血清胃蛋白酶原和胃泌素-17在胃癌和癌前病变筛查中的价值

背景:我国是胃癌高发地区,有研究指出,血清胃蛋白酶原(PG)和胃泌素-17(G-17)水平可用于胃癌的筛查。目的:探讨血清PG和G-17水平筛查胃癌前病变和胃癌的价值。方法:选取2016年3月—2016年10月苏州大学附属第一医院经胃镜和病理学检查确诊的211例患者,以67名健康者作为对照。应用ELISA法检测血清PGⅠ、PGⅡ、G-17和Hp-IgG抗体水平。结果:与对照组相比,萎缩性胃炎组PGⅠ水平、PGR显著降低(P0.01);低级别上皮内瘤变组、高级别上皮内瘤变组和胃癌组PGⅠ水平、PGR均显著降低(P0.01),G-17水平显著升高(P0.01)。根据ROC曲线,PGⅠ、PGR和G-17诊断胃癌及其癌前病变的最佳界值分别为74.74 ng/mL(敏感性88.3%,特异性78.0%)、6.59(敏感性87.0%,特异性73.8%)、13.02 pmol/L(敏感性54.2%,特异性84.4%)。PGR和G-17为胃癌及其癌前病变的独立预测因素,PGⅠ、PGR和G-17联合诊断胃癌及其癌前病变的敏感性为89.9%,特异性为84.4%。结论:血清PGⅠ、PGR、G-17可作为胃癌及其癌前病变筛查的指标。PG联合G-17诊断胃癌及其癌前病变的敏感性和特异性较单独血清PG或G-17更高。     

幽门螺杆菌阴性早期胃癌的内镜及组织学 特点分析

目的分析并总结幽门螺杆菌（Helicobacter pylori, HP）阴性早期胃癌或高级别上皮内瘤变的内镜及组织学特点。方法检索在解放军总医院第七医学中心2013年1月—2020年1月诊断为早期胃癌或高级别上皮内瘤变的患者,按照HP阴性胃癌诊断标准纳入病例,回顾性分析其临床特点、内镜下表现及组织病理学特点。结果469处早期胃癌/高级别上皮内瘤变中共有10处（21%）HP阴性早期胃癌/高级别上皮内瘤变,其中包括3处印戒细胞癌,3处胃底腺型胃癌,1处胃小凹上皮型腺癌,1处贲门部高级别上皮内瘤变,1处家族性腺瘤性息肉病并发胃高级别上皮内瘤变,及1处Lynch综合征并发胃高级别上皮内瘤变。3处印戒细胞癌内镜下形态均为发白的平坦/凹陷病变,胃下部多见（2/3）。分化型早期胃癌/高级别上皮内瘤变7处,多位于胃中上部（6/7）,隆起型病变（5/7）多见。结论HP阴性早期胃癌或高级别上皮内瘤变内镜常表现为孤立性病灶,其中未分化型癌多表现为胃下部的发白平坦/凹陷病变,而分化型多表现为胃中上部的隆起型病变。     

血清胃蛋白酶原联合高危人群胃镜检查诊断幽门螺旋杆菌感染相关胃癌的价值

目的探讨评价血清胃蛋白酶原(PG)和幽门螺旋杆菌抗体(Hp-Ig G)联合高危人群胃镜检查能否作为早期胃癌及其癌前病变的筛查指标。方法选取该院消化内科收治的经胃镜检查确诊的上消化道疾病患者419例。在进行胃镜检查前抽取空腹静脉血4 ml,分离血清后于-20℃冰箱内保存。以病理学活检结果将受检者分为正常对照组78例、浅表性胃炎组114例、萎缩性胃炎组125例、胃癌组102例。应用酶联免疫吸附试验(ELISA)对受检者空腹血清PGⅠ、PGⅡ和血清HP-Ig G抗体进行定量、定性检测。结果 (1)胃癌组和萎缩性胃炎组与正常对照组PG I水平比较。差异显著(P0.05);胃癌组较正常对照组PGⅡ水平差异显著(P0.05);胃癌组和萎缩性胃炎组与正常对照组PGI/PGⅡ(PGR)之间差异显著(P0.05);(2)在除正常对照组外的341例上消化道疾病受检者中,Hp阳性246例(72.14%)、阴性95例(27.86%);(3)在萎缩性胃炎组中PG I、PGⅡ的水平与Hp的阴性和阳性组存在统计学差异(P0.05);(4)PG结果阳性时,Hp阳性检出率明显高于阴性;PG阴性时,Hp阳性率显著高于阴性。结论血清PGⅠ、PGR的变化水平与Hp感染密切相关;结合血清PGⅠ、PGR及Hp-Ig G抗体检查可以作为胃癌的筛查指标。血清胃蛋白酶原联合高危人群胃镜检查对Hp感染相关胃癌的诊断具有重大价值,值得临床推广应用。     

