机构地区:[1]首都医科大学附属北京同仁医院检验科,北京100730 [2]首都医科大学附属北京同仁医院消化科,北京100730
出 处:《中华检验医学杂志》2016年第10期771-775,共5页Chinese Journal of Laboratory Medicine
摘 要:目的 通过乳胶增强免疫比浊法检测不同胃黏膜病变患者的血清胃蛋白酶原Ⅰ(PGⅠ)、Ⅱ(PGⅡ)水平及PGⅠ/PGⅡ(PGR),探讨其在胃黏膜病变中变化及临床意义。方法 病例对照研究。收集2015年1月至2016年1月于北京同仁医院消化内科和外科就诊并做胃镜检查及病理学检查的患者275例,根据胃镜及组织病理学检查确诊正常对照组20名;慢性非萎缩性胃炎组68例;慢性萎缩性胃炎组76例:其中胃窦部萎缩性胃炎组30例,胃体萎缩性胃炎组26例,多灶性萎缩性胃炎组20例;慢性萎缩性胃炎伴肠上皮化生组28例;慢性萎缩性胃炎伴上皮内瘤变组9例;胃良性溃疡组46例;肠型胃癌组28例。用乳胶增强免疫比浊法检测各组患者空腹血清PGⅠ、PGⅡ的水平,计算PGR值。各组符合正态分布的数据采用ANOVA进行统计学分析,组间采用Mann-Whitney U检验和Kruskal-Wallis检验进行统计学分析。结果 慢性萎缩性胃炎组的血清PGⅠ[(74.23±22.36)ng/ml]及PGR(6.92±2.16)低于正常对照组PGⅠ[(98.94±21.00)ng/ml]及PGR(8.13±2.47),差异有统计学意义(FPGⅠ=18.297,PPGⅠ〈0.01,FPGR=4.713,PPGR〈0.01)。肠型胃癌组的血清PGⅠ[(44.46±26.72)ng/ml]及PGR(3.09±0.83)低于慢性萎缩性胃炎组PGⅠ[(74.23±22.36)ng/ml]及PGR(6.92±2.16),差异有统计学意义(ZPGⅠ=-3.921,PPGⅠ〈0.01,ZPGR=-6.662,PPGR〈0.01)。胃良性溃疡组的PGⅠ[(129.95±43.39)ng/ml]及PGⅡ[(21.09±6.78)ng/ml]高于正常对照组PGⅠ[(98.94±21.00)ng/ml]及PGⅡ[(12.64±1.84)ng/ml],差异有统计学意义(FPGⅠ=10.803,PPGⅠ〈0.01;FPGⅡ=39.130,PPGⅡ〈0.01)。多灶性萎缩性胃炎组的血清PGⅠ[(52.44±10.37)ng/ml]和PGR(5.47±1.59)低于胃窦萎缩性胃炎PGⅠ[(94.95±14.45)ng/ml]和PGR(8.39±1.48),差异有统计学意义(ZPGⅠ=-5.941,PPGⅠ〈0.01;ZPGR=-4.9Objective To evaluate serum level of pepsinogen Ⅰ (PG Ⅰ ), PG Ⅱ , and PG Ⅰ/PG Ⅱ - ratio (PGR) using latex enhanced turbidimetric immunoassay in patients with different gastric mucosal lesions, and to investigate their changes and clinical significance. Methods Case-control study. Two hundred and seventy-five patients who had enteroscopy and pathological examination from the department of gastroenterology and surgery from Beijing Tongren Hospital between January 2015 and January 2016 were enrolled. Endoscopic and histopathological examination confirmed the normal control group ( n = 20), chronic non-atrophic gastritis group ( n = 68 ), chronic atrophic gastritis group ( n = 76), including antral atrophic gastritis ( n = 30 ), gastric body atrophic gastritis ( n = 26 ), and multifocal atrophic gastritis ( n = 20 ) ;intestinal metaplasia group ( n = 28 ), intraepithelial neoplasia group ( n = 9 ), benign gastric ulcer group ( n = 46) and intestinal gastric cancer group ( n = 28). Latex-enhanced immune turbidity method were used to detect the patients fasting serum PG Ⅰ and PG Ⅱ. Then the PGR was calculated. The normally distributed data of each group were statistically analyzed by ANOVA, the data between groups were nalyzed using the Mann-Whitney U test and Kruskal-Wallis test. Results Serum PG Ⅰ [ ( 74. 23 ± 22. 36) ] ng/ml and PGR (6. 92 ±2. 16) in chronic atrophic gastritis group were lower than those in normal controls[ PG Ⅰ (98.94 ± 21.00) ng/ml, PGR 8. 13 ±2.471, (F PGI = 18.297,P PGI 〈0.01,FPGR =4.713,PPGR〈0.01). The serum PG Ⅰ [ ( 44.46 ± 26. 72 ) ng/ml ] and PGR ( 3.09 ± 0. 83 ) in the intestinal type of gastric cancer group were lower than those in the chronic atrophic gastritis group [ PG Ⅰ (74. 23 ± 22. 36) ng/ml, PGR 6. 92 ±2.16], (Z PG I =-3.921,P PG I〈0.01,ZPGR= - 6. 662 , PPGR 〈0.01). PGI [(129.95 ±43.39) ng/ ml]. PG Ⅱ [ (21.09 ±6. 78) ng/ml] in the gastric benign ulcer gr
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