Author(s): Raghu G
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Abstract Fibroblast foci are indicative of idiopathic pulmonary fibrosis and appear to be a cellular attempt to repair the damaged alveolus. Although this progressive, often fatal, clinical syndrome is thought to be dependent on alveolar injury of unknown origin, significant clinical and preclinical evidence points to gastric acid as a causative harmful agent. Graded instillation of various forms of acid in several animal models resulted in aspiration-induced lung injury, including pulmonary fibrosis in pigs. Moreover, compelling clinical data suggest that a high percentage of patients with idiopathic pulmonary fibrosis also experience abnormal esophageal acid exposure, without necessarily experiencing the typical symptoms of gastroesophageal reflux disease (GERD). Aggressive, long-term therapeutic trials of patients with GERD and evaluation of the therapeutic effects on pulmonary disease will allow determination of the real influences of abnormal esophageal acid exposure in the development of idiopathic pulmonary fibrosis.
This article was published in Am J Med
and referenced in Journal of Clinical & Cellular Immunology