新型胃癌筛查评分系统临床应用研究

目的探讨新型胃癌筛查评分系统在胃癌筛查中的应用价值。方法兰州大学第二医院内镜团队在2018年4—12月,依据"中国早期胃癌筛查流程专家共识意见(草案),(2017,上海)"纳入筛查人群451名,开展问卷调查,检测胃蛋白酶原I(PGI)、胃蛋白酶原II(PGII)值、(PGI)/PGII及胃泌素17(G17)水平,幽门螺旋杆菌(Hp)感染阳性率,根据新型评分系统将筛查人群分为低、中、高危组。所有患者进行胃镜检查并对内镜下发现的可疑病灶进行活检+病理诊断。结果 PGI、PGI/PGII水平,低危组中危组高危组;PGII、G17水平,低危组中危组高危组。Hp总感染率60.75%,低危组为33.33%;中危组为50.77%;高危组为60.00%,呈上升趋势。低危组发现11例低级别上皮内瘤变(LGIN);中危组发现腺癌1例,高级别上皮内瘤变(HGIN)4例,LGIN23例,胃癌检出率3.8%;高危组发现HGIN2例,LGIN9例,胃癌检出率13.3%。结论:新型胃癌筛查评分系统可以有效的提高胃癌检出率,避免了医疗资源的浪费。     

Ki-67、p53、P504s在胃癌前病变和早期胃癌中的表达及其意义

背景:胃癌的发生是多因素、多步骤、逐渐进展的过程,发生细胞学和结构异常的同时常存在某些分子表达的异常,涉及多种癌基因的活化和抑癌基因的失活。目的:探讨Ki-67、p53、P504s在正常胃黏膜、萎缩性胃炎伴肠化生、低级别上皮内瘤变、高级别上皮内瘤变和早期胃癌中的表达及其意义。方法:收集2015年1月—2016年12月南京大学医学院附属鼓楼医院44例正常胃黏膜、44例萎缩性胃炎伴肠化生黏膜、41例低级别上皮内瘤变、38例高级别上皮内瘤变和35例早期胃癌组织,以免疫组化法检测Ki-67、p53、P504s表达。结果:Ki-67、p53、P504s在萎缩性胃炎伴肠化生、低级别上皮内瘤变、高级别上皮内瘤变、早期胃癌中的表达阳性率逐渐上升,且均显著高于正常胃黏膜组织(P 0. 05)。结论:Ki-67、p53、P504s表达与胃癌的发生、发展密切相关,参与了胃癌发生的早期过程,检测上述三种分子标记物有助于判断病变的严重程度和进展趋势,有利于提高胃癌前病变和早期胃癌的检出率。     

深度卷积神经网络对胃病变普通内镜图像诊断的研究

目的通过深度卷积神经网络（convolutional neural network,CNN）技术实现胃病变内镜图像的快速、准确人工智能辅助诊断。方法收集2012—2018年北京大学人民医院1 121例胃病变的普通白光内镜图像和病理结果。胃病变图像包括消化性溃疡、早期胃癌及高级别上皮内瘤变、进展期胃癌、胃黏膜下肿瘤共4类,另外还包括无病变正常胃黏膜图像。共17 217张图像作为训练集,使用CNN ResNet-34模型训练分类任务,使用全CNN DeepLabv3模型训练像素分割任务。经过训练后的CNN通过一个测试集评估诊断效能,测试集包括237例胃病变,共1 091张普通内镜图像。计算CNN诊断的准确率、敏感度、特异度、阳性预测值、阴性预测值。结果CNN对于早期胃癌及高级别上皮内瘤变的诊断准确率为78.6%(33/42),敏感度为84.4%(27/32),特异度为60.0%(6/10),阳性预测值87.1%(27/31),阴性预测值54.5%(6/11);对于消化性溃疡的诊断准确率为90.4%(47/52),敏感度为92.7%(38/41),特异度为81.8%(9/11);对于进展期胃癌的诊断准确率为88.1%(52/59),敏感度为91.8%(45/49),特异度为70.0%(7/10);对于胃黏膜下肿瘤的诊断准确率为86.0%(43/50),敏感度为89.7%(35/39),特异度为72.7%(8/11)。所有测试集图像识别时间为42 s。结论CNN可以作为早期胃癌及其他胃病变内镜图像的快速辅助识别方法,识别速度快,准确率高。     

