Circulating acylated ghrelin level decreases in accordance with the extent of atrophic gastritis

We attempted to clarify the significance of atrophic change of gastric mucosa for reduction of plasma ghrelin concentration irrespective of Helicobacter pylori (Hp) infection. Plasma acylated (acyl-)ghrelin concentration in 220 subjects, both with and without atrophic gastritis, was measured with an enzyme immunoassay kit. The extent of atrophic change of gastric mucosa was assessed and graded endoscopically. Hp infection was determined by assay of the anti-Hp antibody with an ELISA assay kit. Plasma acyl-ghrelin concentration was significantly lower in the Hp positive than the Hp negative group, and Hp eradication significantly increased plasma acyl-ghrelin concentrations in Hp positive subjects. Plasma acyl-ghrelin was significantly lower in subjects with severely atrophic gastritis than in those with mild or moderate atrophic gastritis, irrespective of Hp infection or age group (< 60 years old or a parts per thousand 60 years old). In male subjects with a normal body mass index, plasma acyl-ghrelin concentrations in subjects with severely atrophic gastritis were significantly lower than those in subjects with mildly or moderately atrophic gastritis, suggesting that the results of the study are independent of emaciation or obesity. Logistic regression analysis showed that gastric atrophy is the key factor that modulates plasma acyl-ghrelin levels. The results suggest that plasma acyl-ghrelin concentration decreases in accordance with the extent of atrophic change in gastric mucosa irrespective of Hp infection, indicating that the low plasma acyl-ghrelin level of subjects with Hp infection is mainly caused by the progress of atrophic changes in gastric mucosa.