title: Dysplasia-like epithelial atypia in ischemic bowel disease.
abstract: Inflammatory and reactive conditions are known to mimic dysplasia or malignancy in the gastrointestinal tract. Epithelial atypia that closely mimics low-grade dysplasia (LGD) or high-grade dysplasia (HGD) can sometimes be seen in ischemic bowel. To study this phenomenon, we evaluated surgical resections for ischemic enteritis (n = 65) and ischemic colitis (n = 99) that included sections of viable epithelium adjacent to necrosis. Viable epithelium was classified as normal, obviously reactive, LGD-like atypia or high-grade dysplasia (HGD)-like atypia. Cases with available paraffin blocks were characterized immunohistochemically with antibodies to p16, p53, and MIB-1. Fourteen dysplastic lesions in chronic ulcerative colitis served as controls. Dysplasia-like atypia was found in 13 small bowel resections (20%) and 15 colectomies (15%), most common near re-epithelializing erosions. Two colectomies had extensive dysplasia-like atypia, whereas the other 26 demonstrated focal or several foci of atypia. Nine cases contained HGD-like atypia, 15 contained LGD-like atypia, and 4 showed both HGD- and LGD-like atypia. Features indicating subacute-to-chronic ischemia were more frequent in LGD-like atypia (13/15, 87%) than HGD-like atypia (2/9, 22%; P = .003). Dysplasia-like atypia showed overexpression of p16 (73%), p53 (50%), and MIB-1 (92%), but these markers did not reliably distinguish dysplasia-like atypia from true dysplasia in chronic ulcerative colitis (P = .45 for p16, P = .51 for p53, P = .08 for MIB-1). These results underscore the frequency of dysplasia-like atypia in ischemic bowel, which can occasionally be an extensive and worrisome finding. Distinction from true dysplasia requires recognizing the context of the epithelial atypia because cell cycle markers were not helpful in classifying individual cases.
authors.affiliation: Department of Pathology, MD Anderson Cancer Center, Houston, TX.
authors.forename: Susan C
authors.initials: SC
authors.lastname: Abraham
authors.affiliation: Department of Pathology, MD Anderson Cancer Center, Houston, TX.
authors.forename: Melissa W
authors.initials: MW
authors.lastname: Taggart
authors.affiliation: Department of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN.
authors.forename: Edward V
authors.initials: EV
authors.lastname: Loftus
authors.affiliation: Division of Anatomic Pathology, Mayo Clinic, Rochester, MN. Electronic address: wu.tsungteh@mayo.edu.
authors.forename: Tsung-Teh
authors.initials: TT
authors.lastname: Wu
mesh_terms: D017091:Colitis, Ischemic / Q000378:metabolism / Q000473:pathology*; D003093:Colitis, Ulcerative / Q000378:metabolism / Q000473:pathology; D003106:Colon / Q000378:metabolism / Q000473:pathology*; D019941:Cyclin-Dependent Kinase Inhibitor p16; D006801:Humans; D006965:Hyperplasia / Q000378:metabolism / Q000473:pathology; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology*; D019394:Ki-67 Antigen / Q000378:metabolism; D009363:Neoplasm Proteins / Q000378:metabolism; D012189:Retrospective Studies; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: C000614131:CDKN2A protein, human; D019941:Cyclin-Dependent Kinase Inhibitor p16; D019394:Ki-67 Antigen; D009363:Neoplasm Proteins; D016159:Tumor Suppressor Protein p53
keywords: Atypia; Dysplasia; Inflammatory bowel disease; Ischemia; Ischemic colitis; Ulcerative colitis