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      Therapeutics and Clinical Risk Management (submit here)

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


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          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.

          Most cited references97

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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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            Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma.

            The causes of adenocarcinomas of the esophagus and gastric cardia are poorly understood. We conducted an epidemiologic investigation of the possible association between gastroesophageal reflux and these tumors. We performed a nationwide, population-based, case-control study in Sweden. Case ascertainment was rapid, and all cases were classified uniformly. Information on the subjects' history of gastroesophageal reflux was collected in personal interviews. The odds ratios were calculated by logistic regression, with multivariate adjustment for potentially confounding variables. Of the patients interviewed, the 189 with esophageal adenocarcinoma and the 262 with adenocarcinoma of the cardia constituted 85 percent of the 529 patients in Sweden who were eligible for the study during the period from 1995 through 1997. For comparison, we interviewed 820 control subjects from the general population and 167 patients with esophageal squamous-cell carcinoma. Among persons with recurrent symptoms of reflux, as compared with persons without such symptoms, the odds ratios were 7.7 (95 percent confidence interval, 5.3 to 11.4) for esophageal adenocarcinoma and 2.0 (95 percent confidence interval, 1.4 to 2.9) for adenocarcinoma of the cardia. The more frequent, more severe, and longer-lasting the symptoms of reflux, the greater the risk. Among persons with long-standing and severe symptoms of reflux, the odds ratios were 43.5 (95 percent confidence interval, 18.3 to 103.5) for esophageal adenocarcinoma and 4.4 (95 percent confidence interval, 1.7 to 11.0) for adenocarcinoma of the cardia. The risk of esophageal squamous-cell carcinoma was not associated with reflux (odds ratio, 1.1; 95 percent confidence interval, 0.7 to 1.9). There is a strong and probably causal relation between gastroesophageal reflux and esophageal adenocarcinoma. The relation between reflux and adenocarcinoma of the gastric cardia is relatively weak.
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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.

                Author and article information

                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                December 2007
                December 2007
                : 3
                : 6
                : 1035-1145
                [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
                © 2007 Dove Medical Press Limited. All rights reserved

                barrett’s esophagus,evidence-based approach,esophageal adenocarcinoma,endoscopic surveillance


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