Eradication Treatment of Helicobacter pylori Infection: Its Importance and Possible Relationship in Preventing the Development of Gastric Cancer
Bruna Maria Roesler, Sandra Cecília Botelho Costa, José Murilo Robilotta Zeitune
Helicobacter pylori is the most important carcinogen for gastric adenocarcinoma. Bacterial virulence factors are essential players in modulating the immune response involved in the initiation of carcinogenesis in the stomach; host genetic factors contribute to the regulation of the inflammatory response and to the aggravation of mucosal damage. In terms of environmental factors, salt intake and smoking contribute to the development of lesions. Various therapeutic schemes are proposed to eradicate H. pylori infection, which could potentially prevent gastric cancer, offering the greatest benefit if performed before premalignant changes of the gastric mucosa have occurred.
The first isolation of Helicobacter pylori in the 1980s by Marshall and Warren brought to the medical and scientific communities a new understanding of the pathogenesis of diseases that affect the digestive tract. Since then, H. pylori infection has been associated with the development of acute and chronic gastritis, atrophic gastritis, peptic ulcer disease, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma. All patients with H. pylori infection have histological gastritis, which corresponds to classical chronic gastritis and is characterized by the infiltration of neutrophils and other inflammatory cells. However, most patients are asymptomatic for life, while only some will come to develop a digestive disease. Furthermore, when the relationship between H. pylori infection and chronic gastritis was established, investigators began to take interest in the causal role of the bacterium in gastric cancer. On the basis of numerous subsequent epidemiological studies, H. pylori infection was shown to be associated with an increased risk of gastric adenocarcinoma development. Evidence that the presence of H. pylori increases the risk of developing gastric cancer through atrophy and intestinal metaplasia has also been reported, suggesting that H. pylori-positive patients develop these conditions in greater proportion than control subjects. Consequently, in 1994, the World Health Organization's International Agency for Research on Cancer concluded that H. pylori has a causal link with gastric carcinogenesis and was defined as a type I carcinogen, a definite human carcinogen. It is known that gastric cancer involves the interaction of three major factors: the agent (in the great part of the cases, H. pylori) and its pathogenicity, the characteristics of the host, and the external environment.