Etiology and Histomorphology of Esophagogastric Junction Intramucosal Adenocarcinoma (IMC): In Comparison to Esophageal IMC
Hui Zhu, Zhigang Li, Hao Xie, Thomas W Rice, Lisa A Rybicki, John R Goldblum, Xiuli Liu. Cleveland Clinic Foundation, Cleveland, OH; Second Military Medical University, Shanghai, China
Background: While it is clear Barrett Esophagus (BE) predisposes to esophageal adenocarcinoma, controversy exists regarding the etiology of esophagogastric junction (EGJ) adenocarcinoma. The aim of this study is to evaluate the clinical and pathologic features of EGJ IMC and compare them to IMC of the distal esophagus, as these tumors are smaller than more deeply invasive ones and allow for a better comparison of the surrounding mucosal changes which are often obscured by larger tumors.
Design: 149 cases of IMC from an esophagectomy database (1983 – 2010) were identified by reviewing medical charts and slides from these resection specimens. Clinicopathologic features were compared between IMC arising in the esophagus versus EGJ.
Results: Of these 149 cases; 54 cases (36.2%) were EGJ and 95 (63.7%) were esophageal IMC. Mean age and gender were not significantly different between these two groups [(61.8 yrs vs. 64.7, p=0.12; 92.6% male vs. 83.2%, p=0.14)]. Hiatal hernia was present in 87.5% and 90.5% of EGJ and esophageal IMC (p=0.51); hiatal hernia length was shorter in patients with EGJ IMC [median: 3 cm vs. 4 cm, p = 0.007)]. Compared with esophageal IMC, intestinal metaplasia (IM) in the esophagus was absent in 8 of 54 EGJ IMC (14.8% vs. 0%, p<0.001) and lack of dysplasia in IM of the esophagus was noted in patients with EGJ IMC (18.8% vs. 4.2%, p=0.012). Tumor histomorphologic features including macroscopic abnormalities, focality, size, depth of invasion, grade, and lymphovascular invasion were similar. Both EGJ and esophageal IMC had low rates of nodal metastasis (0% and 1.1%). Of the 8 EGJ IMC patients without esophageal IM, 3 had long-standing GERD, 3 had cardia/EGJ IM associated with chronic gastritis (2) and reflux (1), 1 had a clinical history of familial adenomatous polyposis (FAP), and 1 had no apparent gastric or esophageal diseases.
Conclusions: Similar to esophageal IMC, most EGJ IMC arise in patients with reflux disease and intestinal metaplasia with hiatal hernia, but hiatal hernias were shorter compared with esophageal IMC patients. About 7.5% EGJ IMC occurred in patients without GERD and may be associated with H. pylori infection or genetic predilection. Our study supports the current view that EGJ and esophageal IMC in the USA share similar etiology, tumor morphology and clinical behavior.
Wednesday, March 6, 2013 1:00 PM
Poster Session VI # 87, Wednesday Afternoon