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      Barrett’s esophagus: Incidence, etiology, pathophysiology, prevention and treatment

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          Abstract

          Barrett’s esophagus is a metaplastic alteration of the normal esophageal epithelium that is detected on endoscopic examination and pathologically confirmed by the presence of intestinal metaplasia on biopsy. Its major significance is as a predisposing factor for esophageal adenocarcinoma, which carries a high mortality rate and a rapidly growing incidence in the United States. Detection of Barrett’s esophagus allows for endoscopic surveillance in order to detect the potential development of dysplasia and early cancer before symptoms develop, and thereby significantly increases treatment options and may lower mortality from esophageal adenocarcinoma. Much current work in the field is aimed at reducing the risk of progression from Barrett’s esophagus to cancer, and in the identification of biomarkers that may predict progression towards cancer. Barrett’s esophagus is present in 10%–20% of patients with gastroesophageal reflux disease (GERD) and has also been detected in patients who deny classic GERD symptoms and are undergoing endoscopy for other indications. We used an evidence-based approach to describe treatment options for patients with Barrett’s esophagus.

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          Changing patterns in the incidence of esophageal and gastric carcinoma in the United States.

          Incidence rates for esophageal adenocarcinoma previously were reported to be increasing rapidly, especially among white males. Rates for gastric cardia adenocarcinoma also were observed to be rising, although less rapidly. In this article, the authors update the incidence trends through 1994 and further consider the trends by age group. Surveillance, Epidemiology, and End Results (SEER) program data were used to calculate age-adjusted incidence rates for esophageal carcinoma by histologic type and gastric adenocarcinoma by anatomic subsite. Among white males, the incidence of adenocarcinoma of the esophagus rose > 350% since the mid-1970s, surpassing squamous cell carcinoma around 1990. Rates also rose among black males, but remained at much lower levels. To a lesser extent, there were continuing increases in gastric cardia adenocarcinoma among white and black males, which nearly equaled the rates for noncardia tumors of the stomach in white men. The upward trend for both tumors was much greater among older than younger men. Although the incidence also rose among females, rates remained much lower than among males. Previously reported increases of esophageal adenocarcinoma are continuing, most notably among white males. Cigarette smoking may contribute to the trend through an early stage carcinogenic effect, along with obesity, which may increase intraabdominal pressure and predispose to gastroesophageal reflux disease. Further research into esophageal and gastric cardia adenocarcinoma is needed to clarify the risk factors and mechanisms responsible for the upward trends as well as the racial and gender disparities in incidence.
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            Epidemiologic trends in esophageal and gastric cancer in the United States.

            Use of tobacco, moderate to heavy alcohol ingestion, infrequent consumption of raw fruits and vegetables, and low income accounted for more [figure: see text] than 98% of the SCE rates among both African American and white men and for 99% of the excess incidence among African Americans compared to whites in a case-control study in three areas of the United States [14]. Thus, it is likely that declines in the prevalence of smoking and drinking, especially among men, and increased intake of fresh fruits and vegetables may have contributed to the downward incidence and mortality rate trends reported for SCE. In addition, it seems plausible that obesity, GERD, and possibly reductions in H. pylori prevalence have contributed to the upward trends in ACE rates. Reductions in smoking, improved diet, and reductions in H. pylori prevalence probably have contributed to the consistent reductions observed for NGA. Contributing factors are less clear for the rising incidence rates of GCA during the 1970s and 1980s. These incidence rates have not continued to rise in recent years.
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              Observer variation in the diagnosis of dysplasia in Barrett's esophagus.

              The potential value of biopsy surveillance of patients with Barrett's esophagus for dysplasia is diminished by a lack of agreement on the diagnostic criteria for dysplasia. In a preliminary consensus conference, experienced gastrointestinal pathologists from four medical centers agreed on criteria for a five-tiered histologic classification of dysplasia in Barrett's esophagus--negative for dysplasia, indefinite for dysplasia, low-grade dysplasia, high-grade dysplasia, and intramucosal carcinoma. Eight morphologists in the four centers tested the criteria for interobserver agreement by examining a set of coded slides that had been chosen to include some especially difficult interpretative problems in all five histologic classifications. Interobserver agreement of 85 and 87% was achieved in successive reviews when the combined group of high-grade dysplasia and intramucosal carcinoma was compared with the combined group of low-grade dysplasia, indefinite for dysplasia, and negative for dysplasia. Comparison of other groups yielded less agreement. For example, negative for dysplasia could be distinguished from all other diagnoses with an interobserver agreement of 72%. We conclude that experienced gastrointestinal morphologists can diagnose high-grade dysplasia and intramucosal carcinoma with a high degree of agreement and thus can detect those patients who may need immediate rebiopsy or esophageal resection. Either further refinement of histologic criteria or alternate diagnostic methods will be needed to achieve the reproducible diagnosis of indefinite changes and low-grade dysplasia. This is important because patients with such changes theoretically merit closer endoscopic surveillance.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                December 2007
                December 2007
                : 3
                : 6
                : 1035-1145
                Affiliations
                [1 ]Department of Internal Medicine Stanford University School of Medicine, Stanford, California
                [2 ]Division of Gastroenterology and Hepatology, Stanford University School of Medicine Stanford, California
                Author notes
                Correspondence: Lauren B Gerson A149, Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California, 300 Pasteur Dr, Stanford, CA 94305, USA Tel +1 650 723 1380 Fax +1 650 725 8418 Email lgerson@ 123456stanford.edu
                Article
                2387291
                18516262
                © 2007 Dove Medical Press Limited. All rights reserved
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