6000例自然人群上消化道早癌内镜筛查结果分析

目的总结分析6 000例自然人群上消化道癌早诊早治项目消化内镜筛查结果。方法采取整群抽样法,连续三年每年筛查2 000例自然人群,经内镜检查及病理活检,统计分析上消化道癌筛查结果。结果任务完成率100%,高级别上皮内瘤变及癌检出率2.03%(122例),其中高级别上皮内瘤变检出率(早诊率)为81.15%(99/122),治疗率89.8%(79/88),随访率85.71%(402/469)。男性检出率高于女性,年龄≥60岁者检出率高于其它年龄段,经统计学分析,上述差异均有显著性意义(P0.05)。结论内镜配合病理活检能有效筛查上消化道癌;上消化道癌检出率与性别及年龄有关。     

早期胃癌及癌前病变内镜黏膜下剥离术后切缘阳性的危险因素与随访分析

目的探究早期胃癌及癌前病变内镜黏膜下剥离术(endoscopic submucosal dissection, ESD)后切缘阳性的危险因素, 并随访复发情况。方法回顾性收集2015年1月—2020年12月在福建省立医院经ESD治疗的489例早期胃癌及癌前病变患者的内镜、临床及病理资料, 根据切缘情况分为切缘阴性组(371例)、切缘低级别上皮内瘤变(low grade intraepithelial neoplasia, LGIN)组(79例)及切缘高级别上皮内瘤变(high grade intraepithelial neoplasia, HGIN)或癌组(39例)。采用logistic回归分析切缘阳性的危险因素, Kaplan-Meier法和log-rank检验对比不同切缘组复发风险, 采用Cox比例风险回归模型探讨阳性者复发的相关因素。结果 489例患者中, 切缘阳性率24.1%(118/489), 其中HGIN或癌占33.1%(39/118)。病灶面积>10 cm2(OR=1.58, 95%CI:1.13～2.08, P=0.033)、存在溃疡(OR=2.92, 95%C...     

提高对胃低级别上皮内瘤变中高级别上皮内瘤变诊断水平的研究进展

<正>胃黏膜上皮内瘤变是在内镜活检中常常遇到情况,而胃黏膜上皮内瘤变是胃癌非常重要的癌前病变。据文献报道,高级别上皮内瘤变(high-grade intraepithelial neoplasia,HGIN)的癌变率为70%~85%~([1-6]),临床上大多数患者最终选择行外科手术或者内镜下治疗。而对于低级别上皮内瘤变(low-grade intraepithelial neoplasia,LGIN)者,多     

505例胃黏膜上皮内瘤变患者中筛查胃癌的研究

[目的]对胃黏膜上皮内瘤变(IEN)患者开展胃镜的定期随访和筛查胃癌的研究,探索提高临床胃癌检出的有效性。[方法]收集2009年1月~2014年12月间,经胃镜活检病理诊断为胃黏膜IEN患者505例,其中低级别上皮内瘤变(LGIEN)465例,高级别上皮内瘤变(HGIEN)40例,进行定期随访、胃镜复查及病灶活检病理学检查,病理学证实胃癌或有确切病灶的HGIEN者行外科、腹腔镜手术或内镜黏膜剥离术(ESD)治疗,切除标本作病理学检查及胃癌分期。[结果]505例胃黏膜IEN患者经平均21.33个月的随访以及平均3.88次的胃镜复查,共检出胃癌81例,检出胃癌占全组的16.0%,其中早期胃癌51例,占检出胃癌的63.0%;进展期胃癌22例,占检出胃癌的27.2%。另外经胃镜活检病理检出的8例胃癌失访。465例LGIEN患者,检出胃癌57例(12.3%),其中早期胃癌38例(66.7%);40例HGIEN患者,检出胃癌24例(60.0%),其中早期胃癌13例(54.2%)。[结论]通过对胃黏膜IEN患者的定期胃镜随访及病理活检,能有效提高胃癌的检出率,尤其能够在LGIEN中筛查出漏诊的胃癌患者;具有确切病灶的HGIEN者,手术病理证实大多为胃癌患者,因此对胃黏膜IEN患者的定期复查必须实施制度化管理。     

