In a recent article Sifrim and coworkers addressed the issue of the importance of weakly acidic reflux (as measured by 24 hour ambulatory pressure and pH-impedance monitoring) in patients with chronic cough. The presence of asthma, postnasal drip, or the use of ACE inhibitors was ruled out, so that an association with gastro-oesophageal reflux was probable. They found that only 15% of cough bursts were preceded by reflux episodes, which in 4% of cases were weakly acidic and therefore not detectable by conventional automated analysis of oesophageal pH tracings. Though the temporal relationship between acid or weakly acidic reflux and cough was highly significant, it could not be demonstrated in most episodes. In this respect their findings are in agreement with a previous study by Laukka and coworkers, who also used manometry for a more accurate timing of cough. Taken together, the results of the two studies suggest that the pathogenetic mechanisms usually proposed as a link between reflux and cough (micro/macroaspiration of refluxate into airways and vagally mediated cough reflex) may be involved, at best, in a minority of cough episodes. A different explanation has therefore to be formulated, not requiring a strict temporal relationship between reflux and cough. We suggest that such explanation is represented by a low cough threshold induced by repeated reflux. We have previously demonstrated that patients with reflux oesophagitis present a tussive response to minute amounts of inhaled capsaicin. In our series, the temporal relationship between irritant inhalation and cough bursts was so reproducible and immediate that a casual association with a single reflux is unlikely. Rather, our finding strongly suggests the presence of a reduction in cough threshold, related to cumulated effect of repeated oesophageal acid exposures. These lead to nociceptor sensitisation, which has been reported to be reversible by PPI treatment. Actually, in our series of oesophagitis patients, only five days of omeprazole treatment produced a striking improvement in tussive reactivity, so that a dose of capsaicin 15-fold higher was required to elicit cough . Once this acid-driven mechanism is activated, a variety of otherwise subliminal stimuli (smoke, pollution, etc) can cause cough. For this reason, the temporal association of reflux with cough does not appear a reliable criterium to diagnose reflux-associated cough, even using state of the art methodology. Future studies will clarify whether variations in cough threshold after PPI therapy has a role for identifying among patients with cough the ones in whom the symptom is due to reflux.
Reflux associated cough is usually not associated with reflux: role of reduced cough threshold
BENINI, Luigi;FERRARI, Marcello;VANTINI, Italo
2006-01-01
Abstract
In a recent article Sifrim and coworkers addressed the issue of the importance of weakly acidic reflux (as measured by 24 hour ambulatory pressure and pH-impedance monitoring) in patients with chronic cough. The presence of asthma, postnasal drip, or the use of ACE inhibitors was ruled out, so that an association with gastro-oesophageal reflux was probable. They found that only 15% of cough bursts were preceded by reflux episodes, which in 4% of cases were weakly acidic and therefore not detectable by conventional automated analysis of oesophageal pH tracings. Though the temporal relationship between acid or weakly acidic reflux and cough was highly significant, it could not be demonstrated in most episodes. In this respect their findings are in agreement with a previous study by Laukka and coworkers, who also used manometry for a more accurate timing of cough. Taken together, the results of the two studies suggest that the pathogenetic mechanisms usually proposed as a link between reflux and cough (micro/macroaspiration of refluxate into airways and vagally mediated cough reflex) may be involved, at best, in a minority of cough episodes. A different explanation has therefore to be formulated, not requiring a strict temporal relationship between reflux and cough. We suggest that such explanation is represented by a low cough threshold induced by repeated reflux. We have previously demonstrated that patients with reflux oesophagitis present a tussive response to minute amounts of inhaled capsaicin. In our series, the temporal relationship between irritant inhalation and cough bursts was so reproducible and immediate that a casual association with a single reflux is unlikely. Rather, our finding strongly suggests the presence of a reduction in cough threshold, related to cumulated effect of repeated oesophageal acid exposures. These lead to nociceptor sensitisation, which has been reported to be reversible by PPI treatment. Actually, in our series of oesophagitis patients, only five days of omeprazole treatment produced a striking improvement in tussive reactivity, so that a dose of capsaicin 15-fold higher was required to elicit cough . Once this acid-driven mechanism is activated, a variety of otherwise subliminal stimuli (smoke, pollution, etc) can cause cough. For this reason, the temporal association of reflux with cough does not appear a reliable criterium to diagnose reflux-associated cough, even using state of the art methodology. Future studies will clarify whether variations in cough threshold after PPI therapy has a role for identifying among patients with cough the ones in whom the symptom is due to reflux.
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