Autoimmune Gastritis Associated With a Gastric Hyperplastic Polyp: Two Case Reports and Review of its Neoplastic Potential

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Korean J Helicobacter Up Gastrointest Res. 2026;26(1):100-105

Publication date (electronic) : 2026 March 5

doi : https://doi.org/10.7704/kjhugr.2025.0086

Myung-Hun Lee, Sung Eun Kim, Moo In Park, Kyoungwon Jung

Division of Gastroenterology, Department of Internal Medicine, Kosin University College of Medicine, Busan, Korea

Corresponding author Sung Eun Kim, MD, PhD Department of Internal Medicine, Kosin University College of Medicine, 262 Gamcheon-ro, Seo-gu, Busan 49267, Korea E-mail: solefide@hanmail.net

Received 2025 December 2; Revised 2025 December 26; Accepted 2026 January 9.

Abstract

INTRODUCTION

Autoimmune gastritis (AIG) is a chronic atrophic gastritis marked by immune-mediated destruction of parietal cells that causes oxyntic gland atrophy, achlorhydria, and secondary hypergastrinemia [1,2]. AIG commonly co-occurs with other autoimmune diseases, such as Hashimoto’s thyroiditis, type 1 diabetes, Addison’s disease, chronic spontaneous urticaria, myasthenia gravis, and vitiligo [3]. Furthermore, it can be a precursor to a variety of gastrointestinal conditions, including gastric cancer, neuroendocrine tumors, and gastric polyps.

Physiologic alterations in AIG promote mucosal regeneration and intestinal metaplasia, thereby contributing to the development of gastric hyperplastic polyp (GHP). Although these lesions have historically been associated with chronic Helicobacter pylori gastritis, accumulating evidence now indicates that AIG serves as an additional major etiologic factor [4,5]. While GHPs are typically regarded as benign, recent studies highlight that those related to AIG present unique clinicopathologic features, including multiple lesions, body-predominant distribution, and a heightened risk of dysplasia or carcinoma [6]. AIG is infrequently documented in South Korea, especially in conjunction with GHPs. Here, we present two cases of AIG that were incidentally identified during management of GHP.

CASE REPORT

Case 1

A 39-year-old woman underwent a screening upper endoscopy that detected a gastric polyp and subsequently visited the outpatient clinic for polyp removal. She denied any prior medical conditions, including autoimmune disorders, except for a history of anemia. Laboratory evaluation identified normocytic anemia consistent with early iron deficiency (hemoglobin 9.7 g/dL, mean corpuscular volume 83 fL, iron 13 μg/dL, total iron binding capacity 375 μg/dL, ferritin 3.6 ng/mL, transferrin saturation 3.5%). Levels of vitamin B12 (362 pg/mL) and folate (3.67 ng/mL) were within normal limits. Serological analysis revealed pepsinogen I 7.3 ng/mL, pepsinogen II 8.1 ng/mL, PG I/II ratio 0.9, and gastrin >1000 pg/mL.

Endoscopic mucosal resection (EMR) was performed to excise the gastric polyp. A hyperemic polypoid lesion, measuring approximately 8 mm, was identified in the lesser curvature of the middle body of the stomach. During EMR, endoscopic assessment demonstrated atrophic gastritis that was more prominent in the gastric body relative to the antrum (Fig. 1). H. pylori antibody, rapid urease test, and dual-priming oligonucleotide-based multiplex polymerase chain reaction (DPOPCR) assays were all negative. Subsequently, testing for antiparietal cell antibody and anti-intrinsic factor antibody was performed. The result for anti-intrinsic factor antibody was negative, while anti-parietal cell antibody was positive, supporting a diagnosis of AIG. Histopathological analysis revealed elongated, cystically dilated foveolae with stromal edema and inflammatory infiltration, which is typical of a hyperplastic polyp without evidence of dysplasia. The adjacent mucosa exhibited marked oxyntic atrophy and intestinal metaplasia (Fig. 2). The patient was prescribed oral ferrous sulfate and scheduled for routine outpatient follow-up.

Fig. 1.

Endoscopic features observed in Case 1. The surrounding mucosa shows typical corpus-predominant atrophy indicative of autoimmune gastritis, whereas the excised lesion represents a gastric hyperplastic polyp. A and B: White-light endoscopy reveals corpus-predominant atrophic mucosa; a hyperemic, sessile polyp approximately 8 mm in size is observed on the lesser curvature of the mid-body. C: Close-up images of the gastric body depict a smooth-surfaced, reddish lesion set against an atrophic mucosal background. D: Endoscopic mucosal resection is performed utilizing a snare method. E: The post-resection ulcer base exhibits clear margins, with no immediate complications observed.

