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Role of gastric atrophy in mediating negative association between Helicobacter pylori infection and reflux oesophagitis, Barrett’s oesophagus and oesophageal adenocarcinoma
  1. Kenneth E L McColl,
  2. Hirotsugu Watabe,
  3. Mohammad H Derakhshan
  1. Medical Sciences, Gardiner Institute, Western Infirmary, Glasgow, UK
  1. Professor K E L McColl, Medical Sciences, Gardiner Institute, Western Infirmary, Glasgow G11 6NT, UK; K.E.L.McColl{at}

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The incidence of oesophageal adenocarcinoma has increased markedly over the past three decades, particularly in the Western world.1 2 The cancer is considered to be a long-term complication of chronic oesophageal mucosal damage produced by acidic gastric refluxate. The gastric juice, which also contains pepsin and intermittently bile, produces ulceration of the oesophageal squamous mucosa, and in some individuals the mucosa undergoes columnar metaplasia to resemble that of the gastric antrum or small or large intestine. This metaplastic mucosa referred to as Barrett’s oesophagus is believed to be the precursor of oesophageal adenocarcinoma. Though the evidence for the increasing incidence of oesophageal adenocarcinoma is unequivocal and there is also some evidence of an increase in Barrett’s oesophagus,3 the evidence for an increase in the incidence of reflux oesophagitis is less robust. However, this may simply be due to the problem in obtaining reliable population incidence rates for reflux oesophagitis.

The rapid rise in incidence of oesophageal adenocarcinoma indicates a change in the environment, and there is considerable interest in identifying the responsible factor or factors. Increased body weight due to dietary and lifestyle factors is a strong candidate. Body mass index (BMI) has been progressively increasing over the past few decades in the Western world, and there is a strong positive association between BMI and oesophageal adenocarcinoma.4

Another environmental candidate for explaining the rising incidence of oesophageal adenocarcinoma is loss of a protective effect related to Helicobacter pylori infection. The prevalence of H pylori infection has been falling in the Western world over recent decades, thus showing the opposite trend to oesophageal adenocarcinoma.5 In addition, numerous studies have demonstrated a negative association between H pylori infection and reflux oesophagitis, Barrett’s oesophagus and oesophageal adenocarcinoma.610 There is also a plausible, biological mechanism by which …

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  • Competing interests: None.

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