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Idiopathic Pulmonary Fibrosis and Gastroesophageal Reflux. Implications for Treatment

  • 2013 SSAT Plenary Presentation
  • Published:
Journal of Gastrointestinal Surgery Aims and scope

Abstract

Background

Even though the pathogenesis of idiopathic pulmonary fibrosis (IPF) is unknown, there is mounting evidence that abnormal reflux (GERD) and aspiration of gastric contents may play a role in the pathogenesis of this disease.

Aims

The aims of this study were to determine in patients with GERD and IPF: (a) the clinical presentation, (b) the esophageal function, and (c) the reflux profile.

Methods

We compared the clinical presentation, the esophageal function (as defined by high-resolution manometry), and the reflux profile (by dual sensor pH monitoring) in 80 patients with GERD (group A) and in 22 patients with GERD and IPF (group B).

Results

Heartburn was present in less than 60 % of patients with GERD and IPF. Lower esophageal sphincter pressure and peristalsis were normal in both groups, while the upper esophageal sphincter (UES) was more frequently hypotensive in IPF patients (p = 0.008). In patients with GERD and IPF, the proximal esophageal acid exposure was higher (p = 0.047) and the supine acid clearance was slower as compared with patients with GERD only (p < 0.001).

Conclusions

The results of this study show that in patients with GERD and IPF: (a) reflux is frequently silent, (b) with the exception of a weaker UES, the esophageal function is preserved, and (c) proximal reflux is more common, and in the supine position, it is coupled with a slower acid clearance. Because these factors predisposing IPF patients to the risk of aspiration, antireflux surgery should be considered early after the diagnosis of IPF and GERD is established.

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Author information

Authors and Affiliations

  1. Center for Esophageal Diseases, Department of Surgery, University of Chicago Pritzker School of Medicine, 5841 S. Maryland Ave, MC 5031, Room G-207, Chicago, IL, 60637, USA

    Marco E. Allaix, Fernando A. Herbella, Bernardo Borraez Segura & Marco G. Patti

  2. Swallowing Center and Department of Surgery, Loyola University Chicago, Stritch School of Medicine, Chicago, IL, USA

    Piero M. Fisichella

  3. Department of Medicine, University of Chicago Pritzker School of Medicine, Chicago, IL, USA

    Imre Noth

Authors
  1. Marco E. Allaix
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  2. Piero M. Fisichella
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  3. Imre Noth
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  4. Fernando A. Herbella
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  5. Bernardo Borraez Segura
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  6. Marco G. Patti
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Corresponding author

Correspondence to Marco G. Patti.

Additional information

Discussant

Dr. John Hunter (Portland, Oregon): This is a descriptive paper, demonstrating the similarities and differences in reflux pattern and esophageal function in patients with GERD and idiopathic pulmonary fibrosis (IPF). From the outset, we must be careful not to read too much into these data, as the indication for evaluation creates an intrinsic selection bias. The first sentence in the results section says that heartburn was less common in IPF patients than GERD controls. Well, of course, in GERD patients, the indication for study is most commonly heartburn, so you would expect them to report primarily typical reflux symptoms such as heartburn. In IPF, the indication for evaluation is most commonly IPF, so you would expect more pulmonary symptoms and less heartburn. If the authors want to learn whether the percentage of “silent” reflux is higher than expected in IPF patients, you would need to define a suitable control population, such as a cohort of patients with another chronic disease, such as diabetes or kidney failure, and perform pH studies on them, then determine the frequency of heartburn in the pH-positive patients. In such a control population stratified for the presence of GERD, I suspect you would find that at least 40 % denied heartburn symptoms.

So what can we learn from this paper?: While most parameters of esophageal function are not different between GERD and GERD + IPF, there appear to be differences in esophageal function between these groups. IPF patients are more likely to have lower UES pressures, more proximal reflux, especially supine, and diminished esophageal clearance of acid. As the authors point out, this is a set-up for microaspiration, one of the more plausible explanations for IPF. Two questions:

1. Your group B is GERD + IPF. As the indication for testing was IPF, I cannot help but wonder how many IPF patients referred to you proved to have normal pH studies. Said another way, what proportion of the IPF population that you screened did not have GERD, by pH criteria?

2. Are your observations a “chicken or the egg” phenomenon? Could chronic pulmonary disease, with all the physiologic consequences (greater work of breathing, tachypnea, more negative inspiratory pressures) partially or completely explain your observations? Did the IPF create the differences in observed physiology or did proximal GERD, poor clearance, and a weak UES lead to IPF?

Closing Discussant

Dr. Marco Allaix: I want to thank Dr. Hunter for his comments.

In response to his first question, abnormal reflux was found by pH monitoring in 61 % of IPF patients referred for evaluation. Interestingly, however, heartburn was experienced by some IPF patients who had a normal pH monitoring study. This observation stresses again the low sensitivity and specificity of symptoms for the diagnosis of GERD.

Is GERD causing IPF or vice versa? This is a great question, but the answer is not known. We do know however that stopping reflux in IPF patients by a fundoplication can halt the progression of the disease. We also know that stopping reflux after lung transplantation may avoid the development of the bronchiolitis obliterans syndrome (BOS).

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Allaix, M.E., Fisichella, P.M., Noth, I. et al. Idiopathic Pulmonary Fibrosis and Gastroesophageal Reflux. Implications for Treatment. J Gastrointest Surg 18, 100–105 (2014). https://doi.org/10.1007/s11605-013-2333-z

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  • DOI: https://doi.org/10.1007/s11605-013-2333-z

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