Polypoid dysplasia in Barrett's esophagus: A clinicopathologic, immunohistochemical, and molecular study of five cases

Dysplasia in Barrett's esophagus (BE) is a precursor to adenocarcinoma and most commonly occurs as a flat, grossly undetectable lesion. Rarely, dyspla sia in BE may grow as a polypoid lesion. Most BE-associated polypoid dyspla stic lesions have been referred to as "adenomas" because of their histologi cal similarity to a colonic adenoma. BE-associated polypoid dysplastic lesi ons have been less well characterized than the flat type. Therefore, our ai m was to characterize the clinicopathologic and molecular features of five cares of BE-associated polypoid dysplasia and to review the literature on t his entity. The cases were evaluated clinically, histologically, immunostai ned for MIB-1 and p53, and genotyped for loss of heterozygosity (LOH) at th e adenomatous polyposis coli (APC) locus. Mucosal biopsy specimens of five BE patients without dysplasia, and five BE cases with high-grade flat dyspl asia, were used as controls. The study patients were all male (average age, 71 years) who presented with symptoms of gastroesophageal reflux disease. Endoscopically, all five cases had a well-defined sessile or pedunculated p olypoid lesion ranging from 0.4 to 1.5 cm in size in the mid (n = 1) or dis tal (n = 4) esophagus and were associated with specialized-type BE (four lo ng segment, one short segment). Histologically, the polyps consisted of int estinalized epithelium with low- and high-grade dysplasia. All five cases c ontained adenocarcinoma (four within the polyp, one in adjacent BE). All po lyps showed increased cell proliferation in the form of surface MiB-1 stain ing and showed positive p53 staining. Three of three (100%) informative cas es showed LOH at the APC locus in the dysplastic epithelium and in areas of adenocarcinoma. All five flat dysplasia controls also showed surface MIB-1 staining and p53 positivity, and three of three informative controls showe d LOH for APC. None of the nondysplastic BE controls showed any of these fi ndings. Three patients were treated with esophagectomy and two with polypec tomy. All were alive, without metastasis, from 2 months to 6 years later. A literature review of esophageal "adenomas" uncovered 12 cases. Four of the se had no clinical or pathological information, two were, in fact, gastric heterotopic lesions, one was composed entirely of intestinal-type epitheliu m, and five were polypoid dysplastic lesions similar to the cases described here (three male, two female; mean age, 59 years). Four of these five case s were associated with adenocarcinoma in the polyp (two intramucosal, two s ubmucosal). In summary, BE-associated polypoid dysplasia share similar clin ical, pathological, and molecular features as flat dysplasia and are often associated with adenocarcinoma. Thus, we agree with other authors who recom mend that the term adenoma, which usually carries a benign connotation, be abandoned in favor of a descriptive diagnostic term, such as "BE-associated polypoid dysplasia." BE patients with this lesion should be considered str ong candidates for esophageal resection similar to lesions of this kind tha t occur in inflammatory bowel disease. Copyright (C) 1999 by W.B. Saunders Company