• familial adenomatous polyposis
• fundic gland polyposis
• gastric adenoma
• atrophic gastritis
• Helicobacter pylori

The report in this issue of Gut on the impact of Helicobacter pylori infection and mucosal atrophy on gastric lesions in patients with familial adenomatous polyposis (FAP)¹ highlights the complex interplay between genetic and environmental factors in the genesis of malignancy and has therapeutic implications for the management of these patients [see page485]. A similar interplay has been observed in hereditary non-polyposis colorectal cancer where gastric cancer was quite common in earlier generations but has become less common recently, a change paralleling that seen in the general Western population.²

In Western patients with FAP the incidence of gastric adenoma is of the order of 2–6%. The incidence of gastric cancer is little if at all elevated above the general population³ and the major concern with these patients is the high risk of duodenal and periampullary cancer. However, in Japan the risk of gastric cancer in these patients is significantly elevated and a high incidence of gastric adenomas has been recognised for some time.⁴ The incidence of 39% reported in the present study is slightly less than the 50% reported by Iida and colleagues.⁴

The …