Sanjeev Slehria, MD, Prateek Sharma, MD

Disclosures

Curr Opin Gastroenterol. 2003;19(4) 

In This Article

Epidemiology and Pathogenesis

One third of the general population may experience reflux symptoms, yet only a small fraction of patients with gastroesophageal reflux disease (GERD) have Barrett esophagus. Avidan et al.[5] recruited outpatients from the gastroenterology clinic who underwent upper gastrointestinal endoscopy, esophageal manometry, and 24-hour esophageal pH monitoring. A total of 256 case subjects with endoscopically and histologically proven Barrett esophagus were compared with a control group of 229 subjects with nonerosive reflux disease. As compared with patients with nonerosive reflux disease, Barrett esophagus was strongly associated with more reflux episodes and occurred more frequently among subjects with hiatus hernia and those who consumed large amounts of alcohol or cigarettes. Moreover, frequent reflux episodes, hiatus hernia, smoking, and alcohol consumption were also risk factors for an increased length of Barrett mucosa. Total esophageal mucosal acid contact time at pH less than 4 was a significant risk factor for an increased length but not the presence of Barrett esophagus. Intake of aspirin or nonsteroidal anti-inflammatory drugs was similar in patients with and without Barrett esophagus. In summary, patients with Barrett esophagus were characterized by the presence of risk factors usually indicative of severe types of GERD.

Are younger patients with Barrett esophagus different from those older than 50 years of age? This study examined 136 Barrett esophagus patients from Scotland and 50 male and 51 female Barrett esophagus patients from Southern England, matched for sex, age, and year of diagnosis with patients with uncomplicated reflux esophagitis.[6] There were no differences in smoking or alcohol drinking habits between patients younger and older than 50 years of age. However, in patients younger than 50 years, 31% of men and 71% of women had a body mass index greater than 30 (obese) vs 11% and 13%, respectively, for the general population. In those older than age 50, 14% of men and 19% of women had a body mass index greater than 30. Therefore obesity may be a risk factor for Barrett esophagus in young patients only.

A familial predisposition to Barrett esophagus and esophageal adenocarcinoma has been reported, but large case-control studies are lacking. In a recent study, a structured questionnaire on GERD symptoms and family history was administered to patients with Barrett esophagus, esophageal adenocarcinoma, or gastroesophageal junction adenocarcinoma and control subjects.[7] The presence of a family history (either a first- or second-degree relative with Barrett esophagus, esophageal adenocarcinoma, or gastroesophageal junction adenocarcinoma) was significantly higher among case subjects compared with controls (24% vs 5%; P < 0.005).

The exact reason for development of high-grade dysplasia (HGD) or esophageal adenocarcinoma in patients with Barrett esophagus is not well understood. To characterize risk factors for the development of HGD or esophageal adenocarcinoma, 2,170 patients without GERD, 1,189 patients with Barrett esophagus without dysplasia, and 131 patients with HGD/cancer were evaluated.[8*] The patients with HGD/cancer were significantly older (P = 0.011) and of white ethnicity, 89% vs 75% in non-GERD vs 83% in Barrett esophagus with dysplasia (P = 0.006). In addition, HGD/cancer patients had longer segments of Barrett compared with controls. Smoking and alcohol consumption were not significant between the various groups. It has been recently demonstrated that the cytokine milieu in Barrett esophagus is distinct compared with esophagitis and uninflamed normal esophageal squamous mucosa. In Barrett esophagus, the inflammatory profile is characterized by a relative increase in the T-helper 2 type cytokines interleukin-4 and -10. In 50 patients with LSBE, inflammation was maximal at the proximally displaced squamocolumnar junction characterized by a greater than twofold increase in proinflammatory interleukin-8 and interleukin- expression.[9] It may be possible that specific cytokine responses contribute to the localization of inflammatory and malignant complications within Barrett esophagus.

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