Fig. 2.

Histopathological examination of the gastric hyperplastic polyp removed in Case 1 reveals no evidence of dysplasia or neoplastic transformation. A and B: Low-power microscopic examination of the polyp demonstrates elongated, branching, and cystically dilated foveolar epithelium, characteristic of a hyperplastic polyp (hematoxylin-eosin [H&E], ×2 and ×40). C and D: Intermediate magnification highlights foveolar hyperplasia, the presence of edema, and mild lymphocytic infiltration in the lamina propria (H&E, ×80 and ×100). E: High-power examination shows scattered lymphoplasmacytic infiltrates with an almost complete absence of normal parietal cells (arrows), consistent with autoimmune atrophy of the corpus (H&E, ×200).

Case 2

A 66-year-old man with type 2 diabetes and decompensated liver cirrhosis undergoing follow-up, who had previously undergone cholecystectomy, presented to the outpatient clinic following concerns about an increase in the size of a gastric polyp detected during screening upper endoscopy within the past year. Laboratory findings revealed white blood cell count 2850/μL, hemoglobin 12.0 g/dL, platelets 121000/μL, prothrombin time-international normalize rate 1.16 (78%), total protein 7.8 g/dL, albumin 4.5 g/dL, total bilirubin 1.37 mg/dL, aspartate aminotransferase 31 U/L, alanine aminotransferase 20 U/L, alkaline phosphatase 55 U/L, Gamma-glutamyl transferase 30 U/L, and HbA1c 6.5%. Serum pepsinogen I was 13.6 ng/mL, pepsinogen II was 6.5 ng/mL, prostaglandins I/II ratio was 2.1, and gastrin level was 472.4 pg/mL. Endoscopy revealed body-dominant atrophic gastritis and identified an erythematous polyp measuring approximately 10 mm on the greater curvature of the proximal antrum (Fig. 3). The degree of atrophy in the gastric antrum was less pronounced than in the corpus. Based on these findings, AIG was suspected and both anti-parietal cell antibody and anti-intrinsic factor antibody assays were performed. The anti-intrinsic factor antibody test was negative, while the anti-parietal cell antibody test was positive. H. pylori antibody, rapid urease test, and DPO-PCR were all negative. EMR was performed and histology confirmed a hyperplastic polyp without evidence of dysplasia (Fig. 4). The patient was scheduled for regular follow-up at the outpatient clinic.

Fig. 3.

Endoscopic findings from Case 2 highlight that, despite the location of the polyp in the antrum, the nearby mucosa presents subtle manifestations of autoimmune corpus gastritis, which may be easily missed during routine assessment. A-C: White-light endoscopy identifies corpus-predominant atrophic mucosa with a hyperemic, sessile polyp measuring about 10 mm on the greater curvature of the proximal antrum. D: Submucosal lifting via injection is performed prior to EMR, delineating a clearly defined lesion. E: The post-resection ulcer base following EMR is secured with hemostasis clips; no immediate complications are noted. EMR, endoscopic mucosal resection.

Fig. 4.

Histopathological features of the resected gastric hyperplastic polyp (Case 2). No evidence of dysplasia is observed, confirming that the lesion is a benign hyperplastic polyp developing within an autoimmune gastritis-associated mucosal background. A: Low-power microscopic image illustrating a hyperplastic polyp characterized by elongated, branching foveolar epithelium and cystic dilatation (hematoxylin-eosin [H&E], ×2). B: At intermediate magnification, the section demonstrates foveolar hyperplasia associated with stromal edema and mild, chronic inflammatory infiltration in the lamina propria (H&E, ×40). C: High-power microscopy reveals the presence of chronic inflammatory cells and decreased normal oxyntic glands (arrows), features that are compatible with autoimmune-type changes in the corpus within the background mucosa (H&E, ×200).

DISCUSSION

AIG is defined by chronic immune-mediated destruction of oxyntic glands, causing hypochlorhydria, hypergastrinemia, and subsequent reactive epithelial proliferation. This sequence accounts for the frequent development of GHPs in autoimmune backgrounds rather than in H. pylori-associated atrophic gastritis [4,7]. Stolte [8] reported that GHPs mainly develop in active and atrophic AIG, and subsequent studies have corroborated their frequent association with pernicious anemia and gastrin-mediated mucosal regeneration. Therefore, GHPs should be considered not only a benign reactive manifestation but also a visible indicator of the autoimmune milieu within the corpus mucosa.

