Development of Carcinoid Tumors of the Glandular Stomach and Effects of Eradication in Helicobacter Pylori-Infected Mongolian Gerbils

Abstract

The relation between Helicobacter pylori (Hp) eradication and prevention of stomach carcinoid developmenthas hitherto remained unclear. We therefore examined this problem using an Hp-infected and Hp-eradicatedMongolian gerbil (MG) model. Enterochromaffin-like (ECL) lesions (hyperplasia/dysplasia and carcinoid)were histopathologically evaluated in the glandular stomachs of Hp-infected and Hp-eradicated MGs. In addition,serum gastrin levels were analyzed. Hp infection induced significant increase in the development of ECL lesionsin the glandular stomach, as well as serum gastrin levels as compared with non-infected MGs, while Hp eradicationwas associated with significant alleviation. The development of ECL lesions in the glandular stomach stronglycorrelated with titers of anti-Hp antibodies and serum gastrin levels in MGs. In conclusion, Hp infection inducescarcinoid development, and Hp eradication prevents its occurrence in the glandular MG stomach, this beingstrongly linked with reduction in serum gastrin levels.