Gastric hamartomatous inverted polyps (GHIP) are difficult to diagnose accurately because of inversion into the submucosal layer. GHIP are diagnosed using the pathological characteristics of the tumor, including the fibroblast cells, smooth muscle, nerve components, glandular hyperplasia, and cystic gland dilatation. Although Peutz-Jeghers syndrome, juvenile polyposis, and Cowden disease are hereditary, it is rare to encounter 2 cases of monostotic and asymptomatic gastric hamartomas. The pathogeneses of hamartomatous inverted polyps and inverted hyperplastic polyps remain controversial because of the paucity of reported cases. There are 3 hypotheses regarding the pathogenesis of complete gastric inverted polyps. Based on our experience with 2 successive, rare GHIP cases, we affirm the hypothesis that after a hamartomatous change occurs in the submucosal layer, some of these components are exposed to the gastric mucosa and, consequently, form a hypertrophic lesion. In Case 1, our hypothesis explains why a tiny hypertrophic change was first detected on the top of the submucosal tumor using a detailed narrow band imaging-magnified endoscopy. There was no confirmation that the milky white mucous and calcification structures were exuding directly from the biopsy site like Case 1, and in Case 2 the presence of this mucous was indirectly confirmed during an endoscopic submucosal dissection (ESD). Regarding the pathogenesis of GHIP, a submucosal hamartomatous change may occur prior to the growth of hypertrophic portions. An en bloc resection using ESD is recommended for treatment.
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