Gastroesophageal Reflux in Idiopathic Pulmonary Fibrosis: More than a Gut Feeling?

(or the treatment of gastroesophageal reflux) and outcomes in IPF. Patients taking oral antiacid therapy appear to have a slower rate of decline in lung function [5] and improved survival [6] . In addition, there is evidence suggesting that gastroesophageal reflux may be an important cause of acute exacerbation [5, 7–8] . Both acid and nonacid reflux might play an important role, and in this respect, Heliobacter pylori could be an important factor [9] . In this issue of Respiration , Kreuter et al. [10] apply an interesting approach in order to shed more light on the relationship between gastroesophageal reflux, in particular nonacid reflux, and IPF. Their approach was original; they investigated whether H. pylori -containing microaspiration could be involved in IPF pathogenesis by performing PCR screening for H. pylori DNA in lung biopsy specimens of IPF patients. They were not able to demonstrate the presence of H. pylori DNA in lung biopsy tissue from IPF patients. In addition, the authors did not find a correlation between the use of corticosteroids and the presence of reflux (unfortunately, they did not investigate an effect of immunosuppressive agents such as azathioprine). In addition, they found that ex-smokers had less prevalent gastroesophageal reflux than current smokers. While there are many potential explanations for the findings of Kreuter et al. [10] that have little to do with the relationship of gastroesophageal reflux-induced miIdiopathic pulmonary fibrosis (IPF) is a destructive pulmonary disease, characterized by extensive scarring of the lung. This process leads to the loss of pulmonary function, progressive dyspnea, and finally death. For many years, IPF patients were treated with immunosuppressive agents based on the hypothesis that chronic inflammation was the pathobiological driver of disease. Such therapies have now been shown to be ineffective and possibly harmful: combination therapy with high-dose corticosteroids, azathioprine, and acetylcysteine had no impact on disease progression and resulted in higher morbidity and mortality than placebo [1] . Although two antifibrotic agents have now been developed that slow disease progression as measured by FVC decline [2, 3] , the pathogenesis of this fibroproliferative disorder is still largely unknown despite intensive research in the last decades. One of the central issues in the debate over disease pathogenesis at this moment is whether or not gastroesophageal reflux (through causing recurrent microaspiration of gastric contents) plays a role in the development and/or progression of IPF. This has become a particularly important issue as antiacid therapy has received a conditional recommendation for the treatment of IPF in the latest ATS/ERS/JRS/ALAT IPF practice guidelines [4] . Indeed, several retrospective studies have demonstrated an association between gastroesophageal reflux Published online: January 5, 2016