Association of serum pepsinogens and gastrin-17 with Helicobacter pylori infection assessed by urea breath test
BackgroundAssociation of gastric atrophy or cancer with levels of serum pepsinogens, gastrin-17 and anti-Helicobacter pylori IgG antibody have been extensively studied. However, the association of serum pepsinogen and gastrin-17 with H. pylori infection has not been studied in a large population.Aim...
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Frontiers Media S.A.
2022-08-01
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Series: | Frontiers in Cellular and Infection Microbiology |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fcimb.2022.980399/full |
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author | Jun-peng Zhou Jun-peng Zhou Chang-hai Liu Chang-hai Liu Bo-wen Liu You-juan Wang Mohammed Benghezal Mohammed Benghezal Barry James Marshall Barry James Marshall Barry James Marshall Barry James Marshall Hong Tang Hong Tang Hong Li Hong Li |
author_facet | Jun-peng Zhou Jun-peng Zhou Chang-hai Liu Chang-hai Liu Bo-wen Liu You-juan Wang Mohammed Benghezal Mohammed Benghezal Barry James Marshall Barry James Marshall Barry James Marshall Barry James Marshall Hong Tang Hong Tang Hong Li Hong Li |
author_sort | Jun-peng Zhou |
collection | DOAJ |
description | BackgroundAssociation of gastric atrophy or cancer with levels of serum pepsinogens, gastrin-17 and anti-Helicobacter pylori IgG antibody have been extensively studied. However, the association of serum pepsinogen and gastrin-17 with H. pylori infection has not been studied in a large population.AimTo investigate the impact of H. pylori infection on serum levels of pepsinogens and gastrin-17.MethodsA total of 354, 972 subjects who underwent health check-ups were included. Serum levels of pepsinogens and gastrin-17 were measured using the enzyme-linked immunosorbent assay. H. pylori infection was detected using 14C-urea breath test (UBT). Multivariable logistic regression analysis was used to investigate the association of serum pepsinogen and gastrin-17 with H. pylori infection.ResultsH. pylori prevalence was 33.18% in this study. The mean levels of pepsinogens and gastrin-17 were higher, while the mean pepsinogen-I/II ratio were lower among H. pylori-positive than -negative subjects. In H. pylori-positive subjects, pepsinogen and gastrin-17 levels correlated positively, whereas the pepsinogen-I/II ratio correlated negatively with UBT values (e.g., the mean serum level of pepsinogen-I in subjects with UBT values in the range of 100-499dpm, 500-1499dpm, and ≥1500dpm was 94.77 ± 38.99, 102.77 ± 43.59, and 111.53 ± 47.47 ng/mL, respectively). Compared with H. pylori-negative subjects, the adjusted odds ratio (aOR) of having pepsinogen-I ≤ 70 ng/mL in the three H. pylori-positive but with different UBT value groups was 0.31 (p<0.001), 0.16 (p<0.001), and 0.08 (p<0.001), respectively; while the aOR of having G-17>5.70 pmol/L was 4.56 (p<0.001), 7.43 (p<0.001), and 7.12 (p<0.001). This suggested that H. pylori-positive subjects with higher UBT values were less likely to have pepsinogen-I ≤70 ng/mL (a serum marker for gastric atrophy), but more likely to have gastrin-17 >5.70 pmol/L (a marker for peptic ulcer).ConclusionsH. pylori-positive subjects with higher UBT values are unlikely to have gastric atrophy, but may have greater risk of severe gastritis or peptic ulcers. Our study suggests that H. pylori-positive patients with high UBT values may benefit the most from H. pylori eradication. |
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spelling | doaj.art-3948172b56874b5ba7badbe19ed9b2bb2022-12-22T04:00:53ZengFrontiers Media S.A.Frontiers in Cellular and Infection Microbiology2235-29882022-08-011210.3389/fcimb.2022.980399980399Association of serum pepsinogens and gastrin-17 with Helicobacter pylori infection assessed by urea breath testJun-peng Zhou0Jun-peng Zhou1Chang-hai Liu2Chang-hai Liu3Bo-wen Liu4You-juan Wang5Mohammed Benghezal6Mohammed Benghezal7Barry James Marshall8Barry James Marshall9Barry James Marshall10Barry James Marshall11Hong Tang12Hong Tang13Hong Li14Hong Li15West China Marshall Research Center for Infectious Diseases, Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaDivision of Infectious Diseases, State Key Laboratory of Biotherapy and Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaWest China Marshall Research Center for Infectious Diseases, Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaDivision of Infectious Diseases, State Key Laboratory of Biotherapy and Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaDental Department, 363 Hospital, Chengdu, ChinaHealth Management Center, West China Hospital of Sichuan University, Chengdu, ChinaWest China Marshall Research Center for Infectious Diseases, Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaDivision of Infectious Diseases, State Key Laboratory of