In order to clarify the carcinogenesis mechanism from chronic atrophic gastritis toward gastric cancer, we measured the pepsinogen I and II and compared their ratio with several clinical findings.

We measured the preoperative serum pepsinogen I and II by using a radio-immunoassay and compared their ratio with several clinical findings, such as tumor size, mucinous vs non-mucinous tumor, cell differentiation, tumor location, depth of invasion, lymph-node status, Lauren's classification, and peritumoral atrophy in 103 consecutive patients with gastric adenocarcinomas who had received resections at Bundang CHA Hospital during the period from July 2003 to February 2005.

There were significant differences in the serum pepsinogen I/II ratio between patients with mucinous vs non-mucinous tumors (n=4 vs 9 and mean pep I/II=1.29 vs. 2.99, P=0.0288), with tumor size more than and less than 10 cm² (n=55 vs. 48 and mean pep I/II=2.64 vs. 3.24, P=0.0491), and with or without peritumoral atrophy (n=94 vs. 9 and mean pep I/II=2.83 vs. 3.89, P=0.0466). In patients with peritomoral atrophy, the pepsinogen I/II ratio was also lower in larger tumors (n=48 vs. 46 and mean pep I/II=2.44 vs. 3.23, P=0.0083). Well-differentiated carcinomas showed significantly lower serum pep I/II ratios than signet-ring-cell types. There was no correlation between serum pep I/II ratio and tumor location, depth of invasion, lymph-node status, or Lauren's classification.

We proved the existence of a correlation between serum pepsinogen level and musosal atrophy, but these results are not sufficient for clinical application of serum pepsinogen level as a screening tool for gastric cancer.