Abstract
Background & Aim: Serum pepsinogen I:II ratio, a surrogate marker of atrophic gastritis, suggests that some adenocarcinomas at the gastroesophageal junction (GOJ) develop on a background of atrophic gastritis, similar to non-cardia gastric cancer, while others arise on a background of healthy, non-atrophic gastric mucosa similar to oesophageal adenocarcinoma. In this current study, we have directly examined the background gastric body mucosa in patients with junctional adenocarcinomas compared to oesophageal adenocarcinomas and non-cardia gastric cancers. Methods: 127 gastrectomy and oesophagectomy specimens for adenocarcinoma were identified for which clear topographic description allowed assignment to oesophageal, junctional (including cardia) and gastric non-cardia locations. In these gastric body mucosa specimens, well clear of the tumour margin, parietal cells were immunostained using antiH+/K+ ATPase. Parietal cell density was counted in 3 to 5 well-oriented fields (1 square mm each) and expressed as mean parietal cell number per 1 square mm area. Inflammation indicated by polymorphonuclear (PMN) and mononuclear (MN) cells were also scored. Non-parametric statistics were used to compare distributions. Results: Ten (8%) cases lacked well-orientated blocks of body mucosa. The remaining 117 patients included 34 oesophageal, 52 GOJ and 31 non-cardia gastric adenocarcinomas. Median (IQR) parietal cell densities were 836 (173), 602 (389) and 411 (334) per square mm in gastric mucosa of oesophageal, GOJ and non-cardia gastric cancers, respectively (all differences P <0.001) (Figure). Using a parietal cell density of 630/square mm, 85% of oesophageal adenocarcinomas had higher and 84% of non-cardia gastric cancers had lower values. In contrast, 50% of the GOJ adenocarcinomas had values greater than and 50% less than this parietal cell density of 630 square mm. Frequency distribution curves of gastric mucosal parietal cell density indicated monophasic patterns for both oesophageal adenocarcinomas and noncardia gastric adenocarcinomas but a biphasic distribution for junctional adenocarcinomas. The chronic inflammatory cell infiltrate [median, (IQR)] was significantly greater in the gastric body mucosa of the non-cardia gastric adenocarcinomas [3(2)] than the oesophageal adenocarcinomas [0(1)]. The junctional adenocarcinoma again had an intermediate score [1(21)], all p values were <0.01. Conclusion: This study provides direct evidence for marked differences in the gastric mucosal phenotype in patients with oesophageal versus gastric non-cardia cancer, with the former being healthy and uninflamed, but the latter atrophic and inflamed. The background gastric mucosa of GOJ cancer supports them being of two distinct aetiologies, one group resembling oesophageal adenocarcinoma and the other gastric non-cardia cancer.
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