The role of Helicobacter pylori in the pathogenesis of gastric malignancies
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REVIEW
The role of Helicobacter pylori in the pathogenesis of gastric malignancies Woojin Kim • Steven F. Moss
Received: 21 July 2008 / Accepted: 3 August 2008 / Published online: 17 September 2008 ©Springer-Verlag 2008
Abstract Helicobacter pylori is the world’s most common chronic bacterial infection, colonizing more than half of the population globally. Although all strains cause persistent gastric inflammation, most cases are asymptomatic; only 15% result in peptic ulcer disease and less than 2% of cases will develop gastric adenocarcinoma or the even rarer mucosa associated lymphoma (MALT). Considerable evidence implicates H. pylori in the pathogenesis of gastric malignancies - still a major burden in much of the world. Interactions between host factors, environmental factors and specific H. pylori constituents (or virulence factors) are
important in determining the outcome of infection. Despite the relative ease of eradicating H. pylori with 1–2 week course of proton pump inhibitors and antibiotics in individuals, whether to actively seek occult H. pylori infection at the population level to attempt to prevent the burden of H. pylori-associated gastric malignancy remains surprisingly controversial. Keywords Helicobacter pylori • Gastric cancer • MALT lymphoma
Introduction
S.F. Moss (쾷) • W. Kim Gastroenterology Division, Department of Medicine, Rhode Island Hospital/Brown University, Providence, Rhode Island, USA e-mail: [email protected]
Helicobacter pylori is the world’s most common chronic bacterial infection, colonizing more than half of the human population [1]. All H. pylori strains cause some type of gastric inflammation but most cause no symptoms in the host. Infection by highly heterogenous H. pylori species usually occurs during childhood and the bacteria persist within the host unless eradicated by combination antibiotic therapies [2]. It has been estimated that only 15% of infections result in peptic ulcer and less than 2% result in distal (non-cardia) gastric adenocarcinomas, [2] with an even lower rate of mucosa associated lymphoma (MALT). While gastric malignancies are uncommon sequelae of H. pylori infection, the high prevalence of H. pylori contributes to gastric cancer ranking as the second highest cause of global cancer mortality [3]. Interestingly, an inverse relationship of H. pylori with the rarer gastric cancers of the cardia has been demonstrated in Western populations in recent years [4]. Gastric malignancies consist of the more common adenocarcinomas and lymphomas of the gastric mucosa associated lymphoma tissue (MALT lymphomas). It has been
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customary to further divide adenocarcinomas into histological type – either diffuse or intestinal (the latter being numerically dominant in most of the developing world). Although the intestinal type adenocarcinoma has been most studied in its association with H. pylori and has been demonstrated to progress through a cascade of histological steps going from normal mucosa to chronic gastritis and then to atrophic gastritis, int
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