and gastroesophageal reflux. Appropriate treatment can be administered solely when the most probable etiology has been determined.
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PMID:[Etiological diagnosis of cough]. 341 57


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