血清胃蛋白酶原、胃泌素-17与慢性萎缩性胃炎

背景：目前慢性萎缩性胃炎的诊断主要依靠组织病理学检查，但日本、挪威、芬兰等国已实施通过血清胃蛋白酶原（PG）和胃泌素-17（G—17）检测筛查慢性萎缩性胃炎和胃癌。目的：探讨慢性萎缩性胃炎患者血清PGI、PGI／PGI／比值（PGR）和G—17的变化规律。方法：296例于2005年5月-2007年5月在北京友谊医院行胃镜检查且符合入选标准者纳入研究。根据病理诊断将入选病例分为3组：对照组42例，慢性非萎缩性胃炎组148例，慢性萎缩性胃炎组106例。以放射免疫测定检测血清PGⅠ、PGⅡ和G—17水平。结果：慢性萎缩性胃炎组与对照组相比．血清PGI水平和PGR显著降低，G—17水平显著升高（P〈0．05）。随着萎缩程度的加重，胃体萎缩、全胃多灶性萎缩的血清PGI水平和PGR进行性下降（P〈0．01），胃窦萎缩的血清G-17水平进行性下降（P〈0．01）。结论：联合检测血清PG和G—17水平可用于慢性萎缩性胃炎的筛查，如有异常，应进一步行胃镜检查以确诊并指导治疗。     

萎缩性胃炎患者血清胃蛋白酶原和胃泌素水平变化及意义

目的探讨血清胃蛋白酶原（PG）、胃泌素（GS）水平在萎缩性胃炎诊断中的价值。方法采用酶联免疫吸附试验法检测45例萎缩性胃炎患者及20例健康体检者血清PGⅠ、PGⅡ、GS水平,并计算PGR。PGR=PGⅠ/PGⅡ。结果萎缩性胃炎组PGⅠ、PGR水平明显低于对照组,而GS水平明显高于对照组,两组比较P均〈0.05。且随病情进展,萎缩性胃炎患者血清PGⅠ、PGR、GS水平逐渐降低（P均〈0.05）。结论萎缩性胃炎患者血清PGⅠ、PGⅡ水平降低,GS水平升高早期检测二者有助于萎缩性胃炎的诊断及判断病情。     

胃蛋白酶原和胃泌素筛查胃癌及萎缩性胃炎

目的探讨血清胃蛋白酶原(PG)和胃泌素-17(G-17)与胃癌及萎缩性胃炎的关系,并分析幽门螺杆菌感染、服用抑酸药、年龄及性别等多种因素对血清PG和G-17的影响,建立本地区胃癌及萎缩性胃炎的血清学筛查方法。方法选择2013年2月至2013年8月在我院消化内镜中心行胃镜检查符合入选研究标准的100例患者,根据组织病理学诊断将结果分为3组:对照组28例,萎缩性胃炎组52例,胃癌组20例,以免疫放射测定法和放射免疫法检测血清PGⅠ、PGⅡ和G-17水平。结果与正常对照组比较,萎缩性胃炎组、胃癌组的PGⅠ和PGⅠ/PGⅡ比值(PGR)水平均降低(P0.05),萎缩性胃炎组的G-17水平显著降低(P0.01),胃癌组的G-17水平显著增高(P0.01)。采用Bayes判别法分析多种因素、PG和G-17并建立Bayes判别函数作为筛查胃癌及萎缩性胃炎的血清学方法。结论检测血清PG和G-17可以作为一种无创性的筛查胃癌及萎缩性胃炎的方法,适合大规模人群普查。     

血清胃蛋白酶原、胃泌素-17和幽门螺杆菌IgG抗体筛查萎缩性胃炎和胃癌

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（Hpylori）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．pytori-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（EuSA）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D-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．pylon感染与PG水平的变化有关。     

