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With interest we read the article by Hansen et al. (Gut 2007;56:918–25). The authors have to be congratulated on their contribution which profoundly adds to our understanding of the pathophysiology leading to oesophageal and gastric cancer. In addition, the paper points out the difficulties we have to correctly assign tumours of the oesophago‐gastric junction (oesophageal vs gastric?). Cardiac cancers were subtyped for their associations with serum anti‐Helicobacter pylori IgG antibody titer and biochemical markers of loss of gastric secretory function associated with atrophy (pepsinogen I/II ratio and serum gastrin concentration). However, the anatomic criterium to define cardiac carcinoma, that is, tumours centred within 2 cm distal to the oesophago‐gastric junction, is inaccurate. Interpretation of the data should be conducted with the inclusion of clear, anatomical and histopathological criteria.
It is well accepted that cardiac cancer and adenocarcinoma of the oesophagus share epidemiological and pathogenetic features.1,2 After birth the oesophagus is lined by squamous epithelium, whereas the stomach is lined by gastric oxyntic mucosa (with parietal and chief cells).1,3 Due to gastro‐oesophageal reflux, squamous epithelium is damaged and replaced by cardiac mucosa (CM). Thus CM is interposed between squamous and oxyntic mucosa. Via intestinal metaplasia and dysplasia CM may progress towards adenocarcinoma of the oesophagus.1,2,3 Anatomy proves that CM is oesophageal: unlike the stomach, the oesophagus has submucosal glands. Histopathology studies of full‐thickness oesophago‐gastric specimens revealed that CM is only present above submucosal glands, whereas gastric oxyntic mucosa is not underlined by submucosal glands.1 CM is columnar‐lined oesophagus and not stomach.1 Using multilevel biopsy sampling around the endoscopic visible oesophago‐gastric junction in patients with gastro‐oesophageal reflux disease, Ringhofer et al.4 showed that CM cannot be differentiated from gastric oxyntic mucosa by endoscopy. Reflux‐damaged columnar‐lined oesophagus was mistaken as proximal stomach in 51% of the patients.4 Based on histopathology, tumours arising within CM are of oesophageal origin, while those arising within oxyntic mucosa are of gastric origin.1,3
What the authors believe to be a “dual” aetiology are in fact “dual associations”. Their data prove that oesophageal adenocarcinoma arising within CM may be present with or without gastric atrophy and H pylori infection of the stomach.1H pylori may also infect columnar‐lined oesophagus (ie, CM)1,3 and be protective against adenocarcinoma, possibly due to atrophy‐induced changes in the composition of the refluate.1
Taken together, the aetiology of cancers at the oesophago‐gastric junction can only be defined by histopathological criteria: tumours arising within cardiac and oxyntic mucosa are of oesophageal and gastric origin, respectively.1,3 Consequently, cardiac carcinomas have to be treated as oesophageal cancers and tumours arising from oxyntic mucosa as gastric malignancies. Cardiac cancer has a single aetiology, gastro‐oesophageal reflux, but may have associations with H pylori infection and gastric atrophy. The authors are kindly asked to address this issue.
Competing interests: None.