A recent five-year random-controlled trial has shown that photodynamic therapy using photofrin is statistically more effective in eliminating dysplastic growth areas than sole use of a proton pump inhibitor.There is presently no reliable way to determine which patients with Barretts esophagus will go on to develop esophageal cancer, although a recent study found the detection of three different genetic abnormalities was associated with as much as a 79% chance of developing cancer in six years.Endoscopic mucosal resection has also been evaluated as a management technique. Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the stomach into the esophagus.In a variety of studies, nonsteroidal anti-inflammatory drugs (NSAIDS) such as low-dose aspirin (75-300 mg/day) have shown evidence of preventing esophageal cancer in people with Barretts esophagus. Prognosis
Barretts esophagus is a premalignant condition, not a malignant one. Its malignant sequela, esophagogastric junctional adenocarcinoma, has a mortality rate of over 85%. The risk of developing esophageal adenocarcinoma in people who have Barretts esophagus has been estimated to be 6–7 per 1000 person-years, but a cohort study of 11,028 patients from Denmark published in 2011 showed an incidence of only 1.2 per 1000 person-years (5.1 per 1000 person-years in patients with dysplasia, 1.0 per 1000 person-years in patients without dysplasia).The relative risk of esophageal adenocarcinoma is about ten times higher in those with Barretts esophagus than the general population. Most patients with esophageal carcinoma survive less than one year.
The protein AGR2 is elevated in Barretts esophagus and can be used as a biomarker for distinguishing Barrett epithelium from normal esophageal epithelium.The presence of intestinal metaplasia in Barretts esophagus represents a marker for the progression of metaplasia towards dysplasia and eventually adenocarcinoma. This factor combined with two different immunohistochemical expression of p53, Her2 and p16 leads to two different genetic pathways that likely progress to dysplasia in Barretts esophagus. Also intestinal metaplastic cells can be positive for CK 7+/CK20-. Epithelial dysplasia
After the initial diagnosis of Barretts esophagus is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer:  development of epithelial dysplasia (or "intraepithelial neoplasia"). Among all metaplastic lesions, around 8% were associated with dysplasia. particularly a recent study demonstrated that dysplastic lesions were located mainly in the posterior wall of the esophagus.Considerable variability is seen in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high-grade dysplasia in Barrett be confirmed by at least two fellowship-trained GI pathologists prior to definitive treatment for patients. For more accuracy and reproducibility, it is also recommended to follow international classification systems, such as the "Vienna classification" of gastrointestinal epithelial neoplasia (2000). Management
Many people with Barretts esophagus do not have dysplasia.