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For more than a quarter of a century it has been widely accepted that the majority of gastric cancers arise through a multistep process starting with chronic gastritis and progressing through atrophy, intestinal metaplasia (IM), and dysplasia to invasive carcinoma.1 Corpus atrophy results in hypochlorhydria, which favours carcinogen formation, while atrophic gastritis and metaplasia are hyperproliferative states that favour mutagenesis. Thus atrophy and metaplasia are generally held to be premalignant conditions although the strength of the association is disputed. More recently, it has been established that infection withHelicobacter pylori is a major risk factor for gastric carcinogenesis and, in keeping with this, infection has been directly implicated in the development of atrophy and IM.2-4 This poses the question “Can eradication ofH pylori reverse these premalignant conditions and interrupt the atrophy-carcinoma sequence?” In order to answer the question one first has to understand the biology and natural history of these conditions and then explore the possibilities for their reversal.
The nature of atrophy
Atrophy in the stomach is conventionally (and simply) defined as “loss of glands”. Such loss may follow ulceration with destruction of the glandular layer or, more frequently, result from a prolonged inflammatory process in which multiple glandular units separately undergo destruction. However, atrophy can also be thought of as “a loss of specialised cells”. Under this broader definition it is possible to include loss of parietal and chief (zymogenic) cells without glandular destruction. Such partial or “pre-atrophy” has been described in human autoimmune gastritis5 and is frequently encountered in animal models of both autoimmune gastritis6 and chronicHelicobacter infection.7 In these latter situations oxyntic cells are replaced within the intact glandular tubules by mucous neck cells (MNC). More interestingly, partial loss of parietal cells and replacement by MNC is a frequent but largely unrecognised …
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