Enterochromaffin-like Cell Hyperplasia as Identification Marker of Autoimmune Gastritis in Patients With Helicobacter pylori Infection in the Context of Gastric Premalignant Lesions

To the Editor:—With interest, we read the article “Features That Aid Identification of Autoimmune Gastritis in a Background of Active Helicobacter pylori Infection” by Choudhuri et al.¹  The authors found that full-thickness oxyntic mucosa inflammation combined with oxyntic gland loss and enterochromaffin-like (ECL) cell hyperplasia may help identify patients with autoimmune gastritis (AIG) with concurrent Heliobacter pylori infection from H pylori–associated gastritis. In a retrospective analysis, 6 of 7 H pylori–positive AIG cases showed loss of oxyntic glands and ECL hyperplasia. In a prospective cohort, oxyntic gland loss was seen in 10 of 11 H pylori–positive AIG cases, with ECL hyperplasia present in 8 cases. No oxyntic gland loss or ECL hyperplasia was seen in 8 controls, either before or 10 years after H pylori eradication, and thus a more careful pathologic examination of biopsies taken from H pylori–positive individuals may allow a better diagnosis for and earlier treatment of AIG patients.

These findings are of importance because recently the management of epithelial precancerous conditions and lesions of the stomach (MAPS 2019) guidelines have indicated that in addition to intestinal metaplasia (IM) and gastric atrophy (GA), AIG diagnosis warrants surveillance of patients for early detection of gastric cancer.²  Several studies have suggested that AIG development is associated with H pylori infection,³  which is also the main risk factor for IM and gastric cancer development. Interestingly, in the cohort of Choudhuri et al,¹  51% of AIG patients presented with concomitant IM. However, none of the controls were IM positive. With a clear link between H pylori, GA, IM, and AIG, it is of importance to know whether the defined pathologic findings also distinguish AIG in H pylori–positive individuals in a background of premalignant lesions. To this end, we examined a cohort of patients who received a diagnosis of gastric precancerous lesion (GPL), including GA and/or IM. Based on pathology availability, 7 men and 15 women from the PROREGAL study, with a mean age of 56 ± 12 years, were included for retrospective analysis.⁴  All patients received a diagnosis of GPL by gastroendoscopy, and serum was collected at baseline endoscopy. The presence of anti–parietal cell antibodies was determined by indirect immunofluorescence antibody test and H⁺K⁺ATPase-specific EliA automated enzyme fluoroimmunoassay. H pylori infection was identified based on pathology findings or the presence of anti–H pylori antibodies. A total of 9 of 22 cases were identified as having AIG in the context of H pylori infection based on both pathology and serum tests (Table). ECL cell hyperplasia was present in 6 of these, and all showed mucosal atrophy in the corpus. A total of 13 cases showed H pylori–associated gastritis without AIG, with ECL cell hyperplasia observed in 1 case. However, the serologic results of this patient indicated near-positive anti–parietal cell antibody levels, suggesting that patient was in end-stage AIG.⁵  These data confirm that ECL cell hyperplasia is a prevalent manifestation in AIG, even in patients with previous H pylori infection and already established GPL. Awareness should be raised among clinicians and pathologists to look for AIG in the context of GPL, which may be facilitated by the assessment of ECL hyperplasia in these patients.

The authors thank Ingrid Prytz Berset, MD, PhD, for her assistance in including patients and collecting the patients' medical information.