Department of Pathology, MD Anderson Cancer Center, Houston, TX.
Department of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN.
Hum Pathol. 2014 Jul;45(7):1348-57. doi: 10.1016/j.humpath.2014.03.009. Epub 2014 Apr 4.
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.
已知炎症和反应性疾病可模拟胃肠道的发育不良或恶性肿瘤。在缺血性肠病中,有时可以看到类似于低级别发育不良(LGD)或高级别发育不良(HGD)的上皮异型性。为了研究这一现象,我们评估了 65 例缺血性肠炎和 99 例缺血性结肠炎的手术切除标本,其中包括紧邻坏死的存活上皮组织的切片。将存活上皮组织分为正常、明显反应性、LGD 样异型性或 HGD 样异型性。有石蜡块的病例用 p16、p53 和 MIB-1 抗体进行免疫组织化学染色。慢性溃疡性结肠炎的 14 个发育不良病变作为对照。在 13 例小肠切除术(20%)和 15 例结肠切除术(15%)中发现了发育不良样异型性,最常见于再上皮化的糜烂附近。2 例结肠切除术有广泛的发育不良样异型性,而其他 26 例则表现为局灶性或多发性异型性。9 例含有 HGD 样异型性,15 例含有 LGD 样异型性,4 例同时含有 HGD 和 LGD 样异型性。在 LGD 样异型性(13/15,87%)中,提示亚急性至慢性缺血的特征比 HGD 样异型性(2/9,22%)更为常见(P =.003)。发育不良样异型性显示 p16(73%)、p53(50%)和 MIB-1(92%)的过度表达,但这些标志物不能可靠地区分缺血性肠病中的发育不良样异型性与慢性溃疡性结肠炎中的真正发育不良(p16 的 P =.45,p53 的 P =.51,MIB-1 的 P =.08)。这些结果强调了缺血性肠病中发育不良样异型性的频率,这种异型性偶尔会是广泛而令人担忧的发现。要将其与真正的发育不良区分开来,需要识别上皮异型性的背景,因为细胞周期标志物在分类个别病例时没有帮助。