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Barrett's esophagus was first described in 1950 from Norman Barrett, who reported a case of chronic peptic gathering in the lower esophagus that was defended by epithelium. (1) Barrett's esophagus can be defined simply as columnar metaplasia of the esophagus. Patients who have columnar epithelium that measures 3 cm or more from the gastroesophageal junction are said to have traditional, or "long-segment" Barrett's esophagus, while patients with a measure les than 3 cm have "short-segment" Barrett's esophagus. (2) In 1998 the American corporation of Gastroenterology (ACG) defined Barrett's esophagus as "a change in the esophageal epithelium of any fulness that can be recognized at endoscopy and is confirmed to have intestinal metaplasia by way of biopsy of the tubular esophagus and excepts intestinal metaplasia of the cardia." (3)

Gastroesophageal ebb disease (GERD) is a condition commonly evaluated and managed in the primary care setting. overlooks suggest that approximately 20 percent of U adults have symptoms of GERD at least formerly a week. (4) A subgroup of patients with GERD bring to maturity severe complications that include erosive esophagitis, stricture formation, Barrett's esophagus, and adenocarcinoma of the esophagus. Because Barrett's esophagus is meditation to be associated with the disclosure of adenocarcinoma, it is imperative that primary care physicians be familiar with Barrett's esophagus, its association with GERD and its diagnosis and management.

The overall prevalence of Barrett's esophagus in the general population is difficult to estimate, because approximately 25 percent of bodys with Barrett's esophagus have no symptoms of ebb (5) It is known, however, that the incidence of adenocarcinoma of the esophagus has risen sharply in the past not many decades. The results of individual study (6) note that the incidence of adenocarcinoma in white men has increased by the agency of more than 350 percent since the mid-1970s. Identification of patients at risk for adenocarcinoma of the esophagus is fairly poor. In fact, alone 5 percent of patients who had resection of esophageal adenocarcinoma were known to have Barrett's esophagus before the resection, highlighting the fact that passing from hand to hand screening techniques are relatively ineffective. (7) Perhaps on increasing awareness of Barrett's esophagus, we can better target screening of high-risk patients.

Pathophysiology and Diagnosis

Progression from GERD to adenocarcinoma is conception to follow a stepwise proces It is believed that in all senses of the esophageal epithelium to acid damages the lining, causing chronic esophagitis. The damaged area then heals in a metaplastic proces in which abnormal columnar confined apartments replace squamous cells. This abnormal intestinal columnar epithelium, which is called specialized intestinal metaplasia, can then progres to dysplasia, ultimately leading to carcinoma (8) (Figure 1) The incidence of Barrett's esophagus progressing to adenocarcinoma is estimated to be 05 by 100 patient-years (i.e., one in 200 patients developing carcinoma through year). (9)

[FIGURE 1 OMITTED]

Barrett's esophagus is diagnosed on endoscopy and histology. The line at which the columnar epithelium transitions to the squamous epithelium (i.e., the squamocolumnar junction) is known as the Z-line. Normally, the Z-line corresponds to the gastroesophageal junction. In patients with Barrett's esophagus, the columnar epithelium lengthen outs proximally up the esophagus (Figure 2) As mentioned previously, long-segment Barrett's esophagus measures 3 cm or more from the gastroesophageal junction, while short-segment Barrett's esophagus is les than 3 cm from the gastroesophageal junction. It is unknown whether the natural course or pathogenesis varies between these brace entities or whether short-segment Barrett's esophagus progresse to long-segment disease. It makes faculty of perception that more metaplasia would predispose to more cancer, and the same study (10) has shown this to be the case. However, in every one's mouth guidelines recommend managing long- and short-segment Barrett's esophagus in the same manner. (3)

[FIGURE 2 OMITTED]

Screening

Given the high prevalence of GERD it is physically and financially impossible to veil all patients with GERD symptoms for the unravelling of Barrett's metaplasia. Obviously, patients with alarm symptoms as it is as dysphagia, odynophagia, bleeding, or weight los should be referr promptly for endoscopy. In patients without alarm symptoms, screening guidelines for Barrett's esophagus are somewhat problematic. Symptoms of GERD are usually the reason a patient is referr for evaluation for Barrett's esophagus nevertheless as previously mentioned, many patients are asymptomatic. (5)

generally there is little evidence that screening for Barrett's esophagus decreases the rate of mortality from adenocarcinoma. (11) Several possible reasons for this finding include the older age of patients being studied and the relatively subdued absolute risk of adenocarcinoma of the esophagus. rife studies lack adequate power to display statistical significance. Nevertheless, the ACG states that "patients with chronic GERD symptoms are those greatest in number likely to have Barrett's esophagus and should bear upper endoscopy." (3) With this general guideline in mind, other components of the risk assessment for Barrett's esophagus and esophageal adenocarcinoma may be considered (Table 1) For instance, symptom severity alone is not an accurate marker; however, patients with a protracted history of reflux are at greater risk. Patients who had symptoms of GERD more than three times through week for more than 20 years have a 40-fold increased risk of developing adenocarcinoma. (12)