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We report a gastric foveolar-type hyperplastic polyp of the duodenum harboring mutations in the GNAS and KRAS genes. The lesion was incidentally detected during a routine upper gastrointestinal endoscopy in a man in his 50s. It appeared as a 10-mm elevated lesion located at the superior duodenal angle. The surrounding mucosa showed no endoscopic evidence of gastric foveolar metaplasia (GFM) or heterotopic gastric mucosa (HGM). Endoscopic mucosal resection was performed as diagnostic treatment. Histopathology showed a diffuse, monotonous proliferation of gastric foveolar-type epithelial cells without cytological dysplasia, and immunohistochemical analysis showed diffuse positivity for MUC5AC. Genetic analysis revealed activating mutations in both the GNAS and KRAS genes. Based on these findings, the final diagnosis was a gastric foveolar-type hyperplastic polyp harboring GNAS and KRAS mutations. Such mutations have also been reported in pyloric gland adenomas and gastric-type duodenal adenocarcinomas. Proximal non-ampullary duodenal epithelial tumors are often linked to a gastric-type mucin phenotype with higher malignant potential. Potential precursor lesions for carcinomas proximal to the ampulla include GFM and HGM. This case supports the hypothesis that some duodenal lesions with the gastric-mucin phenotype may harbor molecular alterations typically associated with neoplastic processes despite their non-neoplastic appearance, suggesting a potential role as precursors to neoplasia.

In endoscopic full-thickness resection (EFTR), luminal collapse can occur due to communication between the gastrointestinal lumen and peritoneal cavity, making visualization and procedural continuity difficult. We propose the underwater pressure lumen expansion (UPLE) method, in which hydraulic pressure is applied in a fluid-filled environment to re-expand the collapsed lumen, thereby restoring visualization and allowing continued endoscopic manipulation. The UPLE method was applied during peroral endoscopic tumor resection in a clinical case and in an animal model of EFTR, and its utility was successfully demonstrated.

Enterocolitis is a common gastrointestinal manifestation of immune-related adverse events (irAEs); however, only a few studies have reported on irAE enteritis with localized active inflammation in the small intestine. Here, we report the case of a 74-year-old man who developed diarrhea, abdominal pain, and oral intake difficulty and was subsequently hospitalized after receiving atezolizumab for pulmonary adenocarcinoma. Computed tomography and enterocolonoscopy revealed active inflammation in the small intestine but not in the colon, leading to the final diagnosis of irAE enteritis. After initiating prednisolone at a dose of 60 mg/day, his symptoms improved rapidly, and a follow-up enterocolonoscopy revealed a marked reduction in inflammation. Being a relatively rare gastrointestinal toxicity, irAE enteritis often goes unrecognized due to diagnostic challenges, but can lead to serious AEs such as perforation. Therefore, even if colonoscopy findings are normal, a thorough examination of the small intestine is essential for patients who develop gastrointestinal symptoms while undergoing immune checkpoint inhibitor therapy. We herein report a rare case of irAE enteritis confirmed through endoscopic and pathological examination, which has not been previously reported.

Ulcerative colitis (UC) predominantly affects the colon; upper gastrointestinal involvement (UGI) has been reported, but no established treatments exist. We report two cases of UC with concomitant UGI that showed positive responses to vedolizumab therapy. Case 1 involved a 29-year-old man who developed continuous inflammation extending from the stomach to the jejunum 1 month after an initial UC diagnosis. Intravenous prednisolone provided clinical remission; however, maintenance therapy with oral azathioprine was unsuccessful. Vedolizumab was initiated. Three months later, esophagogastroduodenoscopy (EGD) and colonoscopy confirmed the resolution of inflammation. Case 2 involved a 19-year-old man diagnosed with UGI via endoscopy while being evaluated for nausea and fever during UC treatment. 5-aminosalicylic acid and prednisolone therapies were ineffective; therefore, vedolizumab was administered. Three months later, EGD confirmed mucosal healing. Both patients have maintained clinical remission for >2 years. To our knowledge, this is the first report of UC with UGI involvement that was successfully treated with vedolizumab. These findings suggest that vedolizumab is effective and safe for UGI treatment.