Barrett’s Esophagus
The condition whereby the tubular esophagus is lined with columnar epithelium rather than squamous epithelium was first described by Norman Barrett in 1950. He incorrectly believed it to be congenital in origin. It is now realized that it is an acquired abnormality, occurs in 7 to 10% of patients with GERD, and represents the end stage of the natural history of this disease. It is also distinctly different from the congenital condition in which islands of gastric fundic epithelium are found in the upper half of the esophagus when tissues are examined under laboratory microscopes.
The definition of Barrett’s esophagus (BE) has evolved consid¬erably over the past decade. Traditionally, BE was identified by the presence of columnar mucosa extending at least 3 cm into the esophagus when examined under laboratory microscopes. It is now recognized that the specialized intestinal type epithelium found in the Barren’s mucosa is the only tissue predis¬posed to malignant degeneration. Consequently, the diagnosis of BE is presently made given any length of endoscopically identi¬fiable columnar mucosa that proves on biopsy, with the use of laboratpry microscopes, to show intestinal metaplasia. While long segments of columnar mucosa without in¬testinal metaplasia do occur, they are uncommon and are probably congenital in origin.
The hallmark of intestinal metaplasia is the presence of intesti¬nal goblet cells in tissues whn viewd under the microscope. There is a high prevalence of biopsy-demonstrated intestinal metaplasia at the cardia, on the gastric side of the squamocolumnar junction, in the absence of endoscopic evidence of a columnar-lined esophagus. Evidence is accumulating that these patches of what appears to be Barren’s in the cardia have a sim¬ilar malignant potential as the longer segments, and are precursors for carcinoma of the cardia.
The long-term relief of symptoms remains the primary reason for performing antireflux surgery in patients with BE. Healing of esophageal mucosal injury and the prevention of disease progression are important secondary goals. In this regard, patients with BE are no different than the broader population of patients with gastro¬esophageal reflux. They should be considered for antireflux surgery when patient data suggest severe disease or predict the need for long-term medical management. Most patients with BE are symptomatic. Although it has been argued that some patients with BE may not have symptoms, careful history taking will reveal the presence of symptoms in most, if not all, patients.
Patients with BE have a spectrum of disease ranging from visu¬ally identifiable but short segments, to long segments of classic BE. In general however, they represent a relatively severe stage of gas¬troesophageal reflux, usually with markedly increased esophageal acid exposure, deficient LES characteristics, poor esophageal body function, and a high prevalence of duodenogastroesophageal reflux. Gastric hypersecretion occurs in 44% of patients. Most will require long-term proton pump inhibitor therapy for relief of symptoms and control of coexistent esophageal mucosal injury. Given such profound deficits in esophageal physiology, antireflux surgery is an excellent means of long-term control for most patients with BE. In years past, referral for antireflux surgery was reserved for patients with associated complications such as stricture, ulceration, or pro¬gression of the metaplastic segment. The advent of laparoscopic fundoplication and its successful control of gastroesophageal re¬flux in over 90% of patients have lowered the threshold for referral. Patients with quiescent, uncomplicated BE, particularly young patients, are now considered by many to be excellent candidates for antireflux surgery.
The typical complications in BE include ulceration in the columnar-lined segment, stricture formation, and a dysplasia-cancer sequence. Barrett’s ulceration is unlike the erosive ulceration of reflux esophagitis in that it more closely resembles peptic ulcera¬tion in the stomach or duodenum, and has the same propensity to bleed, penetrate, or perforate. The strictures found in BE occur at the columnar junction, and are typically higher than peptic stric¬tures in the absence of BE. Ulceration and stricture in association with BE were commonly reported prior to 1975, but with the advent of potent acid suppression medication they have become less comm¬on in contrast, the complication of adenocarcinoma developing in Barrett’s mucosa has become more common.
Adenocarcinoma developing in Barrett’s mucosa was considered a rare tumor prior to 1975. Today it occurs in approximately one in every 100 patient¬ years of follow-up, which represents a risk 40 times that of the general population. Most if not all cases of adenocarcinoma of the esophagus arise in Barrett’s epithelium. About one third of all patients with BE present with malignancy when tissues are examined under the microscope.
The long-term risk of progression to dysplasia and adenocarci¬noma, while not the driving force behind the decision to perform antireflux surgery, is a significant concern for both patient and physi¬cian. Although to date there have been no prospective randomized studies documenting that antireflux surgery has an effect on the risk of progression to dysplasia and carcinoma, complete control of re¬flux of gastric juice into the esophagus is clearly a desirable goal. As data accumulate regarding the relative impact of medical and surgical therapy on the natural history of Barrett’s metaplasia, the risk of progression may play a larger role in therapeutic decisions.
