Does chronic microaspiration cause idiopathic pulmonary fibrosis?

Abstract

Idiopathic pulmonary fibrosis is a diffuse fibrotic lung disease of unknown etiology with no effective treatment. Emerging data support a role for chronic microaspiration (ie, subclinical aspiration of small droplets) in the pathogenesis and natural history of idiopathic pulmonary fibrosis. However, the precise relationship between chronic microaspiration and idiopathic pulmonary fibrosis remains unknown. Gastroesophageal reflux, a presumed risk factor for microaspiration, has been strongly associated with idiopathic pulmonary fibrosis with an estimated prevalence of up to 90%. This review aims to describe the relationship between chronic microaspiration and idiopathic pulmonary fibrosis by laying out the clinical and biologic rationale for this relationship and exploring the scientific evidence available. The gaps in our current understanding of the diagnosis of chronic microaspiration and idiopathic pulmonary fibrosis and the ongoing uncertainties in management and treatment will be highlighted. Defining the role of chronic microaspiration in idiopathic pulmonary fibrosis is essential as it has potential clinical, pathobiological, and treatment implications for this deadly disease.

Figure 1. Possible Pathogenetic Mechanism for Chronic Microaspiration in Idiopathic Pulmonary Fibrosis

Gastric fluid can travel in a retrograde fashion through a weakened lower esophageal sphincter (e.g. secondary to a hiatal hernia, traction from the diaphragm, or medications) up into the esophagus. The gastric refluxate can travel as high up as the cricopharyngeal region and enter the airway. Normal host defenses likely clear most gastric refluxate without clinical sequelae. However, in some cases, components of the gastric refluxate (e.g. acid, bile, particulates) may directly injure the lung epithelium. In the genetically or otherwise predisposed patient, chronic microaspiration of gastric refluxate may cause repetitive injury over time leading to granulomatous pneumonitis, dysregulated wound healing, and eventual lung fibrosis. Additionally, progressive pulmonary fibrosis may lead to distortion of the mediastinal structures and traction on the esophagus. This could cause additional weakening of the lower esophageal sphincter, which could in turn lead to microaspiration, lung injury, and the accelerated decline and/or acute respiratory decompensation seen in some patients with idiopathic pulmonary fibrosis.