The role of gastroesophageal reflux in idiopathic pulmonary fibrosis
Section snippets
Histology
Histologic features of idiopathic pulmonary fibrosis include the presence of patchy, nonuniform, and variably distributed interstitial changes at low magnification, as demonstrated by Katzenstein and Myers3 (Figure 1). Histologic variation, with alternating sections of interstitial fibrosis, inflammation, honeycomb changes, and normal lung tissue, is characteristic. Fibrosis consists of eosinophilic collagen, which thickens alveolar septa and forms patchy ridges. Honeycomb changes are
Preclinical evidence
Preclinical evidence of acid aspiration–induced lung injury dates back several decades. In 1952, investigators reported that the degree of lung tissue response (pneumonia, inflammation, fibrosis) in rabbits increased with increasing volume of instilled acid and as pH decreased from 2.5 to 1.5.4 Shortly thereafter, data were reported from a dog model displaying a chemical pneumonitis related to acid damage.5 Gastric juice was found to have rapid distribution in the lung, moving to the periphery
Clinical evidence
A Veterans Administration case-control study (N = 101,366) was conducted from 1981 to 1994, in which subjects with sinus, pharyngeal, laryngeal, and pulmonary diseases were compared with controls without esophagitis or esophageal stricture. Multivariate logistic regression analysis demonstrated that erosive esophagitis was associated with a number of respiratory diseases, including chronic bronchitis, asthma, pneumonia, and, notably, an odds ratio (OR) for pulmonary fibrosis of 1.36 (95%
Gastroesophageal reflux in patients with idiopathic pulmonary fibrosis
To investigate prospectively the possible association of GER and idiopathic pulmonary fibrosis, Tobin et al.17 studied 17 consecutive subjects with biopsy-proven idiopathic pulmonary fibrosis. Along with 8 controls with interstitial lung disease, these study subjects underwent dual-channel, ambulatory esophageal pH monitoring. Sixteen of the 17 subjects had abnormal distal and/or proximal esophageal acid exposure, compared with 4 of 8 controls (P = 0.02). Additionally, for study subjects, the
Conclusion
Evidence concerning the pulmonary implications of GER appears to be mounting. Compelling data indicate that a high percentage of patients with idiopathic pulmonary fibrosis also experience abnormal esophageal acid exposure. Additional outcomes-based studies and therapeutic trials are needed to clarify the association between, and the mechanisms of, GER and lung disease. Considering the high mortality rates associated with idiopathic pulmonary fibrosis, evolving clinical knowledge concerning
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