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Gastroenterologie
a hepatologie

Gastroenterology and Hepatology

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ETHNIC DIFFERENCES IN ESOPHAGEAL ADENOCARCINOMA: HELICOBACTER PYLORI OR GASTROESOPHAGEAL REFLUX?



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Western type societies experienced in the past decades a sharp decline in peptic ulcers and gastric adenocarcinoma ((H. pylori, HP associated disorders) but there has been a precipitous increase in gastroesophageal reflux disease (GERD) and associated complications: Barrett’s esophagus (BES) and esophageal adenocarcinoma (ESACA). The role of HP, curved bacilli first described in 1983, and of the increase in obesity, is unclear in these epidemiological trends. Improved sanitation may decrease prevalence of HP with potential decrease in chronic active gastritis, a pre-malignant condition. There is a speculation that eradication of HP may increase GERD, BES and ultimately ESACA. Also, incompetence of the gastro esophageal junction with hiatus hernia, HH is one of the main causes of gastro esophageal reflux. Mechanisms leading to ESACA are complex: this malignancy can result from reflux- related complications but also from HP-induced metaplasia of the epithelium at the cardia. We hypothesized that we may clarify the mechanisms leading to ESACA by analyzing the cause of ethnic differences observed in our patients: Black Americans in contrast to Whites have very low incidence of BES and of ESACA. Why? Gastric biopsies showed no difference in pre malignant gastric intestinal metaplasia and in HP histological density, although Blacks had more gastric adenocarcinoma. Searching for a factor responsible for lower incidence of BES and ESACA in Blacks we also compared the size of HH and the Body Mass Index (measure of obesity). Blacks have smaller HH but no difference in obesity. Still, the proportion of Blacks with a large HH is too high to explain their low incidence of BES and ESACA. In conclusion: We did not find the HP gastric density, the competence of the gastroesophageal support system or obesity to be major factors explaining the rise in ESACA in white populations. Clinicians should eradicate HP if this is associated with upper GI disorders and they should not be concerned about aggravating GERD that in most cases responds to proton pump inhibitors.

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