摘要
背景:目前萎缩性胃炎和胃癌仍需经过胃镜活检组织病理学检查才可确诊。许多研究显示,血清胃蛋白酶原(PG)Ⅰ、PGⅡ、胃泌素-17(G-17)和幽门螺杆菌(H.pylori)IgG抗体可用于筛查慢性萎缩性胃炎和胃癌。目的:评价能否以血清PGⅠ、PGⅠ/PGⅡ比值(PGR)、G-17和H.pylori-IgG抗体检测筛查萎缩性胃炎,并提高胃癌的早期诊断率。方法:胃癌高发区上海经胃镜检查确诊的458例胃十二指肠疾病患者纳入研究。血清学检查前在胃镜下取多处活检,根据组织病理学检查结果将受检者分为5组:正常对照组(包括轻度非萎缩性胃炎)77例,萎缩性胃炎组92例,胃癌组141例,胃溃疡组58例,十二指肠球部溃疡组90例。以酶联免疫吸附测定(ELISA)定量检测受检者空腹血清PGⅠ、PGⅡ和G-17水平,定性分析血清H.pylori-IgG抗体。结果:萎缩性胃炎组和胃癌组的PGⅠ和PGR水平显著降低(P<0.01);根据接受者操作特征(ROC)曲线,两者诊断萎缩性胃炎的最佳界值分别为82.30μg/L(敏感性85.9%,特异性75.1%)和6.05(敏感性78.3%,特异性71.6%)。萎缩性胃炎组的PGⅠ、PGR和G-17水平与萎缩部位和(或)程度显著相关(P<0.01),萎缩性胃体胃炎PGⅠ和PGR水平降低,G-17水平明显升高,萎缩性胃窦胃炎G-17水平降低。胃癌组G-17水平显著升高(P<0.01),进展期胃癌的PGⅠ和PGR水平较早期胃癌显著降低(P<0.01),但两者G-17水平差异不明显。正常对照组H.pylori-IgG抗体阳性率为54.5%,阳性者的PGⅠ水平显著高于阴性者(P<0.01),但两者G-17水平差异不明显。其余4组的H.pylori-IgG抗体阳性率均大于85%。结论:血清PGⅠ、PGR和G-17水平低下分别是胃体和胃窦萎缩的生物学标志,可根据血清PGⅠ和PGR界值进行萎缩性胃炎的筛查。结合血清G-17水平明显升高而PGⅠ、PGR水平明显降低可进行胃癌筛查。H.pylori感染与PG水平的变化有关。
Currently the diagnosis of atrophic gastritis and gastric cancer are mainly made by endoscopy and histopathology. In recent years, determination of serum pepsinogen （PG） Ⅰ , PG Ⅱ, gastrin-17 （G-17） and Helicobacterpylori （H. pylori） IgG antibodies is regarded as new tests for screening chronic atrophic gastritis and gastric cancer. Aims： To evaluate the use of serum tests： serum PG Ⅰ , PG Ⅰ/PGⅡ ratio （PGR）, G-17 and H. pylori-IgG antibodies to screen atrophic gastritis, so as to increase the early diagnosis rate of gastric cancer. Methods： A total of 458 patients with gastroduodenal diseases diagnosed by gastroscopy in Shanghai, high incidence area of gastric cancer, were recruited, and each of them underwent endoscopy with biopsies before serum tests were performed. These patients were divided into 5 groups based on endoscopic and histopathological findings： 92 patients in atrophic gastritis group, 141 in gastric cancer group, 58 in gastric ulcer group, 90 in duodenal ulcer group, and 77 （including mild non-atrophic gastritis） served as control group. Fasting serum samples for PG Ⅰ and PGⅡ, G-17, and H. pylori-IgG antibodies determination were analyzed by enzymelinked immunosorbent assay （ELISA）. Results： PG Ⅰ and PGR values decreased significantly in both atrophic gastritis and gastric cancer groups （P〈0.01）. For the best discrimination of atrophic gastritis, the cut-off values of PG Ⅰ and PGR calculated by receiver operating characteristic （ROC） curve were 82.30 μg/L （sensitivity 85.9%, specificity 75.1%） and 6.05 （sensitivity 78.3%, specificity 71.6%）, respectively. PG Ⅰ, PGR and G-17 values were related significantly with grades and/or sites of atrophic gastritis （P〈0.01）. Patients with atrophic corpus gastritis had low PG Ⅰ and PGR values and high G-17 level, and patients with atrophic antral gastritis had low G-17 level. G-17 level increased significantly in the gastric cancer group （P〈0.01）. PG Ⅰ and PGR values were significantly lower in patients with advanced gastric cancer than those in patients with early gastric cancer （P〈0.01）, while there was no difference in G-17 level between them. The positivity rate of H. pylori-IgG antibodies was 54.5% in the control group. PG Ⅰ level was higher in H. pylori-positive patients than that in the tt. pylori-negative ones （P〈0.01）, whereas 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. Conclusions： Low serum PG Ⅰ, PGR and G-17 values are biomarkers of atrophic corpus and antral gastritis, respectively. Atrophic gastritis can be screened by serum PG I and PGR values. Screening of gastric cancer can be based on increased serum G-17 level and decreased serum PG Ⅰ and PGR values. H. pylori infection is related to the change of PG level.
出处
《胃肠病学》
2006年第7期388-394,共7页
Chinese Journal of Gastroenterology
基金
上海市重点学科建设项目(No.Y0205)资助