血清胃蛋白酶原检测在慢性萎缩性胃炎筛查中的价值

目的探讨血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅰ/胃蛋白酶原Ⅱ(PGⅠ/PGⅡ)比值(PGR)与慢性萎缩性胃炎的关系,确定其在萎缩性胃炎中的变化规律。方法选择在我院消化科行胃镜检查符合入选研究标准的200例患者,根据组织病理学诊断结果分为慢性非萎缩性胃炎组(135例)和慢性萎缩性胃炎组(65例)。采用化学发光方法定量测定空腹血清PGⅠ、PGⅡ,并计算PGⅠ/PGⅡ比值(PGR)。结果慢性萎缩性胃炎组与非萎缩性胃炎组血清PGⅠ分别为(78.55±15.42)μg/L和(130.51±55.23)μg/L,有显著差异(P<0.05)。PGR分别为4.09±2.15和8.95±5.18,显著差异(P<0.05);以PGⅠ≤70μg/L且PGR≤3.0为界值来计算诊断慢性萎缩性胃炎的敏感性和特异性分别为72.3%和93.3%。结论检测血清PG及PGR可用于慢性萎缩性胃炎的筛查,如有异常,应进一步行胃镜检查以确诊并指导治疗。     

血清胃蛋白酶原和胃泌素-17在胃癌筛选中的作用

胃癌是全球最常见的恶性肿瘤之一,提高胃癌的早期诊断率是降低胃癌的发生率和死亡率的重要手段。近年来血清学检测因简便、便于动态监测而在国外被广泛应用。此文主要介绍血清胃蛋白酶原和胃泌素-17的临床意义及单独或联合检测在胃癌及其癌前病变筛选中的作用,指导进一步研究以寻找适合国内胃癌筛选的最佳方法。     

检测血清胃蛋白酶原和胃泌素-17诊断胃癌的临床价值

目的通过测定血清胃蛋白酶原(PG)Ⅰ、PGⅡ、胃泌素-17(G-17)和H.pylori-IgG抗体来预测胃癌高危,提高胃癌早诊率。方法本研究采用观察性病例-对照研究,共310例受检者纳入研究。在作血清试验前,所有患者均在胃镜下作多处活检,并根据病理结果将受检者分为胃癌组(141例,其中早期胃癌40例、进展期胃癌101例)、正常组(77例)和萎缩性胃炎组(92例)。每一例均用酶联免疫吸附试验(ELISA)定量测定空腹血清PGⅠ、PGⅡ和G-17,定性测定H.pylori-IgG抗体。结果PGⅠ和PGR(PGⅠ/PGⅡ)水平在胃癌组(28.74±11.55μg/L,1.66±1.01)明显低于正常组(123.99±32.25μg/L,10.09±1.89)和萎缩性胃炎组(58.63±25.35μg/L,4.36±2.57)(均P<0.01),根据接受者操作特征曲线(ROC)计算PGⅠ和PGR诊断胃癌的最佳界值分别为57.15μg/L(灵敏度99.3%,特异度84.5%)和2.99(灵敏度92.5%,特异度89.0%);而G-17水平胃癌组(20.86±8.24pmol/L)明显高于正常组(10.39±9.25pmol/L)和萎缩性胃炎组(8.59±6.08pmol/L)(均P<0.01)。根据ROC曲线计算G-17的最佳界值为14.61pmol/L(灵敏度75.2%,特异度71.3%)。进展期胃癌的PGⅠ和PGR水平较早期胃癌明显降低(P<0.01),而G-17差别不明显。萎缩性胃炎组和胃癌组的H.pylori-IgG抗体阳性率均明显高于正常组(P<0.01)。结论结合G-17水平明显升高而PGⅠ、PGR水平显著低下可作胃镜进行胃癌筛查,有助于提高胃癌早诊率。     

胃蛋白酶原在慢性萎缩性胃炎和胃癌筛查中的价值

迄今为止．全球范围内胃癌的发病率和病死率仍居高不下。由于进展期胃癌的预后差,早期筛查、诊断和干预胃肠化生、萎缩性胃炎和早期癌变对提高患者的生存率至关重要。本文旨在介绍胃蛋白酶原及其在筛查萎缩性胃炎和胃癌中的作用。     

