胃蛋白酶原、胃泌素17与胃癌前病变进展风险的纵向研究

Longitudinal Study on the Relationship between Pepsinogen, Gastrin-17 and the Risk of Gastric Precancerous Lesions

摘要: 目的：探讨血清胃蛋白酶原I、II (pepsinogen, PGI、II)与胃泌素-17 (gatrin-17, G-17)在胃癌前病变中的诊断价值。方法：选择2018年1月~10月有消化道症状患者98例，根据胃镜检查及病理结果分为胃溃疡组(32例)、萎缩性胃炎组(21例)、肠上皮化生组(25例)、低级别上皮内瘤变组(20例)，选取同期30例非萎缩性胃炎者作为对照组。应用ELISA法检测比较五组血清PGI、PGII、胃蛋白酶原比值(PGR即PGI/PGII比值)、G-17水平。结果：胃溃疡组PGI、PGII水平明显高于萎缩性胃炎组、肠上皮化生组、低级别上皮内瘤变组及对照组，差异有统计学意义(P < 0.05)；PGR值变化不明显，差异无统计学意义(P > 0.05)。萎缩性胃炎组、肠上皮化生组、低级别上皮内瘤变组中PGI、PGR值低于对照组，差异有统计学意义(P < 0.05)；萎缩性胃炎组、肠上皮化生组、低级别上皮内瘤变组间PGI、PGR水平值比较无明显差异(P > 0.05)。萎缩性胃炎组、肠上皮化生组、低级别上皮内瘤变组与对照组PGII比较无统计学意义(P > 0.05)。萎缩性胃炎组血清G-17水平与对照组比较，差异无统计学意义(P > 0.05)；胃溃疡组、肠上皮化生组、低级别内瘤变组血清G-17均显著高于对照组与萎缩性胃炎组，差异有统计学意义(P < 0.05)。胃溃疡组、肠上皮化生组、低级别内瘤变组间G-17比较，差异无统计学意义(P > 0.05)。结论：血清PGI、PGII、PGR以及G-17的变化对胃癌前病变进展风险有一定的临床价值，值得我们深入研究。

Abstract: Objective: To explore the diagnostic value of serum pepsinogen and gastrin-17 in precancerous lesions of gastric cancer. Methods: From January to October 2018, 98 patients with digestive tract symptoms were divided into three groups according to gastroscopy and pathology: gastric ulcer group (n = 32), atrophic gastritis group (n = 21), intestinal metaplastic group (n = 25) and low grade intraepithelial neoplastic group (n = 20). In the same period, 30 healthy subjects were selected as the control group. ELISA method was used to detect and compare the levels of serum PGI, PGII and PGR, G-17 in the five groups. Results: The level of PGI, PGII in gastric ulcer group was significantly higher than that in atrophic gastritis group, intestinal metaplastic group, low grade intraepithelial neoplastic group and control group (P < 0.05), but there was no significant difference in PGR value between the two groups (P > 0.05). PGI and PGR values in atrophic gastritis group, intestinal epithelial metaplasia group and low-grade intraepithelial neoplasia group were lower than those in control group (P < 0.05). There was no significant difference in PGI and PGR levels between atrophic gastritis group, intestinal metaplasia group and low-grade intraepithelial tumor group (P > 0.05). There was no significant difference in PGII between atrophic gastritis group, intestinal metaplastic group and low grade intraepithelial neoplastic group compared with the control group (P > 0.05). There was no significant difference in serum G-17 level between atrophic gastritis group and control group (P > 0.05), but the serum G-17 level in gastric ulcer group, intestinal metaplastic group and low grade intratumor group was significantly higher than that in control group and atrophic gastritis group (P < 0.05). There was no significant difference in G-17 between gastric ulcer group, intestinal metaplastic group and low grade intratumoral degeneration group (P > 0.05). Conclusions: The changes of serum PGI, PGII, PGR and G-17 have certain clinical value in the diagnosis of precancerous lesions of gastric cancer, which is worthy of further study.