Barrett's Esophagus: Upper Digestive Tract Disorder
Barrett's esophagus occurs when cells in the lining of the esophagus, also known as the esophageal mucosa, are replaced by cells that are more resistant to acid, a process called metaplasia.
Causes of Barrett's esophagus
Normally, the esophageal mucosa is lined with multiple layers of flattened, scale-like cells. When these cells are damaged by gastric acid in individuals with gastroesophageal reflux, they are replaced with a single layer of cells that are similar to those that line the stomach and small intestine. A 2008 study suggests that eating a diet high in meat, fast-food, soft drinks, alcohol, and coffee may contribute to the risk of Barrett's esophagus.
Symptoms and diagnosis of Barrett's esophagus
Typically, Barrett's esophagus causes no symptoms, but it should be suspected in people with chronic GERD. An upper endoscopy (either traditional or via an esophageal capsule) is used to diagnose Barrett's esophagus. If the condition is present, the doctor will see tongue-like protrusions above the gastroesophageal junction.
Samples of tissue (called biopsy samples) are taken from these projections and examined under the microscope to look for precancerous changes called dysplasia.
Treatment of Barrett's esophagus
Barrett's esophagus increases the risk of esophageal cancer. In fact, about 0.5% of people with Barrett's esophagus develop cancer of the esophagus each year. To reduce the risk, it's important to control GERD and undergo an upper endoscopy and a biopsy of the esophageal mucosa every three to five years.
If biopsies indicate severe dysplasia or esophageal cancer, surgery is usually performed. Most of the esophagus is removed and the stomach is pulled up into the chest cavity and attached to what remains of the esophagus.
However, new guidelines suggest that an alternative to surgery may be endoscopy mucosal resection. This procedure can be used to remove any nodules or small polyps that are seen during a traditional endoscopy.
The doctor injects a solution into the nodule that forms a blister under it and decreases bleeding. The nodule is then lifted up while a wire loop cauterizes it from underneath and removes it.
A less invasive option is photodynamic therapy, a relatively new treatment that uses a light-sensitizing agent (such as Photofrin) plus a laser to kill sensitized cancerous and precancerous cells. The light-sensitizing agent is injected into a vein. When the agent is exposed to the laser, it produces a chemical reaction that destroys the cancerous and precancerous cells.
In a recent study, individuals who underwent photodynamic therapy were more likely to have a complete reversal of their dysplasia than people who did not receive the therapy. Two years after treatment with Photofrin, only 20 percent of these patients had cancer compared with 50 percent of those who did not receive the therapy.
The risks of photodynamic therapy include esophageal strictures and temporary sensitivity to the sun.
Two new ablation therapieswhich use heat or radiofrequency energy to destroy the abnormal cells on the esophageal wallsshowed promise in a 2006 clinical trial. About 70 percent of participants who had radiofrequency ablation or argon plasma coagulation benefited, but these procedures are still considered experimental.