血清胃蛋白酶原与胃泌素检测对慢性萎缩性胃炎的诊断价值

目的探讨血清胃蛋白酶原Ⅰ（PGⅠ）、胃蛋白酶原Ⅰ/胃蛋白酶原Ⅱ（PGⅠ/PGⅡ）比值（PGR）和胃泌素-17（G-17）与慢性萎缩性胃炎的关系,确定其在萎缩性胃炎中的变化规律。方法 选择在我院消化科行胃镜检查符合入选研究标准的300例患者,根据组织病理学诊断结果分为慢性非萎缩性胃炎组（202例）和慢性萎缩性胃炎组（98例）。采用酶联免疫吸附试验（ELISA）方法定量测定空腹血清PGⅠ、PGⅡ和G-17水平,并计算PGⅠ/PGⅡ比值（PGR）。采用14C-或13C-呼气试验和快速尿素酶试验两种方法联合判定幽门螺杆菌（Hp）感染情况。结果 慢性萎缩性胃炎组与非萎缩性胃炎组相比,血清PGⅠ分别为128.55±61.42μg/L和150.61±75.33μg/L,比较有显著差异（P〈0.05）。PGR分别为10.09±5.15和10.95±7.18,比较无显著差异（P〉0.05）;G-17分别为9.68±15.51pmol/L和18.93±18.92pmol/L,比较有显著差异（P〈0.05）。Hp阳性组PGR（8.96±7.72）与阴性组（11.63±5.56）比较有显著差异（P〈0.05）;Hp阳性组PGⅠ（125.39±65.90μg/L）与阴性组（154.19±65.13μg/L）比较有显著差异（P〈0.05）;Hp阳性组G-17（10.91±15.50pmol/L）与阴性组（10.68±19.12pmol/L）比较无显著差异（P〉0.05）。结论 联合检测血清PG和G-17水平可用于慢性萎缩性胃炎的筛查,如有异常,应进一步行胃镜检查以确诊并指导治疗。Hp感染与PG水平的变化有关。     

胃蛋白酶原、胃泌素-17和幽门螺杆菌IgG抗体对胃癌筛查的价值探讨

目的探讨胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原I/胃蛋白酶原II(PGR)、胃泌素-17(G-17)联合检测以及幽门螺杆菌(H.pylori)IgG抗体对胃癌筛查的价值。方法选取2018年1月至2019年8月合肥市第二人民医院诊疗的正常对照者72例,慢性萎缩性胃炎患者32例,胃溃疡患者35例,胃息肉患者72例,胃癌患者60例作为研究对象,分别检测5组血清PGⅠ、PGR、G-17水平及H.pylori抗体IgG,分别绘制PGⅠ、PGR、G-17单独检测以及联合检测的ROC曲线进行诊断效能评价。结果慢性萎缩性胃炎组、胃癌组血清PGⅠ水平、PGR水平显著低于对照组(P<0.05),其他组与对照组差异无统计学意义(P>0.05)。胃癌组血清G-17水平显著高于对照组(P<0.05),其他组与对照组差异无统计学意义(P>0.05)。通过绘制ROC工作曲线,发现单独检测PGⅠ、PGR和G-17时曲线下面积为0.924、0.754、0.801;PGⅠ、PGR和G-17水平单项检测的的敏感性分别为86.1%、83.3%和64.3%,特异性分别为85.7%、64.3%和88.9%;综合预测模型曲线下面积为0.948,敏感性和特异性为94.4%和87.5%。结论血清PGⅠ、PGR和G-17水平以及H.pylori抗体IgG联合检测优于各项指标单独检测,可用作早期胃癌的筛查指标。     

Screening of atrophic gastritis and gastric cancer by serum pepsinogen, gastrin-17 and Helicobacter pylori immunoglobulin G antibodies

OBJECTIVE: 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. METHODS: 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. RESULTS: 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 µg/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. CONCLUSIONS: Low serum PGI, PGR and G‐17 values are biomarkers of atrophic antral gastritis. Atrophic corpus gastritis can be screened by lower serum PGI, PGR and high G‐17 values. [Correction added after online publication on 2 February 2007: the preceding sentence has replaced one that read ‘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.     

