Abstract
The aim of this article was to review the roles of Helicobacter pylori-induced antralization in gastric carcinogenesis and its implications in clinical practice. A search of PubMed/PubMed Central, Web of Science, and China National Knowledge Infrastructure was performed in December 2018 to retrieve all literature related to antralization (or antralisation), pyloric (or pseudopyloric) glands, pyloric (or pseudopyloric) metaplasia, or pyloric (or pseudopyloric) gland metaplasia, and spasmolytic polypeptide-expressing metaplasia (or SPEM). Among the synonyms, antralization and SPEM, which are derived in the same mechanisms at the molecular, cellular and tissue levels, are more commonly used in recent studies. Antralization (or SPEM) is associated with H. pylori infection, atrophic gastritis and intestinal metaplasia, while H. pylori eradication may reverse antralization. It is proposed that H. pylori infection leads to inflammation in the gastric mucosa and apoptosis of the epithelial cells of the proximal stomach, including gastric incisura, body and fundus. The stem cells proliferate and transform into mucous cells and form antral-type mucosa (i.e. antralization). Subsequently, H. pylori-induced antralization, if not controlled, may develop into atrophic gastritis, intestinal metaplasia, dysplasia, and early intestinal-type gastric cancer. Although many biomarkers, including the spasmolytic polypeptide and mucin 6, are specifically expressed in the gastric mucosa with antralization, none of them are evaluated for the clinical diagnosis of antralization. H. pylori-induced antralization (or SPEM) is believed to be an initiating and reversible stage of gastric carcinogenesis. Identification of antralization would help make an early intervention to cease or even reverse the process toward the development of gastric cancer. Currently, the “gold standard” for diagnosing antralization is pathology, which is invasive and time consuming. A non-invasive and convenient method that accurately and specifically diagnoses antralization is urgently required.
Highlights
According to the latest global cancer data released by the WorldHealth Organization, gastric cancer was responsible for over 1,000,000 new cases in 2018 and an estimated 783,000 deaths, making it the fifth most frequently diagnosed cancer and the third leading cause of cancer death.[1]
The international consensus on the prevention and treatment of gastric cancer recommends the detection and monitoring of precancerous lesions, including atrophic gastritis, intestinal metaplasia, and dysplasia and diagnosis of early gastric cancer,[4] which is virtually based on the theory on intestinal-type gastric cancer pub
In 1998, with the in-depth investigation of gastric mucosal histology, Xia et al.[16] observed that H. pylori infection was associated the presence of antral-type mucosa in gastric incisura, which was further associated with atrophic gastritis and intestinal metaplasia
Summary
Health Organization (commonly known as WHO), gastric cancer was responsible for over 1,000,000 new cases in 2018 and an estimated 783,000 deaths (equating to 1 in every 12 deaths globally), making it the fifth most frequently diagnosed cancer and the third leading cause of cancer death.[1]. In 1998, with the in-depth investigation of gastric mucosal histology, Xia et al.[16] observed that H. pylori infection was associated the presence of antral-type mucosa in gastric incisura, which was further associated with atrophic gastritis and intestinal metaplasia They coined a term “antralization” for this histological change. The authors reported later that antralization was present at the edge of proximal gastric ulcers and disappeared after H. pylori eradication in a substantial proportion of patients.[17] In 1999, Schmidt et al.[18] reported a metaplasia lineage in the stomach that expresses spasmolytic polypeptide ( called trefoil factor 2 or TFF2) that is associated with gastric cancer The authors defined this lineage as spasmolytic polypeptide-expressing metaplasia (SPEM), which is believed to share the same histological origin, i.e. they are derived in the same mechanisms at the molecular, cellular and tissue levels. We use “antralization”, where appropriate, to emphasize the carcinogenic roles and clinical implications of this histological change, as we believe that antralization is more suitable to describe the transition of the specialized glands in the gastric body or at the body-antrum junction by mucous-secreting glands
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