Development of plasma ghrelin level as a novel marker for gastric mucosal atrophy after Helicobacter pylori eradication

Hideki Mori; Hidekazu Suzuki; Juntaro Matsuzaki; Kaori Kameyama; Koji Igarashi; Tatsuhiro Masaoka; Takanori Kanai

doi:10.1080/07853890.2021.2024875

Development of plasma ghrelin level as a novel marker for gastric mucosal atrophy after Helicobacter pylori eradication

Ann Med. 2022 Dec;54(1):170-180. doi: 10.1080/07853890.2021.2024875.

Authors

Hideki Mori^{1

2}, Hidekazu Suzuki^{2

3}, Juntaro Matsuzaki^{2

4}, Kaori Kameyama⁵, Koji Igarashi⁶, Tatsuhiro Masaoka^{2

7}, Takanori Kanai²

Affiliations

¹ Translational Research Center for Gastrointestinal Diseases (TARGID), University of Leuven, Leuven, Belgium.
² Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
³ Division of Gastroenterology and Hepatology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Japan.
⁴ Division of Pharmacotherapeutics, Keio University Faculty of Pharmacy, Tokyo, Japan.
⁵ Department of Diagnostic Pathology, School of Medicine, Showa University, Yokohama Northern Hospital, Kanagawa, Japan.
⁶ Bioscience Division, TOSOH Corporation, Kanagawa, Japan.
⁷ Department of Gastroenterology and Hepatology, International University of Health and Welfare, Mita Hospital, Tokyo, Japan.

Abstract

Background and aim: The severity of atrophic gastritis is significantly associated with the risk of gastric cancer. Although the current gold standard for assessing the gastric cancer risk is esophagogastroduodenoscopy with a pathological examination, the development of less-invasive biomarkers is warranted for efficient risk stratification of gastric cancer. Serum pepsinogens (PGs) are biomarkers used to predict the extent of gastric mucosal atrophy; however, they are not an accurate reflection of gastric mucosal atrophy after Helicobacter pylori eradication. The present study was conducted to investigate the usefulness of plasma ghrelin levels as a marker for gastric mucosal atrophy, and as a risk stratification marker for gastric cancer, even after H. pylori eradication.

Methods: Patients who received H. pylori eradication treatment were enrolled in the study. The severity of gastric mucosal atrophy was evaluated both endoscopically and histologically. Serum pepsinogen and plasma ghrelin levels were measured before and at 1, 12, 24, and 48 weeks after treatment. The study was approved by the Research Ethics Committee of the Keio University School of Medicine (no. 20140102; 8 July 2014).

Results: Eighteen patients completed the study protocol. Total and acyl plasma ghrelin levels demonstrated no significant change from before treatment to 48 weeks after eradication; however, there was a significant difference between open-type and closed-type atrophic gastritis. The PG I/II ratio increased significantly from 48 weeks after H. pylori eradication. The severity of the histological intestinal metaplasia scores correlated inversely with plasma total ghrelin levels from before to 48 weeks after H. pylori eradication.

Conclusion: Plasma levels of ghrelin correlate well with the level of gastric mucosal atrophy, even after H. pylori eradication.KEY MESSAGESGhrelin plasma levels are associated with the progression of endoscopic atrophic gastritis, even at 48 weeks after H. pylori eradication.Ghrelin plasma levels are also associated with increased severity of histological intestinal metaplasia 48 weeks after H. pylori eradication.Pepsinogen I/II ratios increased immediately after H. pylori eradication and are inappropriate for assessing atrophic gastritis after H. pylori eradication.

Keywords: Ghrelin; atrophic gastritis; gastric cancer; intestinal metaplasia; pepsinogen.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Atrophy / complications
Atrophy / pathology
Biomarkers
Gastric Mucosa / pathology
Ghrelin
Helicobacter Infections* / complications
Helicobacter Infections* / diagnosis
Helicobacter Infections* / drug therapy
Helicobacter pylori*
Humans

Substances

Biomarkers
Ghrelin

Grants and funding

This work was supported by a Grant-in-Aid for Scientific Research B (25293178, to H.S.) and a Grant-in-Aid for Challenging Exploratory Research (26670065, to H.S.) from the Japan Society for the Promotion of Science (JSPS); by a MEXT-Supported Program for the Strategic Research Foundation at Private Universities (S1411003, to H.S.); by Princess Takamatsu Cancer Research grants (13 -24513, to H.S.); and by Keio Gijuku Academic Development Funds (to J.M. and H.S.).