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1 Division of Pulmonary and Critical Care Medicine, Dept of Medicine, and 3 Gastrointestinal Motility Clinic, Dept of Surgery, University of Washington, Seattle, WA, USA. 2 Dept of Respiratory and Critical Care Medicine, Singapore General Hospital, Singapore.
CORRESPONDENCE: G. Raghu, Division of Pulmonary and Critical Care Medicine, University of Washington Medical Center, Campus Box 356522, Seattle, WA 98195, USA. Fax: 1 2065982105. E-mail: graghu{at}u.washington.edu
Keywords: Aspiration, cryptogenic fibrosing alveolitis, gastro-oesophageal reflux disease, idiopathic pulmonary fibrosis, usual interstitial pneumonia
Received: March 28, 2005
Accepted August 31, 2005
The aim of this prospective study was to determine the prevalence and characteristics of acid gastro-oesophageal reflux (GER) in patients with idiopathic pulmonary fibrosis (IPF).
Sixty-five consecutive patients with well-defined IPF were subjected to 24-h pH monitoring and oesophageal manometry. A total of 133 consecutive patients with intractable asthma and symptoms of GER were used as comparisons.
The prevalence of abnormal acid GER in IPF patients was 87%, with 76% and 63% demonstrating abnormal distal and proximal oesophageal acid exposures, respectively. Abnormal acid GER was significantly more common in IPF patients than asthma patients. Only 47% of IPF patients experienced classic GER symptoms. Despite treatment with standard doses of proton pump inhibitors (PPIs), 12 out of 19 patients receiving PPIs during the 24-h pH monitoring had abnormal oesophageal acid exposures by pH probe. There was no correlation between IPF severity and acid GER severity.
In conclusion, abnormal acid gastro-oesophageal reflux is highly prevalent, but often clinically occult in patients with idiopathic pulmonary fibrosis. Standard doses of proton pump inhibitors may not suppress the acid gastro-oesophageal reflux in this population. Therefore, further studies are needed to determine if acid abnormal gastro-oesophageal reflux represents an important risk factor for idiopathic pulmonary fibrosis development or progression, and if optimal suppression of acid gastro-oesophageal reflux slows the progression of idiopathic pulmonary fibrosis and/or decreases episodic exacerbations of idiopathic pulmonary fibrosis.
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