In East Asia, the clinical identification of AIG remains difficult. Despite increased disease awareness, standard screening endoscopy still primarily targets H. pylori-associated gastritis. Corpus-dominant atrophy is frequently ascribed to past infection or normal aging, while systematic serologic assessments—including pepsinogen I/II ratio, fasting gastrin, and anti-parietal cell antibody testing—are rarely adopted in health-check protocols [9,10]. Consequently, many patients receive a diagnosis only after considerable mucosal damage or clinical evidence of nutritional deficiency has already occurred.

Multiple recent studies have described these diagnostic obstacles, consistently underscoring the lack of AIG detection, the limitations inherent in both endoscopic and serologic diagnostic approaches, and the potential for GHPs to undergo neoplastic transformation in autoimmune contexts. Table 1 summarizes the principal findings from these key publications [1,4,6,10,11].

Table 1.

Recent literature and reviews addressing autoimmune gastritis and hyperplastic polyps

A recent case report from China documented a GHP containing high-grade intraepithelial neoplasia in an autoimmune setting, highlighting the carcinogenic risk linked to chronic AIG-driven mucosal changes [6]. Upon AIG diagnosis, the potential for neoplastic progression—including adenocarcinoma and type I gastric neuroendocrine tumors—demands regular endoscopic monitoring and prompt management of iron and vitamin B12 deficiency.

In Case 1, pronounced corpus atrophy combined with elevated gastrin levels clearly indicated an autoimmune etiology; in contrast, Case 2 exhibited an antral lesion and comparatively mild body atrophy, which could readily be mistaken for non-specific chronic gastritis. Nevertheless, serologic assessment suggested hypochlorhydria and positive anti-parietal cell antibodies, supporting AIG as the etiology.

Although anti-intrinsic factor antibody is considered a specific marker for AIG, its diagnostic sensitivity is low, reported to be approximately 25%–30%, and positivity is more frequently observed in advanced or late-stage disease [9,12]. Therefore, a negative intrinsic factor antibody result does not exclude the diagnosis of AIG.

The serologic abnormalities observed in some patients, such as profoundly reduced pepsinogen I/II ratios and markedly elevated serum gastrin levels, may warrant closer evaluation for vitamin B12 and iron deficiency and more intensive monitoring. However, serologic markers are influenced by multiple factors, including the extent of gastric atrophy, residual acid output, Helicobacter pylori status, and proton pump inhibitor use. Consequently, there is insufficient evidence to reliably infer an individual patient’s disease duration or precise disease stage from specific serologic cutoff values [13].

Current evidence supports a comprehensive diagnostic approach incorporating anti-parietal cell antibodies, endoscopic findings, histopathologic features of oxyntic gland atrophy, and serologic biomarkers such as pepsinogen levels and serum gastrin [12]. This comparison demonstrates that AIG can manifest across a broad morphological range—from substantial atrophy to only slight mucosal alteration—and underscores the importance of integrating serologic and endoscopic findings for accurate diagnosis.

Furthermore, Chen et al. [14] have recently advanced the understanding of AIG by characterizing the endoscopic features associated with early-stage disease in patients who do not display visible atrophy. The investigators identified yellowishwhite cobblestone-like elevations and irregular collecting venules located in the gastric body, which histologically correspond to pseudo-hypertrophy of parietal cells and G-cell hyperplasia. These observations demonstrate that AIG can be detected prior to the development of atrophy, emphasizing the clinical importance of recognizing such subtle endoscopic findings during standard screening [14]. Integrating these early morphologic indicators in conjunction with serologic assessment may help reduce delayed diagnosis and facilitate earlier identification of AIG.

In this context, the present cases add to the accumulating evidence that GHPs identified in H. pylori-negative, body-predominant atrophic mucosa should raise suspicion for underlying autoimmune pathology. Accordingly, when an endoscopist observes a GHP within atrophic gastric body mucosa, a systematic approach involving H. pylori testing, consideration of AIG if negative, followed by serum biomarker analysis and targeted biopsy of the gastric body, could limit underdiagnosis and facilitate prompt detection of precancerous changes.

AIG represents a distinct pathophysiologic basis for body atrophy that frequently remains unrecognized in routine clinical practice. The two cases described herein indicate that the presence of small hyperplastic gastric polyps confined to body atrophic mucosa, absent H. pylori infection, may function as an observable surrogate marker for underlying AIG.

Endoscopists are encouraged to thoroughly evaluate corpus-dominant atrophic changes and consider relevant serologic tests—including pepsinogen profile, gastrin, and anti-parietal cell antibody—whenever GHPs are detected in this context. Improving awareness of both classic and subtle presentations of early-stage AIG may enhance diagnostic precision and support optimal long-term follow-up for this frequently underdiagnosed disorder.

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