Sep 18 2013
Researchers from Australia have found that the rate of gastroesophageal reflux disease (GERD) is twice as high in patients with chronic obstructive pulmonary disease (COPD) or bronchiectasis as in people without lung disease.
Furthermore, the researchers found evidence for pulmonary aspiration of gastric contents among these patients which, if confirmed in future studies, could support the hypothesis that this contributes to lung disease severity.
The study participants were 27 patients with mild or moderate COPD and 27 with moderate or severe bronchiectasis as well as 17 controls.
Ambulatory 24-hour esophageal pH monitoring showed that 37% of COPD patients and 40% of bronchiectasis patients had reflux compared with 18% of controls. All controls with GERD had asymptomatic distal reflux, while eight COPD patients had distal reflux only and two had proximal and distal reflux. In bronchiectasis, seven patients had distal reflux only, three had proximal and distal reflux, and two had proximal reflux only.
And of 48 participants from whom sputum was collected, seven with bronchiectasis and nine with COPD tested positive for pepsin in at least one sample, indicating reflux aspiration.
However, there was no significant difference in the proportion of COPD and bronchiectasis patients with pepsin detected according to the presence of GERD. Nor was there any association between pepsin detection or GERD diagnosis and spirometry results, the authors report.
Writing in Respirology, the team, led by Annemarie Lee (University of Melbourne, Victoria, Australia), says the results “confirm that proximal and distal reflux in both patient populations is not confined to those [with] advanced disease, but [is] also present in mild to moderate COPD and bronchectasis.”
And, noting that five of 12 bronchiectasis patients diagnosed with GERD had clinically silent disease, they add that the study also highlights the value of 24-hour esophageal monitoring for diagnosing GERD in these patients
Lee and colleagues also report that they had difficulty recruiting an adequate number of patients for such an invasive study, which could explain why they found no association between sputum pepsin and proximal reflux – something they suggest should be explored in future studies.
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