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Serum pepsinogen levels can quantify the risk of development of metachronous gastric cancer after endoscopic resection

Authors :
Jun Kato
Mikitaka Iguchi
Kosaku Moribata
Hideyuki Tamai
Kazuhiro Fukatsu
Toru Niwa
Yasuhide Yamamoto
Takao Maekita
Izumi Inoue
Kenichiro Nakachi
Yoshimasa Maeda
Takeichi Yoshida
Yoshiyuki Mori
Naoki Shingaki
Masao Ichinose
Hisanobu Deguchi
Source :
International Journal of Cancer. 139:1150-1156
Publication Year :
2016
Publisher :
Wiley, 2016.

Abstract

We have previously reported that serum pepsinogen (PG) can quantify the level of gastric mucosal atrophy, and that H. pylori eradication reduces cancer development in subjects with mild atrophy identified by serum PG levels. The aim of this study was to elucidate the predictive ability of serum PG levels for the development of metachronous gastric cancer (MGC) after endoscopic resection (ER) of primary cancer in association with H. pylori eradication. A retrospective chart review was performed, and 330 patients who underwent ER for initial early gastric cancer were enrolled. Presence or absence of H. pylori, serum PG levels, and endoscopic atrophy at ER were evaluated. H. pylori eradication was performed at the patient's request after ER. The incidence of MGC in these patients was analyzed. Of 330 patients, 47 developed MGC. Endoscopic extensive atrophy was observed more frequently in patients with MGC (p = 0.001). Although PG I or PG II alone did not significantly differ according to development of MGC, the proportion of PG I/II ≤ 3.0, which is one of the criteria of PG test-positive, was significantly higher in patients with MGC (83 vs. 69%, p = 0.04). H. pylori eradication after ER did not affect MGC development (p = 0.2). On multivariate analysis, serum PG I/II ratio ≤ 3.3 was significantly associated with the development of MGC (hazard ratio: 3.66, 95% confidence interval: 1.47-12.25, p = 0.004). The risk of MGC after ER could be quantitatively predicted by the PG I/II ratio regardless of H. pylori status.

Details

ISSN :
00207136
Volume :
139
Database :
OpenAIRE
Journal :
International Journal of Cancer
Accession number :
edsair.doi...........8d4975eae74f571fe8ccaf9b80cb3de7