Synthetic orally active angiotensin-converting enzyme (ACE) inhibitors have been successfully used in the treatment of congestive heart failure and hypertension, particularly in hypertensive subjects with increased renin-angiotensin-aldosterone-system activity. Adverse skin reactions, angioneurotic oedema and rapidly decreasing lung function in asthmatics have been reported following medication with ACE inhibitors. Furthermore, these drugs have been associated with a persistent dry cough in subjects without previous known bronchial hyper-reactivity. There is reason to believe that an ACE inhibitor-induced cough is due to an increased inflammatory state in the airways of susceptible individuals, and that this cough might thereby have pathophysiological features in common with the cough seen as an early symptom of asthma. All inflammatory responses, wheal and flare reactions, infiltration of neutrophils, eosinophils, basophils and monocytes were enhanced by ACE inhibitors. A dose-response relationship for the proinflammatory effect of the ACE inhibitor has been demonstrated.

Forty eight patients with moderate to severe asthma were enrolled in a double blind crossover study designed to evaluate the effects of ranitidine treatment, 150 mg twice daily for four weeks, on gastro-oesophageal reflux, asthma control, and bronchial reactivity. All 48 had a history of reflux symptoms and 27 had in addition reflux associated respiratory symptoms. Thirty two patients had objective evidence ofacid reflux on 24 hour pH monitoring (pH ofless than 4 for more than I % of the 24 hours) and 27 patients had a positive result in the acid perfusion test. Reflux symptoms were significantly improved after ranitidine treatment. Ranitidine treatment was associated with modest improvements in nocturnal asthma and daily use of inhaled bronchodilator drugs but there was no significant change in bronchial reactivity, lung function, peak flow, or the number of eosinophils in the blood. Comparisons between the effect of ranitidine treatment on asthma control were performed between patients with and without a history of reflux associated respiratory symptoms, with and without a positive result in the acid perfusion test, and with and without objective evidence of gastrooesophageal reflux. A history of reflux associated respiratory symptoms was the only factor that predicted an improvement in asthma control after ranitidine treatment. These results indicate that antireflux treatment will produce only small improvements in asthma control in asthmatic patients with a history of gastro-oesophageal reflux.

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