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Barrett�s Esophagus and Esophageal Cancer: The dark side of the acid reflux epidemic

Published Date
Author Drew Schembre, MD, FASGE, FACG

Heartburn (which was once considered an annoying result of over-eating) has matured into a full-blown medical condition better known as gastro-esophageal reflux or GERD.

GERD, or the sensation of acid or other gastric fluids washing up into the chest or mouth, affects as many as 1 in 5 adults in the US on a monthly basis with up to 6% experiencing symptoms 2 or more times per week. Estimates suggest that about 5% of those who suffer from reflux will develop a potentially pre-malignant condition called Barrett’s esophagus (BE). Named after the British thoracic surgeon who erroneously suggested the condition resulted from a congenitally short esophagus, BE is characterized by “specialized intestinal lining” replacing normal squamous epithelium (ie, wet skin, like the lining of the mouth) in the lower esophagus in response to long-term, repetitive exposure to stomach acid.

While this may seem like a protective adaptation—Barrett’s tissue will not ulcerate and develop scarring the way squamous tissue does—it is inherently unstable and can progress to cancer. The risk for developing adenocarcinoma of the esophagus for people with BE is more than 30 times greater than for people without it.

Luckily, the absolute risk of progression from BE to cancer is relatively low. BE progresses to esophageal cancer at the rate of around 0.2% per year. Further, cancer doesn’t usually develop suddenly. Instead, it progresses through a series of stages termed “dysplasia” meaning bad or unfavorable changes that can be identified on biopsies collected at endoscopy. These changes progress from:

  • Barrett’s tissue without dysplasia. This condition does not usually warrant treatment but can be followed by endoscopy every 3-5 years.
  • Low-grade dysplasia. Subtle abnormalities become apparent but progression to cancer is still slow and infrequent. This stage can be treated or followed closely.
  • High-grade dysplasia. Here progression to cancer is much more common, occurring in 5-25% of individuals each year. Treatment is highly recommended.
  • Intra-mucosal cancer. Cancer cells remain confined to the most superficial layer of the esophagus and are at very low risk for metastasizing. This can sometimes be treated without surgery at an expert center.
  • Invasive cancer where cancer cells penetrate deeper layers of the esophagus and begin to spread to lymph nodes and distant sites. At this stage, superficial treatments offer little benefit and surgery and/or chemo and radiotherapy are usually necessary.

What are the symptoms of Barrett’s esophagus?

No specific symptoms indicate the presence of Barrett’s esophagus and up to 40% of people who have the condition don’t experience classic heartburn symptoms. The condition most commonly affects middle aged white men but can affect women and members of other ethnicities as well. Obesity, smoking and family history may increase the risk not only of developing Barrett’s esophagus but also likelihood of progression to cancer.

How is Barrett’s esophagus diagnosed?

No blood tests or x-rays (even CT or MRI scans) can detect Barrett’s. Endoscopy with biopsy remains the standard method for diagnosing Barrett’s and is recommended for individuals who suffer from frequent reflux symptoms (weekly or more often) that have persisted for several years. This is a low-risk test (much like a colonoscopy without the bowel prep) but does usually require sedation. Correctly identifying dysplasia can be tricky for many pathologists and may require review by an expert. If there is any question of high-grade dysplasia or early cancer on biopsies, the slides should be sent to a center of excellence for a second opinion.

What is surveillance strategy?

If a person has undergone endoscopy and this has not demonstrated Barrett’s esophagus it is extremely unlikely that it will develop after age 30. Once Barrett’s esophagus has been detected, most experts recommend repeat endoscopy with biopsies every 3-5 years in order to detect the development of dysplasia or cancer. If dysplasia is discovered, surveillance intervals need to be shortened or definitive treatment undertaken.