Gastric Cancers Emerging after H. pylori Eradication Arise Exclusively from Non-Acid-Secreting Areas

Gastric Cancers Emerging after H. pylori Eradication Arise Exclusively from Non-Acid-Secreting Areas
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DOI:
10.1620/tjem.226.45
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发表时间:
2012-01-01
影响因子:
2.2
通讯作者:
Shimosegawa, Tooru
Shimosegawa, Tooru
中科院分区:
医学4区
文献类型:
--
作者:
Iijima, Katsunori;Abe, Yasuhiko;Shimosegawa, Tooru

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虽然幽门螺杆菌(H. pylori)根除对胃癌的后续发展具有一定的抑制作用,即使在成功根除后仍有散发的胃癌病例。H. pylon的根除仍有待澄清。在这项研究中,采用刚果红色素内镜,这是能够可视化的酸分泌胃底粘膜,我们调查的地形关系的酸分泌模式的发生部位的胃癌根除后出现。前瞻性入组了14例根除后新发胃癌的连续患者,定义为根除后至少2年发现的病变。用刚果红染色内镜评价肿瘤是否来自泌酸区或非泌酸区。从这两个地区采取的活检标本进行组织学评价和免疫组化Ki-67和p53。从根除到随后发生胃癌的平均时间为74(44)个月。5例患者有2个癌病灶,因此14例患者共有19个病灶。刚果红染色内镜检查显示,所有19个病变完全来自非酸分泌区。组织学检查显示持续的过度增殖和积累的p53蛋白是经常检测到的非酸分泌区。根除后残留的非泌酸区似乎已经存在基因改变(如p53突变),这些区域可能是根除后胃癌发生的起源。确定这些高风险地区应该是一个有前途的方法,估计个人的癌症风险后,根除。
Although Helicobacter pylori (H. pylori) eradication has some inhibitory effects on the subsequent development of gastric cancer, there are sporadic cases of gastric cancer even after successful eradication. The pathogenesis of gastric cancer emerging after H. pylon eradication remains to be clarified. In this study, employing Congo-red chromoendoscopy, which is capable of visualizing the acid-secreting fundic mucosa, we investigated the topographic relationship of the acid secretion pattern to the occurrence site of gastric cancers emerging after eradication. Fourteen consecutive patients who suffered from new gastric cancer after eradication, defined as lesions that were discovered at least 2 years after the eradication, were prospectively enrolled. Whether the neoplasias arose from acid-secreting or non-acid-secreting areas was evaluated with Congo-red chromoendoscopy. Biopsy specimens taken from the two areas were subjected to histologic evaluation and immunohistochemistry for Ki-67 and p53. The mean period from the eradication to the subsequent occurrence of gastric cancer was 74 (44) months. There were two cancer lesions in 5 cases, and thus there was a total 19 lesions from 14 cases. Congo-red chromoendoscopy revealed that all 19 lesions arose exclusively from non-acid-secreting areas. Histological examination revealed sustained hyperproliferation and accumulation of p53 protein was frequently detectable in non-acid-secreting areas. Genetic alteration such as p53 mutation seems to be already present in the residual non-acid-secreting areas after eradication, areas that could be the origin of gastric carcinogenesis after eradication. Identification of such high-risk areas should be a promising approach for estimating the individual cancer risk after eradication.