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Traditional teaching holds that the normal stomach has three types of mucosae. The oxyntic mucosa of the gastric body and fundus has glands with parietal cells that secrete acid, and chief cells that secrete digestive enzymes. The mucosa of the antrum is comprised of mucus-secreting cells and endocrine cells that produce gastrin, which regulates acid production by the oxyntic mucosa. Finally, the most proximal portion of the stomach (the gastric cardia), a region with ill-defined borders, allegedly is lined by ‘cardiac mucosa’ comprised almost exclusively of mucus-secreting cells. Cardiac mucosa has been assumed to function as a buffer zone, preventing the damage that might result if the acid-sensitive, squamous mucosa of the oesophagus joined directly with the acid-secreting oxyntic mucosa of the gastric body. This dogma went unchallenged until 1997, when Chandrasoma proposed that cardiac mucosa is not a normal structure, but rather is acquired when GORD causes columnar metaplasia of squamous epithelium in the distal oesophagus.1 Furthermore, he contended that cardiac mucosa evolves into the intestinal metaplasia of Barrett's oesophagus in the setting of persistent GORD. Recent studies by investigators in Glasgow provide support for Chandrasoma's proposals.
In an earlier investigation, the Glasgow group studied the gastro-oesophageal junction (GOJ) region of 51 healthy volunteers.2 No subject had abnormal acid reflux by conventional pH monitoring in which a pH electrode was positioned 5 cm above the lower oesophageal sphincter (LOS). Using pH electrodes positioned within the LOS, however, significant differences …