Biotherapy and Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaWest China Marshall Research Center for Infectious Diseases, Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaDivision of Infectious Diseases, State Key Laboratory of Biotherapy and Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaHelicobacter pylori Research Laboratory, School of Biomedical Sciences, Marshall Centre for Infectious Disease Research and Training, University of Western Australia, Nedlands, WA, AustraliaSchool of Biomedical Engineering, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, Shenzhen, ChinaWest China Marshall Research Center for Infectious Diseases, Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaDivision of Infectious Diseases, State Key Laboratory of Biotherapy and Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaWest China Marshall Research Center for Infectious Diseases, Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaDivision of Infectious Diseases, State Key Laboratory of Biotherapy and Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, ChinaBackgroundAssociation of gastric atrophy or cancer with levels of serum pepsinogens, gastrin-17 and anti-Helicobacter pylori IgG antibody have been extensively studied. However, the association of serum pepsinogen and gastrin-17 with H. pylori infection has not been studied in a large population.AimTo investigate the impact of H. pylori infection on serum levels of pepsinogens and gastrin-17.MethodsA total of 354, 972 subjects who underwent health check-ups were included. Serum levels of pepsinogens and gastrin-17 were measured using the enzyme-linked immunosorbent assay. H. pylori infection was detected using 14C-urea breath test (UBT). Multivariable logistic regression analysis was used to investigate the association of serum pepsinogen and gastrin-17 with H. pylori infection.ResultsH. pylori prevalence was 33.18% in this study. The mean levels of pepsinogens and gastrin-17 were higher, while the mean pepsinogen-I/II ratio were lower among H. pylori-positive than -negative subjects. In H. pylori-positive subjects, pepsinogen and gastrin-17 levels correlated positively, whereas the pepsinogen-I/II ratio correlated negatively with UBT values (e.g., the mean serum level of pepsinogen-I in subjects with UBT values in the range of 100-499dpm, 500-1499dpm, and ≥1500dpm was 94.77 ± 38.99, 102.77 ± 43.59, and 111.53 ± 47.47 ng/mL, respectively). Compared with H. pylori-negative subjects, the adjusted odds ratio (aOR) of having pepsinogen-I ≤ 70 ng/mL in the three H. pylori-positive but with different UBT value groups was 0.31 (p<0.001), 0.16 (p<0.001), and 0.08 (p<0.001), respectively; while the aOR of having G-17>5.70 pmol/L was 4.56 (p<0.001), 7.43 (p<0.001), and 7.12 (p<0.001). This suggested that H. pylori-positive subjects with higher UBT values were less likely to have pepsinogen-I ≤70 ng/mL (a serum marker for gastric atrophy), but more likely to have gastrin-17 >5.70 pmol/L (a marker for peptic ulcer).ConclusionsH. pylori-positive subjects with higher UBT values are unlikely to have gastric atrophy, but may have greater risk of severe gastritis or peptic ulcers. Our study suggests that H. pylori-positive patients with high UBT values may benefit the most from H. pylori eradication.https://www.frontiersin.org/articles/10.3389/fcimb.2022.980399/fullHelicobacter pyloripepsinogengastrin-17urea breath testgastric cancer |
spellingShingle | Jun-peng Zhou Jun-peng Zhou Chang-hai Liu Chang-hai Liu Bo-wen Liu You-juan Wang Mohammed Benghezal Mohammed Benghezal Barry James Marshall Barry James Marshall Barry James Marshall Barry James Marshall Hong Tang Hong Tang Hong Li Hong Li Association of serum pepsinogens and gastrin-17 with Helicobacter pylori infection assessed by urea breath test Frontiers in Cellular and Infection Microbiology Helicobacter pylori pepsinogen gastrin-17 urea breath test gastric cancer |
title | Association of serum pepsinogens and gastrin-17 with Helicobacter pylori infection assessed by urea breath test |
title_full | Association of serum pepsinogens and gastrin-17 with Helicobacter pylori infection assessed by urea breath test |
title_fullStr | Association of serum pepsinogens and gastrin-17 with Helicobacter pylori infection assessed by urea breath test |
title_full_unstemmed | Association of serum pepsinogens and gastrin-17 with Helicobacter pylori infection assessed by urea breath test |
title_short | Association of serum pepsinogens and gastrin-17 with Helicobacter pylori infection assessed by urea breath test |
title_sort | association of serum pepsinogens and gastrin 17 with helicobacter pylori infection assessed by urea breath test |
topic | Helicobacter pylori pepsinogen gastrin-17 urea breath test gastric cancer |
url | https://www.frontiersin.org/articles/10.3389/fcimb.2022.980399/full |
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