Speaker's Highlight

• Don Sin University of British Columbia, St. Paul Hospital (Canada)
  Kenneth R. Chapman Toronto General Hospital Research Institute (Canada)
• Parameswaran Nair McMaster University (Canada)
  Carolyn Calfee UCSF (U.S.A.)
• Gregory P. Downey University of Colorado School of Medicine (U.S.A.)
  David A. Schwartz University of Colorado School of Medicine (U.S.A.)
• Neil Schluger Tuberculosis Control Branch, California Department of Public Health (U.S.A.)
  Nick Kim Critical Care & Sleep Medicine, University of California San Diego (U.S.A.)
• Nicola Hananiah Baylor College of Medicine (U.S.A.)
  Jae-Joon Yim Seoul National University College of Medicine (Republic of Korea)
• Koichiro Asano Tokai University School of Medicine (Japan)
  Diahn-Warng Perng Taipei Veterans General Hospital (Taiwan)
• Konstantinos Kostikas University of Ioannina (Greece)
  Karin Klooster University Medical Center Groningen (Kingdom of the Netherlands)

• Gastroesophageal reflux in idiopathic pulmonary fibrosis: a review

  For decades, respiratory physicians have observed that many people with idiopathic pulmonary fibrosis (IPF) also describe heartburn, throat clearing, or a chronic nocturnal cough. Outpatient clinics in Sydney and Melbourne now routinely screen for gastroesophageal reflux disease (GORD) at the time of IPF diagnosis, and the Lung Foundation Australia lists it as a comorbidity worth attention. Whether reflux drives fibrosis or simply travels alongside it remains debated.

  The practical message is that reflux is potentially modifiable, even if scarring is not. Treating it may ease cough, reduce exacerbations, and improve quality of life. Australian guidance is pragmatic, with tailored treatment preferred to blanket prescribing.

  What idiopathic pulmonary fibrosis looks like

  IPF is a chronic, progressive interstitial lung disease characterised by scarring of the lung parenchyma without an identifiable trigger. High-resolution computed tomography typically shows honeycombing, traction bronchiectasis, and a usual interstitial pneumonia pattern. Australian registry data report a median age at presentation in the late sixties and a male predominance, although women are not uncommonly affected.

  Breathlessness on exertion and a dry, persistent cough are usually the first symptoms that prompt review. Lung function declines gradually, and many patients eventually need ambulatory or home oxygen. Median survival without disease-modifying treatment is in the range of three to five years from diagnosis, although individual outcomes vary considerably.

  The condition behaves differently from chronic obstructive pulmonary disease or asthma. Cigarette smoking is a recognised risk factor, but the disease is not driven by smoking alone. Ageing, genetic susceptibility, and recurrent epithelial injury all contribute. Reflux sits within that injury hypothesis.

  How reflux may influence fibrotic lung disease

  The leading mechanistic theory is microaspiration. Small volumes of gastric content rise beyond the upper oesophageal sphincter and reach the larynx and lower airways, exposing delicate alveolar tissue to acid, pepsin, and bile. Repeated injury is thought to drive abnormal wound repair and fibroblast activation, producing the scar that characterises IPF.

  A second pathway involves vagal reflexes. Acid in the distal oesophagus can trigger cough and airway irritation through shared neural pathways, even without frank aspiration. This may partly explain the chronic cough that troubles so many people with fibrotic lung disease. Both pathways are biologically plausible, and most patients probably have elements of both.

  A hiatus hernia worsens the picture by displacing the lower oesophageal sphincter from the diaphragmatic crura. Obesity, ageing, and some medications also predispose to reflux. Because these factors are common in the demographic typical of IPF, screening at diagnosis makes sense.

  Diagnostic pathways for reflux in IPF

  Assessment usually begins with a careful history. Heartburn, acid brash, hoarseness, throat clearing, and cough that worsens after meals or on lying down are all suggestive. In fibrotic lung disease, classical heartburn is sometimes absent, and atypical symptoms such as chronic cough or throat irritation may dominate.

  Objective testing is reserved for cases where the diagnosis is uncertain or surgery is being considered. Common investigations include:

  • 24-hour oesophageal pH monitoring, which quantifies acid exposure in the distal oesophagus
  • High-resolution oesophageal manometry, which assesses motility and lower sphincter function
  • Upper endoscopy, which detects erosive oesophagitis, Barrett's oesophagus, or hiatus hernia
  • Sputum or exhaled breath pepsin testing, an emerging research tool for identifying those who aspirate

  In Australian tertiary centres such as Royal Prince Alfred Hospital in Sydney or Royal Adelaide Hospital, these tests are coordinated between respiratory and gastroenterology teams. Access is more limited in remote regions, where telehealth and selective referral play a larger role.

