血清胃蛋白酶原检测对胃癌和慢性胃炎的意义

The diagnostic value of serum pepsinogen in gastric diseases and chronic gastritis

目的比较血清胃蛋白酶原（PG）在不同胃疾病中的水平，探讨其诊断胃部疾病的价值。方法选取已行胃镜检查的患者214例，按胃镜病理诊断结果分为非萎缩性胃炎组（70例）、萎缩性胃炎组（86例）、胃癌组（58例）。采用化学发光法定量测定患者空腹血清PGI和PGU，并计算PGI与PGII比值（PGR）。结果胃癌组PGI明显高于萎缩性胃炎组[（78．41±55．42）μg／L比（53．10±30．08）μg／L]，差异有统计学意义（P〈0．05），但与非萎缩性胃炎组比较差异无统计学意义（P〉0．05）；胃癌组PG Ⅱ明显高于萎缩性胃炎组和非萎缩性胃炎组[（23．26±17．80）μg／L比（13．12±10．23）、（13．78±9．26）μg／L]，PGR明显低于萎缩性胃炎组和非萎缩性胃炎组（3．67±2．03比4．88±1．82、5．24±1．88），差异有统计学意义（P〈0．05）。共有165例行幽门螺杆菌（Hp）检测，其中阳性29例（Hp阳性组），阴性136例（Hp阴性组）。Hp阴性组和Hp阳性组PGI比较差异无统计学意义[（60．46±45．49）μg／L比（72．41±31．85）μg／L，P〉0．05]；Hp阳性组PG Ⅱ明显高于Hp阴性组[（19．58±1．57）μg／L比（14．09±13．21）μg／L，PGR明显低于Hp阴性组（3．82±O．18比4．99±0．18），差异有统计学意义（P〈0．05）。结论与非萎缩性胃炎、萎缩性胃炎患者相比，胃癌患者PG Ⅱ明显升高，PGR明显下降，PG I与胃癌的危险性无关。用PG Ⅱ联合PGR预测胃癌的高危人群有一定价值，且对于Hp感染的判断有一定的帮助。

Objective To compare the levels of the serum pepsinogen （PG） in the gastric diseases, and explore the diagnostic value in gastric diseases. Methods Two hundred and fourteen patients who had undergone endoscopy were selected, and the patients were divided into 3 groups according to the results of endoscope pathological diagnosis： chronic superficial gastritis （CSG） group （70 cases）, chronic atrophic gastritis （CAG） group （86 cases） and gastric cancer （GC） group （58 cases）. The quantitative chemiluminescence method was used to test serum PG I and PG Ⅱ and the PG I/PG Ⅱ ratio （PGR） was calculated. Results The PG I in GC group was significantly higher than that in CAG group： （78.41 ± 55.42） μg/L vs. （53.10 ± 30.08）μg/L, and there was statistical difference （P〈O.05）. There was no statistical difference in PG I between GC group and CSG group （P 〉 0.05）. The PG Ⅱ in GC group was significantly higher than that in CAG group and CSG group： （23.26 ± 17.80） μg/L vs. （13.12± 10.23） and （13.78± 9.26） μg/L, the PGR was significantly lower than that in CAG group and CSG group： 3.67±2.03 vs. 4.88 ± 1.82 and 5.24 ±1.88, and there were statistical differences （P 〈 0.05）. Helicobacterpylori （Hp） was detected in 165 patients, with positive in 29 cases （Hp positive group） and negative in 136 cases （Hp negative group）. There was no statistical difference in PG I between Hp negative group an Hp positive group： （60.46 ±45.49） μg/L vs. （72.41 ± 31.85） μg/L, P 〉 0.05. The PG Ⅱ in Hp positive group was significantly higher than that in Hp negative group： （19.58 ± 1.57） μg/L vs. （14.09 ± 13.21） μg/L, the PGR was significantly lower than that in Hp negative group： 3.82±0.18 vs. 4.99 ± 0.18, and there were statistical differences （P 〈 0.05）. Conclusions Compared with that in the CSG and CAG patients, the PG II in GC patients increases significantly, while PGR descends significantly, but PG Ⅰ has no correlation with the risk of GC. The PG Ⅱ combined with PGR can predict people with high risk of GC, and help with the judgment of Hp infection.