Gastric ghrelin expression associated with Helicobacter pylori infection and chronic gastritis in obese patients.

BACKGROUND

Helicobacter pylori is a major pathogen of stomach. Ghrelin is secreted from the stomach, and it plays a role in the coordination of eating behavior, and facilitates fat storage and weight regulation. The effects of H. pylori infection on gastric ghrelin production are still not well known. Recent exciting studies linked H. pylori infection to ghrelin, then to obesity. The aim of the present study is to investigate gastric ghrelin immunoreactivity associated with H. pylori infection, chronic gastritis and the clinical correlation in obese patients.

METHODS

The histologic findings of stomach were examined in 156 patients who were undergoing laparoscopic vertical-banded gastroplasty for obesity. Ghrelin immunoreactivity was evaluated immunohistochemically with an anti-ghrelin antibody, and the density of ghrelin-positive cells determined per total glands of the gastric mucosa. Relationship between density of ghrelin-positive cells, histopathology of chronic gastritis scored by the Sydney system and clinical correlation was analyzed.

RESULTS

H. pylori was present in 62 (39.7%) out of 156 patients. The density of ghrelin-positive cells was significantly lower for H. pylori-infected patients. There was a significant stepwise decrease in density of ghrelin-positive cells, with progression of histological severity of chronic inflammation, neutrophil activity and glandular atrophy in the corpus. Obese patients positive for H. pylori were associated with older age and abnormal plasma triglyceride level, but not with sex, body mass index, liver function tests or glucose level. There was no relationship between density of gastric ghrelin-positive cells and body mass index.

CONCLUSIONS

H. pylori infection has a negative impact on density of gastric ghrelin-positive cells in obese patients. Impaired density of gastric ghrelin-positive cells is associated with neutrophil activity, chronic inflammation and glandular atrophy induced by H. pylori infection. The potential role of H. pylori infection and density of gastric ghrelin-positive cells on the development of obesity and their biological significance warrants further investigation.