Abstract

We present the case of a 69-year-old female undergoing esophagogastroduodenoscopy for iron-deficiency anemia investigation. She reported intermittent bloating, nausea and vomiting. A pedunculated polyp was identified arising from the greater curvature of the middle gastric body, with a long fibroelastic stalk (30mm) and a 60mm congestive head that prolapsed towards the pyloric ring, causing a complete gastric outlet obstruction (GOO). An en-block polypectomy was performed. An intraprocedural oozing bleeding from a large visible vessel at the residual stalk was managed using endoloop®. Histo-immunohistochemistry showed a R0-resection of a mixed-type gastric pyloric gland adenoma (PGA) positive for MUC-5AC and MUC-6 mucins, in a surrounding H. pylori-negative non-atrophic chronic gastritis. She became asymptomatic with anemia resolution. Adenomas account for up to 10% of gastric polyps. Histologically, they are categorized into intestinal, foveolar, pyloric and oxyntic types (1). PGA is a rare subtype, accounting for less than 3% of all gastric polyps (2). PGAs are usually solitary at gastric body, and occur in association with autoimmune gastritis, H. pylori and chemical gastritis (2). A normal background gastric mucosa has also been described (35.8%) (3). PGAs are devoid of apical mucin cap and label by both MUC-5AC and MUC-6 (2). Choi et al. (3) defined three PGA immunohistochemical phenotypes: pure pyloric-type (25.4%), with strong MUC-6 expression; predominant foveolar-type (3%), with MUC-5AC diffuse expression but ≤10% of MUC-6 expression and no foveolar differentiation; and mixed-type (61.2%), with variable MUC-5AC/MUC-6 expression. Most PGAs are asymptomatic, but clinically significant because of their potential for malignant transformation (12-47%) and complications, including gastrointestinal bleeding and obstruction (1, 3). GOO is rare, causing intermittent symptoms by polyp intussusception (ball-valve-syndrome) (4, 5). PGA management is challenging, depending on size, morphology and location. This case illustrates a successful endoscopic resection as a minimally invasive procedure of a doubly complicated PGA.

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