Related Experiment Video
Updated: Oct 13, 2025

Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors
Published on: February 16, 2024
Intestinal-type gastric dysplasia in Helicobacter pylori-naïve patients
Kotaro Shibagaki1, Ayako Itawaki2, Yoichi Miyaoka3
1Department of Endoscopy, Shimane University Hospital, Zip code 693-8501, 89-1 Enya, Izumo, Japan. kotaro@med.shimane-u.ac.jp.
Abstract:
Gastric dysplasia and gastric cancer in Helicobacter pylori (Hp)-naïve patients usually exhibit a gastric phenotype, reflecting gastric mucosa without intestinal metaplasia (IM). We showed that intestinal-type gastric dysplasia (IGD) rarely occurs in the Hp-naïve stomach. In the last 10 years, we treated 1760 gastric dysplasia and gastric cancer patients, with 3.6% (63/1760) being Hp-naïve. Among these, ten were diagnosed with 14 IGDs and enrolled in this retrospective analysis. All lesions were observed by white-light endoscopy (WLE) and narrow-band imaging with magnification endoscopy (NBIME). We analyzed their endoscopic and microscopic features and patient demographics. Five men and five women aged 64 ± 21 years were included. WLE showed the depressed lesions mimicking a benign raised erosion in the prepyloric compartment. Multiple growths were confirmed in 30% (3/10) of patients. NBIME showed a near-regular microstructure and capillaries in 50% (7/14) of lesions with a gastritis-like appearance. Histologically, background mucosa was non-atrophic pyloric gland tissue, but 40.0% of samples (4/10) contained sporadic IM. Most of the lesions (8/14) were low-grade dysplasia, and others had a high-grade component, with one progressing to intramucosal carcinoma. The neoplastic surface was widely covered with foveolar epithelium in 57.1% (8/14). Immunohistochemically, neoplastic cells expressed CDX2 in all patients (14/14), MUC2 and CD10 in 92.9% (13/14), MUC5AC in 14% (2/14), and no expression of MUC6, showing an intestinal phenotype. Ki-67 was overexpressed with a mean labeling index of 58.3 ± 38.5%, and p-53 was overexpressed in 92.9% (13/14), regardless of the dysplastic grade. The IGD rarely occurs in Hp-naïve patients with distinctive clinicopathologic characteristics.
Related Concept Videos
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Gastritis-I: Introduction and Types
Acute gastritis presents as a sudden inflammation triggered by various stressors to the stomach lining, such as exposure to corrosive agents, local irritants like aspirin and other NSAIDs, alcohol consumption, radiation therapy, physical trauma, severe burns, sepsis,...
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...