  Treatment considerations and current evidence

  Antacid therapy with proton pump inhibitors is the most commonly prescribed treatment. Observational studies have suggested slower decline in lung function among IPF patients taking PPIs, although randomised trials have not confirmed a definitive mortality benefit. H2 receptor antagonists are sometimes used as an alternative or for night-time breakthrough symptoms.

  Antifibrotic therapy with nintedanib or pirfenidone remains the cornerstone of disease-modifying treatment for IPF. Both are listed on the Australian Pharmaceutical Benefits Scheme, which makes them accessible at subsidised cost to eligible patients. Gastrointestinal side effects such as diarrhoea and nausea are common, and clinicians typically separate dosing from meals and coordinate PPI use to improve tolerability.

  Laparoscopic fundoplication is considered when reflux is refractory to medication or when objective testing confirms ongoing acid exposure. Evidence in IPF comes mainly from small case series, and surgery is not undertaken lightly given anaesthetic risk. Decisions are made by a multidisciplinary team that often includes thoracic surgeons, respiratory physicians, and dietitians.

  Therapy	Primary purpose	Evidence in IPF	Main limitation
  Proton pump inhibitors	Reduce gastric acid	Observational benefit on FVC decline	Mixed randomised evidence
  H2 receptor antagonists	Reduce gastric acid	Limited specific data	Less effective than PPIs
  Laparoscopic fundoplication	Mechanical reflux control	Small case series support	Surgical and anaesthetic risk
  Antifibrotics (nintedanib, pirfenidone)	Slow fibrosis progression	Strong randomised evidence	Do not directly treat reflux

  Living with reflux and IPF in daily life

  Day-to-day management begins with simple measures that often help. Elevating the head of the bed, avoiding late meals, and weight reduction where appropriate can all reduce reflux episodes. Smaller, more frequent meals are usually better tolerated than large, rich ones, especially for patients already coping with reduced appetite from antifibrotic therapy.

  Bushfire smoke is an additional respiratory burden during Australian summers. During poor air quality in Sydney, Melbourne, or regional NSW, patients are advised to stay indoors, use protective masks, and monitor air quality indices. Avoiding additional airway irritants alongside managing reflux helps protect already scarred lungs.

  Topics worth raising at the next clinic visit include:

  • Whether current symptoms warrant objective reflux testing
  • Whether PPI therapy is still needed, or whether the dose can be reviewed
  • Whether dietary changes are reducing cough or exacerbations
  • How to coordinate reflux treatment alongside other medications

  Australian healthcare context and access

  Specialist IPF care in Australia is concentrated in tertiary centres such as The Alfred in Melbourne, Royal Prince Alfred in Sydney, and Royal Adelaide Hospital. Multidisciplinary interstitial lung disease clinics unite respiratory physicians, rheumatologists, radiologists, and pathologists. Waiting times vary, and patients in rural or remote regions may rely on outreach clinics or telehealth for follow-up.

  Aboriginal and Torres Strait Islander peoples face higher rates of chronic respiratory disease and additional barriers to specialist care. The Australian Institute of Health and Welfare has documented persistent gaps in respiratory outcomes. Culturally safe services are gradually expanding, but many patients still rely on outreach or telehealth for specialist review.

  Future directions and ongoing research

  Research is increasingly focused on identifying which IPF patients are most likely to benefit from reflux treatment. Sputum pepsin, exhaled breath biomarkers, and advanced oesophageal impedance are being studied as tools to detect occult aspiration. Personalised approaches may eventually replace today's pragmatic prescribing.

  Several clinical trials are evaluating PPIs and fundoplication in carefully selected IPF populations. Australian investigators are contributing to international registries and collaborative studies, helping to define the relationship between reflux, ageing, and fibrosis. The hope is that future guidelines will allow treatment to be matched to the patient most likely to benefit.

  For patients and clinicians today, the most useful step is to take reflux symptoms seriously at the time of IPF diagnosis, assess them with a structured history, and treat them pragmatically with lifestyle measures and, where appropriate, antacid therapy alongside disease-modifying antifibrotics.

  Richard Russell Nuffield Department of Clinical Medicine, University of Oxford (United Kingdom)
• Mona Bafadhel King’s College London (United Kingdom)
  David Jackson Guy’s and St Thomas’ Hospital, King’s College London (United Kingdom)
• James Chalmers University of Dundee (United Kingdom)
  David Price University of Aberdeen (United Kingdom)