Revealing autoimmune gastritis: Polypoid nodule scar development after endoscopic submucosal dissection for early gastric cancer

Abstract

Endoscopic submucosal dissection (ESD), the standard treatment for early gastric cancer, typically results in homogeneous flat scars. However, in some cases, polypoid nodule scars (PNS) may develop, complicating the cancer recurrence assessment. This case report describes a 60-year-old man with a history of Helicobacter pylori infection who underwent two ESD procedures: first for early antral gastric cancer and then for gastric body adenoma. Subsequently, an erythematous protruding lesion developed at the antral ESD scar site. Lesion biopsy revealed regenerative and hyperplastic tissue growth, consistent with PNS. Despite H. pylori eradication therapy and discontinuation of potassium-competitive acid blockers and H₂-receptor antagonists, the lesion continued to enlarge. PNS growth may be caused by excessive mucosal regeneration and enhanced antral peristalsis, suggesting that hypergastrinemia, which may enhance these effects, may be an underlying cause. Further, elevated serum gastrin levels, decreased pepsinogen levels, the presence of antiparietal cell antibodies, and consistent pathological findings confirmed autoimmune gastritis (AIG). This case highlights the diagnostic challenges of AIG, especially in cases of active or previous H. pylori infection because typical endoscopic features may be obscured. Persistent PNS after ESD warrants the consideration of excessive mucosal regeneration and enhanced peristalsis, with AIG as a potential cause because of its association with hypergastrinemia. To our knowledge, this is the first case report describing a potential link between AIG and PNS.

Keywords: Helicobacter pylori; autoimmune gastritis; endoscopic submucosal dissection; gastrin; polypoid nodule scar.

FIGURE 1

(a) Type 0–IIc early gastric cancer is approximately 10 mm in diameter, erythematous, and located on the posterior wall of the gastric antrum. The background mucosa shows atrophic changes and intestinal metaplasia. (b) The resection site after endoscopic submucosal dissection. (c) An intestinal adenoma, approximately 5 mm in diameter, is observed on the posterior wall of the gastric body. Background mucosal atrophy is also observed. (d) The resection site after endoscopic submucosal dissection.

FIGURE 2

(a) Two months after the first endoscopic submucosal dissection (ESD) of the gastric antrum, the polypoid nodule scar (PNS) has gradually enlarged to approximately 20 mm in diameter. (b) Five months after the first ESD of the gastric antrum, the PNS has continued to enlarge, reaching approximately 30 mm in diameter and exhibiting an increasingly irregular shape, despite switching from vonoprazan to H₂‐receptor antagonist therapy. (c) Ten months after the first ESD of the gastric antrum, the PNS has continued to enlarge, reaching approximately 35 mm in diameter with a rough lobulated surface, despite successful H. pylori eradication. (d) Two years after the second ESD of the gastric body, no PNS is observed in the post‐ESD ulcer area of the gastric body.

FIGURE 3

(a) A biopsy of the gastric body shows degeneration and loss of parietal cells; Decreased glandular density due to the progression of pseudopyloric gland metaplasia (mucous neck cell proliferation), foveolar elongation, and intense lymphocytic infiltration, mainly into tissues deeper than the isthmus, can be seen. Intestinal metaplasia is also observed (hematoxylin and eosin [HE] staining, × 40). (b) Magnified view of the area is indicated by the red frame in Figure 3a (HE staining, × 80). (c) Chromogranin A staining shows linear, tubular, and nodular hyperplasia of enterochromaffin‐like cells. (d) A biopsy of the greater curvature of the gastric antrum shows focal intestinal metaplasia. However, the degree of atrophy in the pyloric glands is less severe than in the oxyntic glands of the gastric body, with scarce lymphocytic infiltration. G‐cell hyperplasia is also observed (HE staining, × 40).

FIGURE 4

(a) Endoscopic images before H. pylori eradication show diffuse erythema and intestinal metaplasia in the gastric antrum which is associated with H. pylori infection. (b) Marked atrophy is also observed in the gastric body. (c) Endoscopic images after H. pylori eradication show that although intestinal metaplasia remains, no atrophic changes are observed in the gastric antrum because the inflammation has resolved, and the mucosa appears glossy. (d) In contrast, the gastric body exhibits marked atrophic changes.