CASE REPORT: POST-MEGASTENT DUODENAL POLYP

Abstract

Introduction
 Most duodenal polyps are non-neoplastic. Instead, they represent regenerative/hyperplastic nodules of foveolar epithelium or Brunner gland proliferation (38%). Other less common polyps include heterotopic (6%) and neoplastic lesions (11%) (1). Adenomas of intestinal type are the most common (89%), followed by adenomatous lesions that present a gastric phenotype: PGAs (8%) and foveolar-type adenomas (3%) (2).
 Non-neoplastic duodenal polyps, most of which represent regenerative inflammatory (pseudo) polyps, are predominantly localized in the bulb (80%) (1). The majority are associated with duodenitis, especially in the setting of peptic injury, and are less commonly associated with inflammatory bowel disease or rare conditions such as primary immunodeficiencies. (3). Histologically, non-neoplastic duodenal polyps may resemble gastric hyperplastic polyps and frequently show metaplastic foveolar epithelium with active inflammation and/or erosion, reactive epithelial changes, seamless transition with the surrounding epithelium, and surface maturation. They may also simply be composed of granulation tissue. It is worth underscoring that some of these polyps are neoplastic. Some hyperplastic polyps harbor KRAS and BRAF mutations and tend to show serrated features, similar to their microvascular colonic counterparts (4). Duodenal hyperplastic polyps with KRAS mutation may represent precursor lesions of duodenal traditional serrated adenomas (4). The polypoid heterotopic gastric mucosa is another frequent type of duodenal polyps. As opposed to the peptic injury-induced foveolar metaplasia, lesions of this type also contain clusters of oxyntic glands under the surface of the foveolar epithelium. Duodenal gastric heterotopia is associated with FGPs and PPI therapy.