The Association Between Barrett’s Esophagus and Helicobacter pylori
Helicobacter Pylori (H.pylori) particularly the cytotoxin associated A gene (CagA) producing strain is associated with decreased levels of adenocarcinoma and Barrett's esophagus, mainly due to corpus atrophy and decreased gastric acid secretion, which is a predisposing factor for epithelial change in the esophagus (Barrett's esophagus) and then to adenocarcinoma. There were early reports in the 90s suggesting that with the eradication of H.pylori there would be an increase in Gastroesophageal reflux symptoms(GERD) and Barrett's esophagus.(1) With the trend mainly seen in western societies that have low rates of H.pylori infection and higher rates of Barrett's esophagus and Adenocarcinoma, far east countries such as China showed negative association
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Helicobacter Pylori (H.pylori) is a curved gram negative bacterium that mainly infects the stomach mucosa , it is urease positive and can neutralize the gastric mucosa and is associated with gastric carcinomas and peptic ulcers. The urease can also break Urea to Ammonia and that in turn can neutralize stomach acid, allowing the organism to survive and multiply in the mucosa. The decrease in acid can have positive effects despite the complications and effects of infection by H.pylori, mainly by reversing the progression of Barrett's metaplasia which is caused by gastric acid secretion to the epithelium of distal one third of esophagus, causing a change in cellular structure to a metaplastic columnar shape that is more resistant to gastric reflux as a result of Gastroesophageal reflux or GERD, but can also lead to Adenocarcinoma. The incidence of Barrett's esophagus lies between 5 to 15% of patients with long standing GERD, and many patients do not show any symptoms, in addition to reflux esophagitis which is characterized by inflammation and is caused by GERD. H.pylori is inversely related to diseases caused by GERD such as Barrett's metaplasia and in turn Adenocarcinoma, and studies have been conducted to investigate the mechanisms behind the effect of GERD over the decrease of BE and Adenocarcinoma
