Observational Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 21, 2016; 22(47): 10440-10449
Published online Dec 21, 2016. doi: 10.3748/wjg.v22.i47.10440
Relationship between ghrelin, Helicobacter pylori and gastric mucosal atrophy in hemodialysis patients
Hitomi Ichikawa, Mitsushige Sugimoto, Yukitoshi Sakao, Shu Sahara, Naro Ohashi, Akihiko Kato, Ken Sugimoto, Takahisa Furuta, Akira Andoh, Tadashi Sakao, Hideo Yasuda
Hitomi Ichikawa, Mitsushige Sugimoto, Yukitoshi Sakao, Shu Sahara, Naro Ohashi, Ken Sugimoto, Hideo Yasuda, First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan
Mitsushige Sugimoto, Division of Digestive Endoscopy, Shiga University of Medical Science Hospital, Otsu, Shiga 520-2192, Japan
Yukitoshi Sakao, Tadashi Sakao, Hamana Clinic, Hamamatsu, Shizuoka 434-0037, Japan
Akihiko Kato, Blood Purification Unit, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan
Takahisa Furuta, Center for Clinical Research, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan
Akira Andoh, Department of Gastroenterology, Shiga University of Medical Science Hospital, Otsu, Shiga 520-2192, Japan
Author contributions: Ichikawa H, Sugimoto M, Sakao Y, Sahara S, Ohashi N and Yasuda H contributed to study conception and design; Ichikawa H, Sakao Y, Ohashi N and Sakao T contributed to data acquisition; Ichikawa H, Sugimoto M and Sakao Y contributed to data analysis and interpretation: Ichikawa H and Sugimoto M wrote the paper; Kato A, Sugimoto K, Furuta T and Andoh A contributed to editing.
Supported by the Japanese Association of Dialysis Physicians, No. 2014-2.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board of Hamamatsu University School of Medicine.
Informed consent statement: All study patients provided informed written consent prior to study enrollment.
Conflict-of-interest statement: None of the authors have any conflicts of interest related to this study.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Mitsushige Sugimoto, MD, PhD, Division of Digestive Endoscopy, Shiga University of Medical Science Hospital, Seta Tsukinowa-cho, Otsu, Shiga 520-2192, Japan. sugimo@belle.shiga-med.ac.jp
Telephone: +81-77-5482618 Fax: +81-77-5482618
Received: July 27, 2016
Peer-review started: August 1, 2016
First decision: August 22, 2016
Revised: October 18, 2016
Accepted: November 13, 2016
Article in press: November 13, 2016
Published online: December 21, 2016
Processing time: 145 Days and 13.2 Hours
Abstract
AIM

To investigate the relationship between plasma ghrelin level, Helicobacter pylori (H. pylori) infection status and the severity of atrophy in hemodialysis patients.

METHODS

One hundred eights patients who received hemodialysis and 13 non-hemodialysis H. pylori-negative controls underwent gastroduodenoscopy to evaluate the severity of gastric atrophy. Serum levels of pepsinogen (PG) were measured as serum markers of gastric atrophy. H. pylori infection was evaluated by anti-H. pylori IgG antibody, rapid urease test and culture test. We classified H. pylori infection status as non-infection, present infection and past infection. In addition, plasma acyl-ghrelin and desacyl-ghrelin levels were measured by enzyme-linked immunosorbent assay.

RESULTS

Infection rate of H. pylori was 45.4% (49/108). Acyl-ghrelin level in the non-infection group (39.4 ± 23.0 fmol/mL) was significantly higher than in the past (23.4 ± 19.9 fmol/mL, P = 0.005) and present infection groups (19.5 ± 14.0 fmol/mL, P < 0.001). Furthermore, desacyl-ghrelin level in the non-infection group (353.2 ± 190.2 fmol/mL) was significantly higher than those in the past (234.9 ± 137.5 fmol/mL, P = 0.008) and present infection groups (211.8 ± 124.2 fmol/mL, P < 0.001). Acyl-ghrelin was positively correlated with the PG I level and PG I/II ratio (|R| = 0.484, P < 0.001 and |R| = 0.403, P < 0.001, respectively). Both ghrelins were significantly decreased in accordance with the progress of endoscopic atrophy (both P < 0.001) and acyl-ghrelin was significantly lower in patients with mild, moderate and severe atrophy (24.5 ± 23.1 fmol/mL, 20.2 ± 14.9 fmol/mL and 18.3 ± 11.8 fmol/mL) than in those with non-atrophy (39.4 ± 22.2 fmol/mL, P = 0.039, P = 0.002 and P < 0.001, respectively).

CONCLUSION

In hemodialysis patients, plasma ghrelin level was associated with the endoscopic and serological severity of atrophy related to H. pylori infection.

Keywords: Acyl-ghrelin; Desacyl-ghrelin; Helicobacter pylori; Hemodialysis; Pepsinogen

Core tip: Ghrelin enhances the orexigenic effect, protein anabolism, anti-inflammatory actions and cardiovascular protection in hemodialysis patients. Helicobacter pylori (H. pylori) infection and gastric mucosal atrophy affect ghrelin level in subjects with normal renal function. However, it is unclear whether ghrelin in hemodialysis patients relates to H. pylori status or gastric mucosal atrophy. This study demonstrated that plasma ghrelin level was associated with endoscopic and serological severity of atrophy related with H. pylori infection in hemodalysis patients. Therefore, eradication therapy of H. pylori before the progression of atrophy might improve ghrelin level associated with nutrition status, such as protein-energy wasting.