-
Stay Connected
Get the latest news on exciting speakers, workshops & learning opportunities at ISDE 2021.
Subscribe for Updates
Barrett's oesophagus develops when chronic gastro-oesophageal reflux changes the squamous lining of the lower oesophagus to columnar mucosa. Intestinal metaplasia can progress through dysplasia to oesophageal adenocarcinoma, making detection before cancer important. The condition may cause no symptoms. Learn more about リウマチ性疾患の骨粗鬆症治療と骨折リスク評価の実践.
Chronic GERD is common, but gastroscopy for every reflux patient would be inefficient and carry avoidable risk. Screening for Barrett's oesophagus in patients with chronic GERD should therefore be selective, based on reflux burden and additional risk factors, and guided by patient preferences and current Australian practice.
Commonly used guidance, including ACG criteria, recommends endoscopic screening for men with GERD plus another risk factor, such as older age, obesity, smoking, family history or ancestry associated with higher prevalence. Routine screening is not advised for the general population, while evidence for women without additional risk factors is limited.
Assessment should combine persistent reflux symptoms with age, body mass index, smoking and family history. Dysphagia, odynophagia, unintentional weight loss, anaemia or gastrointestinal bleeding are not screening features; they require prompt diagnostic evaluation rather than routine surveillance.
Screening means upper gastrointestinal endoscopy with high-definition inspection and biopsy. The squamocolumnar junction should be documented, and the Seattle protocol requires targeted biopsy of visible lesions plus systematic samples from the oesophagus and gastro-oesophageal junction. Histology confirms intestinal metaplasia and checks for dysplasia.
Endoscopy usually requires preparation and sedation, with small risks of bleeding, perforation and anaesthetic complications. Where locally available, a TFF3 cytology sponge can help select patients for endoscopy, but it does not replace endoscopic assessment in many pathways.
Before referral, a clinician should confirm that symptoms represent reflux. For unproven GERD in a high-risk patient, ambulatory reflux monitoring, often off acid suppression, can document acid exposure and reflux-event association. Alarm symptoms should not be delayed for testing, and PPI response alone is less useful when reflux diagnosis is uncertain.
Medication and comorbidity review matters before sedation. For some patients with rheumatic disease, a clinical review of osteoporosis and fracture risk illustrates why steroid exposure, bone health and procedural safety may matter alongside reflux. Anticoagulants, frailty and previous anaesthetic problems should also be considered.
Patients should follow the endoscopy unit's fasting and medication instructions. Smoking cessation, weight management, smaller meals and avoiding late-night eating may ease reflux, but lifestyle changes do not replace assessment of Barrett's risk.
If no dysplasia is found, follow-up depends on segment length, previous histology and earlier examination quality. Many short segments without dysplasia are checked every few years rather than annually, while longer segments or prior dysplasia need closer surveillance. Frailty and life expectancy may justify stopping surveillance.
Low-grade dysplasia should be confirmed by a specialist gastrointestinal pathologist, often with repeat endoscopy or endoscopic resection. Confirmed short-segment Barrett's oesophagus may suit ablation after endoscopic eradication therapy. ISDE coverage of acid suppression and progression notes that PPIs control reflux and may slow progression, but they do not reliably reverse established metaplasia.
Australian referral usually begins with a GP, who assesses symptoms and risk before referring to gastroenterology. Medicare may subsidise medically referred gastroscopy through the MBS, although private procedures can involve out-of-pocket charges. PPIs are available from community chemists, with certain strengths and indications subsidised by the PBS.
Specialist endoscopy is concentrated in cities such as Melbourne, Sydney, Brisbane, Adelaide and Perth. People in regional, rural and remote areas may travel further or wait longer, so telehealth triage, local preparation and coordinated transport matter. Public waiting lists and procedure capacity also shape safe screening.
Aboriginal and Torres Strait Islander communities require equitable, culturally safe care, including local involvement, interpreter support and respect for different family and health-service experiences. Generalising risk estimates from overseas cohorts can miss local variation. Australia's high rates of obesity and smoking make individual risk assessment especially important.
Direct evidence that endoscopic screening reduces mortality remains limited. Most evidence comes from observational studies, models and cancer-detection rates, while treatment thresholds and risk scores continue to evolve. New imaging, biomarkers and less invasive sampling may improve targeting, but none removes the need for careful pathology and surveillance.
The ISDE 2021 virtual congress, held from 27 to 30 September, brought together work on reflux, metaplasia, dysplasia and endoscopic therapy. Archived sessions can help interpret new data, but presentations do not replace local guidelines, pathology review or individual consent. Future Australian research should include rural patients and communities underrepresented in screening studies.
The practical message is to avoid two extremes: missing high-risk disease and sending every reflux sufferer for gastroscopy. Focused assessment of reflux certainty, age, obesity, smoking, family history and patient goals can identify those for whom endoscopic screening is most appropriate.
What the reader should remember is that selective screening, accurate Seattle-protocol biopsy and risk-matched surveillance work together. Acid suppression alone cannot undo established Barrett's oesophagus, and dependable follow-up is essential after the result.