Introduction
Atrophic gastritis (AG) of the corpus mucosa, a condition caused by Helicobacter pylori (Hp) infection or gastric autoimmunity and at increased gastric cancer risk, is characterized by loss of native oxyntic glands leading to impaired gastric acid secretion. Loss of gastric acidity alters gastric motility, impairs digestion and promotes bacterial overgrowth. Despite considered often symptomless, dyspepsia may be a presentation symptom of AG whose diagnosis requires oesophagogastroduodenoscopy (OGD) with multiple biopsies. AG is burdened by a substantial diagnostic delay and dyspepsia has been reported as relevant for this delay. The timely diagnosis of this precancerous condition may be clinically relevant. The primary aim of this study was to assess the prevalence of AG in patients undergoing OGD for dyspepsia.
Aims & Methods
A multicentre Italian study was conducted (Nov 2025-Mar 2026) including consecutive adult outpatients undergoing OGD for dyspepsia. OGD was performed with multiple biopsies according to the updated Sydney system. AG was defined histologically by loss of oxyntic glands replaced by atrophic and/or metaplastic mucosa restricted to the corpus (autoimmune AG) or extended to the antrum (multifocal AG). Clinical features (gender, age, 1st degree gastric tumour family history, autoimmune comorbidities, histological Hp positivity, PPI use, and cholecystectomy) and dyspepsia subtype, post-prandial distress syndrome (post-prandial fulness and/or early satiation)(PDS), epigastric pain syndrome (epigastric pain and/or burning)(EPS), or overlap syndrome (PDS+EPS), were collected. Patients with alarm features, serious gastrointestinal or systemic comorbidities, previous gastric surgery, and under follow-up for AG were excluded. Differences between dyspeptic patients with new AG diagnosis and without AG diagnosis were assessed.
Results
194 patients (66.5% female, median age 58(18-88) years) were included. Gastric tumour family history was reported in 17%, autoimmune comorbidity in 16.8%, PPI use in 25.8%, and cholecystectomy in 7.7%. Regarding dyspepsia subtype, 23.2% had PDS, 32.1% EPS. and 44.7% overlap syndrome. Active Hp infection was detected in 15.5% of patients.
29 patients received a new AG diagnosis (n=8(4.1%) autoimmune AG, n=21(10.8%) multifocal AG), showing a crude AG prevalence of 14.9% (number of dyspeptic patients needed to scope for a new AG diagnosis=6.7). Of the 29 newly diagnosed AG patients, 7(24.1%) and 5(17.2%) were aged less than 50 or 40 years, respectively.
No significant differences between AG and non-AG patients were found in terms of gender (65.5% vs 66.7%,p=0.89), age (62 vs 58 years, p=0.21), gastric tumor family history (12.5% vs 18.1%,p=0.51), autoimmune comorbidities (10.0% vs 18.2%,p=0.37), active Hp infection (24.1% vs 13.9%,p=0.16), PPI use (24.0% vs 26.2%,p= 0.82), cholecystectomy (4.2% vs 8.3%,p=0.48). Overlap of PDS+EPS was less common in AG compared to non-AG (25.9% vs 47.8%, p=0.03). Prevalence of PDS-subtype (29.6% vs 22.1%, p=0.46) and EPS-subtype (44.4% vs 30.1%, p=0.379) was not different between groups.
Conclusion
AG prevalence in patients undergoing OGD for dyspepsia was 14%, with a substantial proportion of dyspeptic patients under 50 years of age, who - according to current guidelines - could have been managed without endoscopy, missing AG diagnosis.
Dyspepsia caused by AG seems not to display typical clinical features making challenging an a priori high clinical suspicion of AG. Thus, in patients with dyspepsia, AG should be kept in mind as an underlying condition at gastric cancer risk, even in younger patients.
References
Lahner E, et al. Dig Liv Dis 2019; Lahner E, et al. Dig Liv Dis 2025; Lenti MV, et al. Aliment Ther Pharm 2019; Massironi S, Expert Rev Gastroenterol Hepatol 2025; Sbarigia C Expert Rev Gastroenterol Hepatol 2025.
