Observational Study
Copyright ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 7, 2020; 26(25): 3673-3685
Published online Jul 7, 2020. doi: 10.3748/wjg.v26.i25.3673
Type I and type II Helicobacter pylori infection status and their impact on gastrin and pepsinogen level in a gastric cancer prevalent area
Lin Yuan, Jun-Bo Zhao, Ying-Lei Zhou, Ya-Bin Qi, Qiong-Ya Guo, Hai-Hui Zhang, Muhammad Noman Khan, Ling Lan, Chang-He Jia, Yan-Rui Zhang, Song-Ze Ding
Lin Yuan, Jun-Bo Zhao, Ying-Lei Zhou, Ya-Bin Qi, Qiong-Ya Guo, Hai-Hui Zhang, Muhammad Noman Khan, Ling Lan, Chang-He Jia, Yan-Rui Zhang, Song-Ze Ding, Department of Gastroenterology and Hepatology, People's Hospital of Zhengzhou University, Henan Province, China
Lin Yuan, Jun-Bo Zhao, Ying-Lei Zhou, Ya-Bin Qi, Qiong-Ya Guo, Hai-Hui Zhang, Muhammad Noman Khan, Ling Lan, Chang-He Jia, Yan-Rui Zhang, Song-Ze Ding, Henan Provincial People’s Hospital, Henan Province, China
Ying-Lei Zhou, Ya-Bin Qi, Qiong-Ya Guo, Hai-Hui Zhang, Muhammad Noman Khan, Ling Lan, Chang-He Jia, Yan-Rui Zhang, Song-Ze Ding, Henan University School of Medicine, Zhengzhou 450003, Henan Province, China
Author contributions: Yuan L, Lan L, Zhang YR and Ding SZ designed the research; Yuan L, Zhao JB, Zhou YL, Qi YB, Guo QY, Zhang HY, Khan MN and Jia CH collected clinical data and performed experiments; Yuan L analyzed the data; Yuan L and Ding SZ wrote the paper; Ding SZ revised the article; All authors have approved the final version of the manuscript.
Supported by National Natural Science Foundation of China, No. U1604174; Henan Provincial Government-Health and Family Planning Commission, No. 20170123; Henan Provincial Government-Health and Family Planning Commission Research Innovative Talents Project, No. 51282; and Henan Provincial Government-Science and Technology Bureau, No. 142300410050.
Institutional review board statement: This study was approved by the Ethics Committee of People’s Hospital of Zhengzhou University (ID: 2019-KY-No. 10), Zhengzhou, China.
Conflict-of-interest statement: Authors declare no competing interests.
Data sharing statement: No additional data are available.
STROBE statement: The authors have read the STROBE Statement, and the manuscript was prepared and revised according to the STROBE Statement.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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/
Corresponding author: Song-Ze Ding, MD, PhD, Chief Doctor, Professor, Department of Gastroenterology and Hepatology, People’s Hospital of Zhengzhou University, No. 7 Weiwu Road, Jinshui District, Zhengzhou 450003, Henan Province, China. dingsongze@hotmail.com
Received: January 4, 2020
Peer-review started: February 24, 2020
First decision: March 27, 2020
Revised: April 8, 2020
Accepted: June 4, 2020
Article in press: June 4, 2020
Published online: July 7, 2020
Processing time: 185 Days and 11.6 Hours
Abstract
BACKGROUND

Type I Helicobacter pylori (H. pylori) infection causes severe gastric inflammation and is a predisposing factor for gastric carcinogenesis. However, its infection status in stepwise gastric disease progression in this gastric cancer prevalent area has not been evaluated; it is also not known its impact on commonly used epidemiological gastric cancer risk markers such as gastrin-17 (G-17) and pepsinogens (PGs) during clinical practice.

AIM

To explore the prevalence of type I and type II H. pylori infection status and their impact on G-17 and PG levels in clinical practice.

METHODS

Thirty-five hundred and seventy-two hospital admitted patients with upper gastrointestinal symptoms were examined, and 523 patients were enrolled in this study. H. pylori infection was confirmed by both 13C-urea breath test and serological assay. Patients were divided into non-atrophic gastritis (NAG), non-atrophic gastritis with erosion (NAGE), chronic atrophic gastritis (CAG), peptic ulcers (PU) and gastric cancer (GC) groups. Their serological G-17, PG I and PG II values and PG I/PG II ratio were also measured.

RESULTS

A total H. pylori infection rate of 3572 examined patients was 75.9%, the infection rate of 523 enrolled patients was 76.9%, among which type I H. pylori infection accounted for 72.4% (291/402) and type II was 27.6%; 88.4% of GC patients were H. pylori positive, and 84.2% of them were type I infection, only 11.6% of GC patients were H. pylori negative. Infection rates of type I H. pylori in NAG, NAGE, CAG, PU and GC groups were 67.9%, 62.7%, 79.7%, 77.6% and 84.2%, respectively. H. pylori infection resulted in significantly higher G-17 and PG II values and decreased PG I/PG II ratio. Both types of H. pylori induced higher G-17 level, but type I strain infection resulted in an increased PG II level and decreased PG I/PG II ratio in NAG, NAGE and CAG groups over uninfected controls. Overall PG I levels showed no difference among all disease groups and in the presence or absence of H. pylori; in stratified analysis, its level was increased in GC and PU patients in H. pylori and type I H. pylori-positive groups.

CONCLUSION

Type I H. pylori infection is the major form of infection in this geographic region, and a very low percentage (11.6%) of GC patients are not infected by H. pylori. Both types of H. pylori induce an increase in G-17 level, while type I H. pylori is the major strain that affects PG I and PG IIs level and PG I/PG II ratio in stepwise chronic gastric disease. The data provide insights into H. pylori infection status and indicate the necessity and urgency for bacteria eradication and disease prevention in clinical practice.

Keywords: Helicobacter pylori; Chronic gastric diseases; Gastrin-17; Pepsinogen; Gastric cancer

Core tip: Type I and type II Helicobacter pylori (H. pylori) infection status and their impact on gastrin-17 and pepsinogen level in chronic gastric diseases have not been studied in this high gastric cancer risk area. Our results show that type I H. pylori infection is the major form of infection, and a very low percentage (11.6%) of gastric cancer patients are not infected by H. pylori. Both type I and type II H. pylori induce an increase in gastrin-17 level, while type I H. pylori is the major strain that affects pepsinogen (PG) I, PG II level and PG I/PG II ratio in stepwise gastric disease in this geographic area.