Commentaries

Role of gastric atrophy in mediating negative association between Helicobacter pylori infection and reflux oesophagitis, Barrett’s oesophagus and oesophageal adenocarcinoma

Kenneth E L McColl, Hirotsugu Watabe, Mohammad H Derakhshan

Medical Sciences, Gardiner Institute, Western Infirmary, Glasgow, UK

Correspondence to:
Professor K E L McColl, Medical Sciences, Gardiner Institute, Western Infirmary, Glasgow G11 6NT, UK; K.E.L.McColl@clinmed.gla.ac.uk

The first 150 words of the full text of this article appear below.

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.

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• Fassan, M., Rugge, M., Parente, P., Tieppo, C., Rugge, M., Battaglia, G. (2009). The Role of Helicobacter pylori in the Spectrum of Barrett's Carcinogenesis. Cancer Prevention Research 2: 94-94 [Full Text]