Barrett’s oesophagus: Current controversies

Abstract

Oesophageal adenocarcinoma is rapidly increasing in Western countries. This tumour frequently presents late in its course with metastatic disease and has a very poor prognosis. Barrett’s oesophagus is an acquired condition whereby the native squamous mucosa of the lower oesophagus is replaced by columnar epithelium following prolonged gastro-oesophageal reflux and is the recognised precursor lesion for oesophageal adenocarcinoma. There are multiple national and society guidelines regarding screening, surveillance and management of Barrett’s oesophagus, however all are limited regarding a clear evidence base for a well-demonstrated benefit and cost-effectiveness of surveillance, and robust risk stratification for patients to best use resources. Currently the accepted risk factors upon which surveillance intervals and interventions are based are Barrett’s segment length and histological interpretation of the systematic biopsies. Further patient risk factors including other demographic features, smoking, gender, obesity, ethnicity, patient age, biomarkers and endoscopic adjuncts remain under consideration and are discussed in full. Recent evidence has been published to support earlier endoscopic intervention by means of ablation of the metaplastic Barrett’s segment when the earliest signs of dysplasia are detected. Further work should concentrate on establishing better risk stratification and primary and secondary preventative strategies to reduce the risk of adenocarcinoma of the oesophagus.

Gastroesophageal reflux disease, Barrett esophagus, and esophageal adenocarcinoma – where do we stand?

“…Premalignant condition for EAC development is Barrett esophagus (BE), a disorder characterized by abnormal transformation of the squamous epithelium. BE is strongly associated with prolonged gastro-esophageal reflux of gastric and bile acids ( 1 , 3 , 4 ). Since patients with BE carry 30-40 times higher risk for EAC than general population, it is not surprising that in the last 10-20 years the research interest in BE has been growing ( 3 ).…”

“…People with high body mass index, especially those with high waist circumference, have increased intraabdominal pressure and decreased lower esophageal sphincter tonus. These are often accompanied by hiatal hernia and delayed gastric emptying, which increase the risk of reflux of gastric and bile acids ( 1 , 4 , 5 , 10 , 11 ). Prolonged exposure to gastric acid in GERD causes esophageal mucosa damage.…”

“…However, in obese people chronic inflammation and metaplastic changes of esophageal mucosa cells are promoted by inflammatory cytokines from the visceral fatty tissue ( 4 , 5 ). Visceral fat is metabolically active and produces a variety of cytokines that promote chronic inflammation and affect esophagogastric motor activity ( 1 , 4 , 5 , 11 ). Another factor linking obesity and GERD are hormones, namely increased estrogen activity, which is often observed in obese people.…”

“…However, endoscopic screening of all GERD patients is considered to be too expensive, as the disease prevalence is extremely high. Some authors suggest performing endoscopic screening only in high-risk GERD patients, ie, patients with longstanding reflux symptoms or obese patients ( 4 ). However, around 40% of EAC patients do not have a history of heartburn, thus surveillance will only target a portion of at-risk patients ( 4 , 12 ).…”

“…Some authors suggest performing endoscopic screening only in high-risk GERD patients, ie, patients with longstanding reflux symptoms or obese patients ( 4 ). However, around 40% of EAC patients do not have a history of heartburn, thus surveillance will only target a portion of at-risk patients ( 4 , 12 ). There is also the question whether a single upper GI endoscopic screening is enough or endoscopy should be repeated ( 1 , 4 , 12 ).…”