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Original Article

Use of endoscopic assessment of gastric atrophy for gastric cancer risk stratification to reduce the need for gastric mapping

ORCID Icon, , , &
Pages 402-407 | Received 10 Oct 2019, Accepted 01 Mar 2020, Published online: 28 Mar 2020
 

Abstract

Background/Aims: Stratification for gastric cancer risk typically involves histologic grading of gastric biopsies. This study aimed to compare endoscopic assessment of gastric atrophy and histologic gastric mapping for gastric cancer risk stratification in a region with relatively high risk of gastric cancer.

Methods: Endoscopic and histologic gastric cancer risk stratification were compared in Vietnamese patients with functional dyspepsia. Endoscopic gastric atrophy was graded according to the Kimura-Takemoto classification. High-risk histologic lesions were defined as gastric dysplasia, Operative Link on Gastritis Assessment (OLGA) gastritis stage III/IV, intestinal metaplasia in both the antrum and the corpus or incomplete intestinal subtype at any site. Two experienced pathologists, blinded to endoscopic information, jointly examined all specimens and reached a consensus. The presence of high-risk histologic lesions was compared among patients with different endoscopic grades of gastric atrophy.

Results: There were 280 subjects (mean age, 46.1 ± 10 years, and male, 50%). The numbers of patients with moderate/severe grade of endoscopic gastric atrophy and high-risk histologic lesions were 126 (45.0%) and 46 (16.4%), respectively. The sensitivity, specificity, positive and negative likelihood ratios of moderate/severe endoscopic atrophic grade for detecting high-risk histologic lesions were 93% (95% CI 86%−100%), 65% (95% CI 58%−71%), 2.64 (95% CI 2.18 − 3.18) and 0.10 (95% CI 0.03 − 0.30), respectively.

Conclusions: Gastric cancer risk assessment using endoscopic or histologic methods provided similar results such that the absence or a mild grade of endoscopic gastric atrophy would preclude the need for histologic mapping.

Acknowledgements

The authors gratefully acknowledge the critical review of Professor David Y. Graham, MD; Professor of Medicine, Molecular Virology and Microbiology, Baylor College of Medicine.

Disclosure statement

No potential conflict of interest was reported by the author(s).

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