Pepsinogens and Gastrin Demonstrate Low Discrimination for Gastric Precancerous Lesions in a Multi-Ethnic United States Cohort

Clin Gastroenterol Hepatol. 2022 Apr;20(4):950-952.e3. doi: 10.1016/j.cgh.2021.01.009. Epub 2021 Jan 10.

Authors

Robert J Huang¹, Sungho Park², Jeanne Shen³, Teri Longacre³, Hanlee Ji⁴, Joo Ha Hwang²

Affiliations

¹ Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University, Stanford, California. Electronic address: rjhuang@stanford.edu.
² Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University, Stanford, California.
³ Department of Pathology, Stanford University, Stanford, California.
⁴ Division of Oncology, Department of Medicine, Stanford University, Stanford, California.

PMID: 33434656
DOI: 10.1016/j.cgh.2021.01.009

Abstract

Early identification of gastric precancerous lesions, including atrophic gastritis (AG) and intestinal metaplasia (IM), may improve gastric cancer detection and prevention. Because AG and IM are generally asymptomatic, many of the estimated 15 million Americans who carry these lesions remain undiagnosed.¹ AG and IM are associated with either active or prior Helicobacter pylori (Hp) infection. Hp infection leads to perturbations in the serum concentration of gastric hormones pepsinogen I (PGI), pepsinogen II, the pepsinogen I/II ratio (PGR), gastrin-17 (G-17), and Hp IgG.²^,³ In East Asia and other regions with high burden of Hp infection and gastric cancer, these biomarkers have been used as screening tools for AG and IM.⁴ However, there exists limited data on the sensitivity and discrimination of these serologic markers in low-Hp-prevalence populations, such as the United States.

MeSH terms

Gastrins
Helicobacter pylori*
Humans
Pepsinogen A
Precancerous Conditions* / diagnosis
Precancerous Conditions* / pathology
Stomach / pathology
United States / epidemiology

Substances

Gastrins
Pepsinogen A