Increased Prevalence of Autoimmune Gastritis in Patients with a Gastric Precancerous Lesion

Xiaopei Guo, Marco W.J. Schreurs, Fleur E. Marijnissen, Michiel C. Mommersteeg, Stella A.V. Nieuwenburg, Michail Doukas, Nicole S. Erler, Lisette G. Capelle, Marco J. Bruno, Maikel P. Peppelenbosch, Manon C.W. Spaander, the Proregal study group, Gwenny M. Fuhler*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

5 Citations (Scopus)
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Abstract

Background: 

Autoimmune gastritis (AIG), characterized with the presence of anti-parietal-cell antibodies (APCA), is a risk factor for gastric cancer. However, AIG may go underdiagnosed, especially in the case of H. pylori infection and the presence of gastric precancerous lesions (GPL), due to the ambiguous pathology and delayed symptom onset. 

Aim: 

Investigate the prevalence and characteristics of AIG in GPL patients. 

Methods:

Prevalence of AIG was determined with the presence of APCA in patients with GPL (n = 256) and the control group (n = 70). Pathological characteristics and levels of gastrin 17 (G17), pepsinogen (PG) I and II and anti-Helicobacter pylori IgG were assessed in GPL cases, and the severity of intestinal metaplasia and gastric atrophy was scored by expert pathologists. 

Results: 

APCA positivity was observed in 18% of cases vs. 7% of controls (p = 0.033). Only 3/256 patients were previously diagnosed with AIG. The presence of APCA was associated with corpus-limited and extended GPL. A receiver operating curve analysis demonstrated that the G17 and PGI/II ratio could identify APCA-positive patients within GPL cases (AUC: 0.884). 

Conclusions: 

The prevalence of AIG is higher in patients with GPL but goes undiagnosed. Using G17 and PG I/II as diagnostic markers can help to identify patients with AIG and improve surveillance programs for patients with GPL.

Original languageEnglish
Article number6152
Number of pages12
JournalJournal of Clinical Medicine
Volume12
Issue number19
DOIs
Publication statusPublished - 23 Sept 2023

Bibliographical note

Publisher Copyright: © 2023 by the authors.

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