Abstract
ABSTRACT Gastroesophageal reflux (GERD) and hidden aspiration of gastric contents are probably involved in the pathogenesis and progression of idiopathic pulmonary fibrosis (IPF). The pathological mechanisms involved are decreased pulmonary distensibility and consequent increase of intrathoracic negative pressure during inspiration, as well as decreased control mechanisms of esophageal motility or lower esophageal sphincter. The prevalence of GERD and oesophageal dysmotility was higher in patients with IPF as compared with general population. Among patients with IPF, 67-76% demonstrated abnormal oesophageal acid exposure. However, no relationship was demonstrated between severity of GERD and severity of IPF. Data are scant on outcomes of antireflux treatment in patients with IPF. Actually, some data suggests that antacid treatment may be deleterious in some IPF patients. After analyzing all the relevant evidence found to date, a causal relationship between GERD, gastric content aspiration and IPF pathogenesis cannot be established. There is scant evidence examining antireflux treatment in idiopathic pulmonary fibrosis patients.
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