A 67-year-old woman underwent a laparoscopic distal pancreatectomy for pancreatic body cancer. On postoperative day (POD) 23, the patient presented with epigastric pain and was diagnosed with delayed peripancreatic fluid collection, which was treated with antibiotics and percutaneous drainage. On POD 51, the patient developed recurrent epigastric pain. Laboratory tests revealed elevated pancreatic enzyme and inflammatory marker levels. Computed tomography revealed acute pancreatitis and a high-density area in the duodenal papilla suggestive of a foreign body. Endoscopic retrograde cholangiopancreatography revealed that the surgical staples were impacted in the minor duodenal papilla and were successfully removed. Although pancreatography did not demonstrate residual staples, three additional staples were subsequently removed from the pancreatic duct. Pancreatitis improved after endoscopic treatment, and the patient was discharged. This case suggests that the migration of staples used during surgery may be a contributing factor to postoperative pancreatitis.
ABSTRACT Endoscopic subepithelial dissection is a minimally invasive treatment for superficial pharyngeal neoplastic lesions, requiring preservation of important neural structures such as the internal branch of the superior laryngeal nerve (ibSLN). We report a case in which red dichromatic imaging (RDI) appeared to improve the visualization of a linear structure presumed to be the ibSLN compared with white‐light imaging (WLI). A 57‐year‐old woman underwent endoscopic subepithelial dissection for a 5‐mm superficial lesion on the pharyngoepiglottic fold. Both WLI and RDI revealed a whitish linear structure beneath the lesion, which was presumed to represent the ibSLN based on its anatomical location and course. The presumed nerve structure appeared to be more clearly delineated with RDI than with WLI before mucosal incision and remained identifiable after submucosal injection and during dissection. This enhanced visualization may have helped guide the selection of the mucosal incision line and dissection plane. En bloc resection was achieved without apparent nerve injury. No dysphagia, hoarseness, or other adverse events occurred postoperatively. These findings suggest that RDI may serve as a useful adjunct for visualization of the structure presumed to represent the ibSLN during pharyngeal endoscopic subepithelial dissection and may support nerve‐preserving strategies.
ABSTRACT Background and Aims Esophageal squamous cell carcinoma (ESCC) detection is crucial for improving survival. While narrow‐band imaging (NBI) improves mucosal visualization, limitations remain. We evaluated the diagnostic performance of the Spectrum‐Aided Vision Enhancer (SAVE), an algorithmic NBI‐like technology reconstructed from white light imaging (WLI). Methods We conducted a retrospective, image‐based exploratory feasibility study to descriptively evaluate the diagnostic performance of WLI, NBI, and SAVE. A dataset of 1350 still endoscopic images (450 each for WLI, NBI, and SAVE) across normal mucosa, dysplasia, and ESCC stages from 158 patients was blindly reviewed by three endoscopists with different experience levels (3, 5, and 15 years). Diagnostic metrics included sensitivity, specificity, accuracy, and reading time. Results For ESCC, SAVE demonstrated diagnostic performance metrics (sensitivity: 0.81–0.97, specificity: 0.85–0.96) that were numerically similar to WLI and NBI. For dysplasia detection, SAVE had lower observed sensitivity (0.39–0.62) compared to NBI (0.55–0.85) across all observers, representing a clinical limitation for precancerous screening in its current format. Mean per‐image reading times were similar across WLI, NBI, and SAVE. Conclusions In this retrospective study, SAVE showed diagnostic potential for ESCC, with observed diagnostic performance metrics numerically similar to those of WLI and NBI in this exploratory dataset, but lacked sensitivity for dysplasia. These findings are hypothesis‐generating and warrant further prospective, multicenter validation to refine the algorithm for early cancer detection.
ABSTRACT Pyloric gland adenoma (PGA) is a rare gastric epithelial neoplasm often associated with autoimmune or metaplastic atrophic gastritis. An 80‐year‐old man underwent serial upper gastrointestinal endoscopy. A small gastric fundus lesion initially resembling a fundic gland polyp (FGP) was followed without biopsy. Over 11 years, it enlarged to 22 mm and became increasingly whitish, against a background described endoscopically as nonatrophic. Biopsy suggested PGA, and the lesion was resected en bloc by endoscopic submucosal dissection. Closely packed pyloric‐type glands showed elongation, tortuosity, branching, and cystic dilatation, with diffuse MUC6 expression and MUC5AC expression restricted to the surface epithelium. The lesion was diagnosed as PGA with low‐grade dysplasia. The adjacent oxyntic mucosa showed no atrophy, lymphoplasmacytic infiltration, or nodular enterochromaffin‐like cell hyperplasia. Without an initial biopsy, whether the lesion was already PGA or developed within a pre‐existing FGP remains unknown. An enlarging or increasingly whitish FGP‐like lesion warrants histologic assessment, even in nonatrophic gastric mucosa.
ABSTRACT Fundic gland polyps (FGPs) may enlarge during long‐term proton pump inhibitor (PPI) therapy, potentially in association with acid suppression and hypergastrinemia. Potassium‐competitive acid blockers (PCABs) provide potent and sustained acid suppression and may induce comparable or greater elevations in serum gastrin levels than PPIs. We report a case of FGPs in which regression was documented after changes in acid‐suppressive therapy, with no subsequent re‐enlargement during long‐term use of PCABs. A woman in her 60s with gastroesophageal reflux disease developed progressive enlargement of FGPs during 7 years of rabeprazole therapy. Rabeprazole was discontinued because of marked redness of the enlarged FGPs and concern for possible bleeding and was replaced with an H2‐receptor antagonist. After reintroduction of rabeprazole, treatment was switched to a PCAB because of insufficient symptom control. Four months after PCAB initiation, esophagogastroduodenoscopy demonstrated marked regression of the FGPs, with no subsequent re‐enlargement during continued PCAB therapy. Serum gastrin levels were elevated at both measurements during PCAB use (491.9 and 753.7 pg/mL). Histological examination revealed similar fundic gland changes characteristic of FGPs in both a residual polyp and the endoscopically non‐polypoid background mucosa, without dysplasia. Because the exact timing of FGP regression could not be determined, the regression observed 4 months after vonoprazan initiation cannot be solely attributed to vonoprazan therapy and may have occurred, at least in part, during the preceding period of PPI discontinuation. Nevertheless, no subsequent re‐enlargement was observed during long‐term vonoprazan therapy. Clinical Trial Registration: Clinical trial registration was not applicable because this was a single case report.