Correlation of serum pepsinogens and gastrin-17 with atrophic gastritis in gastroesophageal reflux patients: a matched-pairs study

Background and Aim: An algorithm (GastroPanel) for the non‐invasive diagnosis of atrophic gastritis has been previously proposed, based on serum pepsinogen‐I, gastrin‐17, and Helicobacter pylori (H. pylori) antibodies. The aim of the present study was to evaluate whether serum markers correlate with and predict gastric atrophy in gastroesophageal reflux disease (GERD) patients. Methods: The baseline data of the prospective ProGERD study, a study on the long‐term course of GERD (n = 6215 patients), served to select patients with atrophic gastritis diagnosed in biopsies from gastric antrum and corpus, and control cases without atrophy. A total of 208 pairs were matched for age, sex, GERD status (erosive vs non‐erosive), presence of Barrett's esophagus, and histological H. pylori status were retrieved. Serum pepsinogen‐I, gastrin‐17, and H. pylori antibodies were determined using specific enzyme immunoassays. Results: A significant negative correlation was found between the degree of corpus atrophy and the level of serum pepsinogen‐I. A previously‐reported negative correlation between the degree of antral atrophy and serum gastrin‐17 could not be confirmed. The low sensitivity (0.32) and specificity (0.70) of the GastroPanel algorithm were mainly due to over diagnosis and under diagnosis of advanced atrophy in the antrum. Conclusion: The diagnostic validity of the GastroPanel algorithm to diagnose gastric atrophy non‐invasively is not sufficient for general use in GERD patients.     

血清胃蛋白酶原、胃泌素-17、幽门螺杆菌抗体检测在筛查胃癌风险人群中的价值分析

胃癌是目前常见的消化道恶性肿瘤之一,死亡率高.早诊早治对于胃癌患者改善预后具有重要意义.血清分子标志物凭借成本较低、简单易行、痛苦小、可动态监测等优点在胃癌及癌前疾病筛查、预后评估等方面发挥着重要的作用,在国内外临床应用较为广泛.本文就血清胃蛋白酶原、胃泌素-17、幽门螺杆菌抗体检测在筛查胃癌风险人群中的价值分析做一综...     

Non-endoscopic diagnosis of multifocal atrophic gastritis; efficacy of serum gastrin-17, pepsinogens and Helicobacter pylori antibodies

BACKGROUND/AIMS: Infection with H. pylori is an important risk factor for the development of gastric cancer and glandular atrophy is an intermediate stage in gastric carcinogenesis. While screening the patients with atrophic gastritis by endoscopy is unrealistic, a concept of "serological gastric biopsy" based on measurement of gastric secretory proteins and peptides should be further validated. We sought to determine if the laboratory panel composed of serum PGI and protein stimulated gastrin-17 might select patients with MAG, and what is diagnostic significance of H. pylori serology in population of high prevalence of H. pylori infection. MATERIAL AND METHODS: 55 consecutive patients of both sexes (M/F 25/30; range of age 55 -81 years) were referred for gastroscopy with antrum and corpus mucosal biopsies. Patients with histological signs of glandular atrophy at any site of the stomach were considered to have multifocal atrophic gastritis. A first blood sample was collected for measurement of basal gastrin-17, pepsinogens and H. pylori IgG-antibodies, and second was taken 20 minutes after use of protein-rich drink to measure stimulated gastrin-17. RESULTS: Signs of mucosal atrophy were found in 19 patients, while 29 patients showed non-atrophic gastritis and seven H. pylori-negative patients had no histological pathology. Low serum level of stimulated gastrin-17 (< 5 pmol/l) and/or pepsinogen I (< 50 microg/l), were found in 16 of 19 patients (84.2%) with and in 7 of 36 patients (19.4%) without atrophy in the histological study. Combining of H. pylori serology with serum levels of secretory peptides had no significant effect on diagnostic sensitivity of the test panel. CONCLUSION: The test panel composed of pepsinogen I and protein stimulated gastrin-17 may be used as the "serological gastric biopsy" detecting multifocal atrophic gastritis. The diagnostic sensitivity of this test panel is not increased by knowledge of H. pylori status.