Cao Qin, Ran Zhi Hua, Xiao Shu Dong
Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiaotong University, China.
J Dig Dis. 2007 Feb;8(1):15-22. doi: 10.1111/j.1443-9573.2007.00271.x.
Currently the screening and diagnosis of gastric cancer and atrophic gastritis are mainly made by endoscopy and biopsy. The aim of this study was to evaluate the use of serum tests: serum pepsinogen I (PGI pepsinogen I/II ratio (PGR), gastrin-17 (G-17) and H. pylori-immunoglobulin G (IgG) antibodies to screen atrophic gastritis and gastric cancer.
A total of 458 patients were recruited, and each underwent endoscopy with biopsies before the serum tests were performed. These patients were divided into five groups based on the endoscopic and histological findings: 92 patients in the atrophic gastritis group, 58 in the gastric ulcer group, 90 in the duodenal ulcer group, 141 in the gastric cancer group (40 early gastric cancer and 101 advanced gastric cancer) and 77 (including mild non-atrophic gastritis) served as a control group. Serum samples for PGI and II, G-17, and H. pylori-IgG antibodies estimation were analyzed by ELISA.
PGI and PGR values decreased significantly both in atrophic gastritis and gastric cancer groups (P<0.01). For the best discrimination of atrophic gastritis, the cut-off values of PGI and PGR were 82.3 microg/L and 6.05, respectively. The PGI, PGR and G-17 values were related significantly with the grades and/or sites of atrophic gastritis (P<0.01). Patients with atrophic corpus gastritis had low PGI and PGR values and high G-17 level, and patients with atrophic antral gastritis had low G-17 level. G-17 increased significantly in the gastric cancer group (P<0.01). PGI and PGR values were significantly lower in patients with advanced gastric cancer than in patients with early gastric cancer, while there was no difference in G-17 level between them. The positivity rate of H. pylori-IgG antibodies was 54.55% in the control group. The PGI level was higher in H. pylori positive patients than in H. pylori negative ones (P<0.001), while there was no difference in G-17 level between them. The positivity rates of H. pylori-IgG antibodies were over 85% in all other four groups.
Low serum PGI, PGR and G-17 values are biomarkers of atrophic antral gastritis. Atrophic be screened by serum PGI and PGR values. Gastric cancer can be screened on the basis of increased serum G-17 and remarkedly low serum PGI and PGR values. The H. pylori infection is related to the change of PG level.
目前胃癌和萎缩性胃炎的筛查与诊断主要依靠内镜检查及活检。本研究旨在评估血清学检测:血清胃蛋白酶原I(PGI)、胃蛋白酶原I/II比值(PGR)、胃泌素-17(G-17)及幽门螺杆菌免疫球蛋白G(IgG)抗体用于筛查萎缩性胃炎和胃癌的应用价值。
共纳入458例患者,在进行血清学检测前均接受了内镜检查及活检。根据内镜及组织学检查结果将这些患者分为五组:萎缩性胃炎组92例,胃溃疡组58例,十二指肠溃疡组90例,胃癌组141例(早期胃癌40例,进展期胃癌101例),77例(包括轻度非萎缩性胃炎)作为对照组。采用酶联免疫吸附测定法(ELISA)分析用于评估PGI、II、G-17及幽门螺杆菌IgG抗体的血清样本。
萎缩性胃炎组和胃癌组的PGI及PGR值均显著降低(P<0.01)。为最佳鉴别萎缩性胃炎,PGI及PGR的临界值分别为82.3μg/L和6.05。PGI、PGR及G-17值与萎缩性胃炎的分级和/或部位显著相关(P<0.01)。胃体萎缩性胃炎患者PGI及PGR值低而G-17水平高,胃窦萎缩性胃炎患者G-17水平低。胃癌组G-17显著升高(P<0.01)。进展期胃癌患者的PGI及PGR值显著低于早期胃癌患者,而二者G-17水平无差异。对照组幽门螺杆菌IgG抗体阳性率为54.55%。幽门螺杆菌阳性患者的PGI水平高于阴性患者(P<0.001),而二者G-17水平无差异。其他四组幽门螺杆菌IgG抗体阳性率均超过85%。
血清PGI、PGR及G-17值降低是胃窦萎缩性胃炎的生物标志物。萎缩性胃炎可通过血清PGI及PGR值进行筛查。胃癌可基于血清G-17升高及血清PGI和PGR值显著降低进行筛查。幽门螺杆菌感染与PG水平变化有关。