Barrett’s and Cancer
Barrett’s Esophagus is a condition in which the glossy, pale pink tissue that lines the esophagus is replaced with salmon-red intestinal tissue due to chronic injury from acid reflux (metaplasia). (1) (2) (3) (4) (5) (6)
This process usually occurs right above the gastric folds, where the stomach ends and the esophagus and stomach meet and is thought to serve as a protective mechanism to make the esophagus more resistant to acid damage. (4) Stretches of Barrett’s 3 cm or longer is called long-segment Barrett’s. Stretches shorter than 3cm is referred to as short segment Barrett’s. (7)
Barrett’s Esophagus is precancerous and can lead to esophageal adenocarcinoma, one of the fastest growing cancers in the US and Western world. (8)
Though patients with Barrett’s Esophagus are at least 10-30 times more likely to develop esophageal cancer than the general population, the annual incidence of BE progressing to esophageal cancer is only about .3-.6%. (3) (8) (9)
A study reported only 10% of BE patients were likely to develop esophageal adenocarcinoma in a 5 year period. (10) Patients with mutated cell growth known as dysplasia have a higher risk (13.4%) of developing esophageal cancer and should be monitored closely. (11)
About 25-40% of BE patients are diagnosed with low-grade dysplasia during follow up. (6) Patients with high-grade dysplasia (HGD) have around a 7% risk of developing cancer every year, making it likely that a 50-year-old with HGD will develop cancer in the next 10 years of his/her life. (12)
High-risk groups for BE include men with over 5 years of chronic GERD/LPR, men over 50 years old, Caucasian race, obesity, smoking, and family history of cancer. (13) Long segment Barrett’s also carries a higher risk for cancer. Barrett’s esophagus has skyrocketed by at least 159% since the 90s. Though there have been significant technological advances that have given us some understanding of BE, the cause, and prevention of the condition is not fully understood. Research has shown that most people with Barrett’s Esophagus are undetected and have no symptoms of GERD/LPR. (7)
BE is first diagnosed by visually inspecting the esophagus with a high definition white-light endoscope. If abnormal tissue is spotted during inspection and Barrett’s is suspected a small sample is dissected with forceps and sent to a pathologist for analysis and confirmation. (13)
A sample can come back as dysplasia-positive, dysplasia-negative, indefinite dysplasia, or either low grade or high-grade dysplasia. (8) Several medical societies recommend regular endoscopic monitoring for patients with Barrett’s esophagus to detect dysplasia or esophageal cancer. (13)
If dysplasia is absent in the initial screening, the American College of Gastroenterology recommends endoscopy checkups every 3 years. (3) Patients with low-grade dysplasia should have annual screenings and patients with untreated high-grade dysplasia should be screened every 3 months. (3)
Barrett’s Esophagus is treated with PPI therapy and endoscopic surgery. PPIs treat Barrett’s esophagus long-term by limiting acid production and allowing the esophagus to heal. (5) This decreases the chances of Barrett’s Esophagus advancing and can lead to partial regression. (5)
Radiofrequency ablation is currently the most common procedure used to flat Barrett’s Esophagus lesions. This procedure applies radiofrequency energy with a 3cm endoscopic balloon to the surface of the esophagus in order to burn off lesions. Dead Barrett’s tissue is scraped off after the first radiofrequency treatment and the procedure is repeated one more time. If the esophagus is allowed to heal in an acid-free environment, normal esophageal tissue can regrow.
Radiofrequency ablation is useful for treating all stages of Barrett’s but is most effective treating BE patients with high grade or low-grade dysplasia. (12) Patients successfully treated with surgery for early esophageal cancer nodules are also recommended to undergo radiofrequency ablation for complete eradication of Barrett’s tissue. (5)
Radiofrequency ablation has been reported to remove all Barrett’s tissue 79-95% of the time and virtually all dysplasia 90-100% of the time. (7) Following radiofrequency ablation anti-reflux medication is usually prescribed to prevent Barrett’s tissue from growing back. Endoscopic surveillance is also required after ablation to monitor progress. (13)
For raised lesions or bumps, endoscopic resection is performed. Endoscopic resection is done with a tubular tool with a needle attached at the end. This tool is passed endoscopically through the mouth and works by cutting the Barrett’s nodules from the esophagus and tying it up with a lasso-like device.
Then, the nodule is either cut off or sucked up into the device for disposal. A benefit endoscopic resections have over radiofrequency ablations is that resections remove deeper segments of esophageal tissue so there is more confidence that all abnormal tissue is removed.
Radiofrequency ablation only applies treatment to the esophageal lining so deeper residual Barrett’s tissue may be missed. (12)
For more advanced cases of Barrett’s Esophagus with infiltration of HGD or cancer in the submucosal layer, an esophagectomy may be performed. (14) An esophagectomy removes portions of the esophagus that are affected with Barett’s or dysplasia and then connects what’s left with the upper esophagus.
This procedure was performed more often in the 1950s for most cases of Barrett’s but has since fallen out of favor due to the high morbidity and mortality of esophagectomies and the invention of newer, safer devices. (6)
Photodynamic Therapy and Cryotherapy
Other types of Barrett’s procedures less commonly used are photodynamic therapy and cryotherapy ablation. Photodynamic therapy is done by giving light sensitive cell-killing drugs to the patient and passing an endoscopic red light to the Barrett’s Esophagus site.
As the red light is applied to the site, the drug in the patient is activated and destroys Barrett’s cells. Cryotherapy ablation sprays Barrett’s Esophagus with liquid nitrogen to freeze the selected site and destroy abnormal cells. (7)
Undetected Barrett’s Esophagus with dysplasia, especially high-grade dysplasia, is likely to develop into esophageal adenocarcinoma. Esophageal adenocarcinoma is the final stage of Barrett’s Esophagus and is one of the fastest growing of all cancers despite the wide availability of PPIs and international treatment guidelines in the West and in developed countries. (3) (10) (13) (15)
Early esophageal cancer is often symptomless and many patients aren’t diagnosed until the disease is at an advanced stage. (13) A common symptom is trouble swallowing food and eventually difficulty swallowing liquids. Treatment for EA is endoscopic resection for early EA and esophagectomy for advanced EA.
The cause of EA is currently unclear but obesity and GERD are believed to play a role. (13) The disease is somewhat mysterious, as more than 40% of esophageal cancer patients have no history of typical GERD symptoms. The five-year survival rate of EA patients is 18%. (13)