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Grading of gastric foveolar-type dysplasia in Barrett's esophagus

机译:在巴雷特食管中胃小叶型不典型增生的分级

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Dysplasia is the gold standard biomarker of cancer risk in Barrett's esophagus, but its diagnosis remains difficult. This is due in part to its multitude of histological appearances. One aspect receiving little attention concerns gastric-type Barrett's dysplasia, which is distinctly different from the well-established intestinal variant. Recognition of gastric-type dysplasia and development of separate grading criteria are required. The prevalence, diagnostic criteria, and natural history of gastric-type Barrett's dysplasia were systematically evaluated in 1854 endoscopic biopsies from a cohort of 200 consecutive Barrett's dysplasia patients. Goblet cells were present in all cases, confirming the utility of this defining feature of Barrett's esophagus. The prevalence of Barrett's gastric-type dysplasia was 15% at the patient level (30 of 200 patients) and 20% at the biopsy level (166 of 852 dysplastic biopsies). Gastric-type dysplasia uniformly showed non-stratified, basally oriented nuclei as the major criterion for distinguishing it from intestinal-type Barrett's dysplasia. As such, loss of nuclear polarity, as the most objective criterion to distinguish intestinal-type low- and high-grade dysplasia, cannot be applied to gastric-type dysplasia. Rather, discriminatory features included increased nuclear size with a high-grade dysplasia cutoff by receiver operating characteristic (ROC) analysis approximating 3–4 times the size of a mature lymphocyte, providing an optimal sensitivity, specificity, and area under the curve of 0.78, 0.90, and 0.90 (95% CI: (0.87, 0.93)), respectively. Crowded, irregular glandular architecture (PPPPPP<0.001). During follow-up, 64% (7 of 11) of patients with pure gastric and 26% (5 of 19) with mixed gastric and intestinal dysplasia underwent neoplastic progression. The recognition of Barrett's gastric-type dysplasia and use of the proposed grading criteria should promote better diagnostic classification of the Barrett's neoplastic spectrum.
机译:不典型增生是巴雷特食管中癌症风险的金标准生物标志物,但其诊断仍然很困难。这部分是由于其大量的组织学表现。很少引起关注的方面涉及胃型Barrett发育异常,与公认的肠道变异明显不同。需要识别胃型发育异常并制定单独的分级标准。在1854年的200例连续Barrett发育不良患者队列中,对胃型Barrett发育不良的患病率,诊断标准和自然病史进行了系统评估。在所有情况下都存在杯状细胞,这证实了Barrett食道这一定义特征的实用性。在患者水平上,Barrett胃型异型增生的发生率为15%(200名患者中的30名),在活组织检查水平(852例发育不良的活检中)为20%。胃型异型增生均匀地显示出非分层的,基础取向的细胞核是区别于肠型Barrett型异型增生的主要标准。因此,作为区分肠型低度和高级不典型增生的最客观标准,核极性的丧失不能应用于胃型不典型增生。相反,歧视性特征包括通过接受者工作特征(ROC)分析得出的核大小增加和高度不典型增生,大约是成熟淋巴细胞大小的3-4倍,从而提供了最佳的敏感性,特异性和0.78曲线下的面积,分别为0.90和0.90(95%CI:(0.87,0.93))。拥挤的不规则腺体结构(PPPPPP <0.001)。在随访期间,有64%(11人中的7人)的纯胃和26%(19人中的5人)的胃和肠混合性异型增生发生了肿瘤进展。对Barrett胃异型增生的认识和建议的分级标准的使用应促进Barrett肿瘤谱的更好的诊断分类。

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