Buttar N S, Wang K K, Sebo T J, Riehle D M, Krishnadath K K, Lutzke L S, Anderson M A, Petterson T M, Burgart L J
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic and Graduate School of Medicine, Rochester, Minnesota, USA.
Gastroenterology. 2001 Jun;120(7):1630-9. doi: 10.1053/gast.2001.25111.
BACKGROUND & AIMS: The identification of any high-grade dysplasia (HGD) in Barrett's esophagus has been considered to be an indication for esophagectomy because of the increased risk of cancer. The aim of this study was to determine if a limited extent of HGD has the same potential for cancer as diffuse HGD.
A retrospective cohort study was performed to assess the risk of developing adenocarcinoma in relationship to the extent of HGD found on endoscopic surveillance. The extent of HGD was defined as focal if cytologic and/or architectural changes of HGD were limited to a single focus of 5 or fewer crypts and diffuse if more than 5 crypts were involved in a single biopsy specimen or if HGD involved more than one biopsy fragment. The relative risk of cancer was assessed using a Cox proportional hazard model, and cancer-free survival was determined using survival curves.
Sixty-seven patients with diffuse HGD and 33 with focal HGD satisfied selection criteria. Cancer-free survival rates at 1 and 3 years were 93% and 86% for focal HGD compared with 62% and 44% for diffuse HGD (P < 0.001). On univariate analysis, extent of HGD (relative risk, 5.36; 95% confidence interval, 1.84-15.56), nodularity on endoscopy (relative risk, 3.98; 95% confidence interval, 1.97-8.04), and lack of acid suppression (relative risk, 2.48; 95% confidence interval, 1.16-5.28) were associated with an increased risk of esophageal adenocarcinoma. Diffuse HGD had a 3.7-fold increase in the risk of esophageal cancer compared with focal HGD (P = 0.02) on multivariate analysis.
Patients with focal HGD are less likely to have cancer during the first year after diagnosis or on subsequent follow-up compared with diffuse HGD.
由于巴雷特食管发生癌症的风险增加，因此将巴雷特食管中任何高级别异型增生（HGD）的识别视为食管切除术的指征。本研究的目的是确定有限范围的HGD与弥漫性HGD是否具有相同的癌变可能性。
进行了一项回顾性队列研究，以评估内镜监测发现的HGD范围与发生腺癌风险之间的关系。如果HGD的细胞学和/或结构改变局限于5个或更少腺管的单个病灶，则将HGD范围定义为局灶性；如果单个活检标本中有超过5个腺管受累，或者HGD累及多个活检片段，则定义为弥漫性。使用Cox比例风险模型评估癌症的相对风险，并使用生存曲线确定无癌生存率。
67例弥漫性HGD患者和33例局灶性HGD患者符合入选标准。局灶性HGD患者1年和3年的无癌生存率分别为93%和86%，而弥漫性HGD患者分别为62%和44%（P<0.001）。单因素分析显示，HGD范围（相对风险，5.36；95%置信区间，1.84 - 15.56）、内镜下结节形成（相对风险，3.98；95%置信区间，1.97 - 8.04）以及未进行抑酸治疗（相对风险，2.48；95%置信区间，1.16 - 5.28）与食管腺癌风险增加相关。多因素分析显示，与局灶性HGD相比，弥漫性HGD的食管癌风险增加3.7倍（P = 0.02）。
与弥漫性HGD相比，局灶性HGD患者在诊断后的第一年或后续随访中发生癌症的可能性较小。