Serum pepsinogen I and gastrin in relation to extent and location of intestinal metaplasia in the surgically resected stomach

A study of 177 patients undergoing distal subtotal gastrectomy indicates that a preoperative serum pepsinogen I (PGI) level below 20 ng/ml predicts the presence of gastric carcinoma and the degree of intestinal metaplasia of the gastric antrum. The serum gastrin level was not predictive of carcinoma or of the degree of intestinal metaplasia. Of the 15 patients with a low serum PG I level, 13 had carcinoma and 2 had atypical polyps. The PG I level in a stored serum sample from 4 of 30 patients fell from normal to abnormal over a period of 8–9 years. Each of these converters had invasive carcinoma of the stomach. This suggests that persons showing a fall in serum PG I to abnormal levels during serial analyses should be evaluated for the possibility of gastric carcinoma.     

LONG‐TERM RESULTS OF GASTRIC CANCER SCREENING USING THE SERUM PEPSINOGEN TEST METHOD AMONG AN ASYMPTOMATIC MIDDLE‐AGED JAPANESE POPULATION

Background and Aim: In order to reduce gastric cancer death, mass screening for gastric cancer has been established in Japan for several decades. Only photofluorography is considered to be an acceptable screening method so far, but recent evidence may show the usefulness of serum pepsinogen (PG) measurement for gastric cancer screening. The aim of the present study was to elucidate the feasibility of measuring serum PG levels for detection of gastric cancers. Methods: Serum PG levels (PGI/PGII) were measured in asymptomatic middle‐aged Japanese between 1991 and 2005. Those with a PGI ≤ 70 ng/mL and PGI/PGII ≤ 3 were defined as having a positive PG test. According to the obtained results of serum PG levels and previous individual records, those with a positive PG test and those with a negative PG test took gastroendoscopy every 2 and 5 years, respectively. Results: The total number of participating individuals was 101 892 (mean age of 48.7 years). In a total of 21 178 planned gastroendoscopies (20.8%), 13 789 (65.1%) underwent gastroendoscopy and 125 gastric cancers were detected, which corresponded to 0.12% of all participants and to 0.91% of those with gastroendoscopy. Early‐stage cancers and intestinal‐type intramucosal cancers accounted for 80% and 39% of all the detected cancers, respectively. Conclusions: Serum PG measurement for mass screening of gastric cancer enabled us to achieve high recruitment for gastroendoscopy in intended individuals, a favorable detection rate of gastric cancer and, in particular, an extremely high proportion of early‐stage gastric cancer in all the detected cancers.     

The role of serum pepsinogen in the detection of gastric cancer

The incidence of gastric cancer is very high in Japan, Korea, and China. Reducing the morbidity and mortality associated with gastric cancer requires early diagnosis, which can be facilitated by applying gastroscopy more frequently in high-risk groups. A strategy of population screening for gastric cancer is currently being adopted in Korea, Japan, and the Matsu region of Taiwan, but using different screening methods. In addition, the history of pepsinogen (PG) in research as a gastric cancer biomarker has varied, in that the use of serum levels of PGI and PGII and the PGI/PGII ratio as gastric cancer screening tools was introduced in Japan before 1990, but in Korea the first research results were only reported in 2008. This review first evaluates the physiology of PG, followed by the usefulness or limitations of serum PG testing with regard to the detection of gastric cancer. Finally, the factors affecting the efficacy of PG tests as a gastric cancer biomarker (i.e., Helicobacter pylori infection status, gender, histopathologic features, and cancer location and depth) are evaluated. It was found that the strategies used to increase the efficacy of PG tests should be individualized in each country according to the seroprevalence of H. pylori.     

Plasma ghrelin concentration correlates with the levels of serum pepsinogen I and pepsinogen I/II ratio--a possible novel and non-invasive marker for gastric atrophy

BACKGROUND/AIMS: Ghrelin, a novel growth-hormone-releasing peptide, has been reported to be localized mainly in the A-like cells in the gastric fundic mucosa. With the extension of gastric inflammation caused by H. pylori infection, gastric mucosal atrophy extends from the antrum to the corpus, which is the predominant site of localization of the ghrelin-producing A-like cells. The present study was designed to investigate the correlation between the plasma ghrelin levels and the extent of gastric mucosal atrophy in patients with chronic gastritis caused by H. pylori infection. METHODOLOGY: Sixty-nine patients with dyspeptic symptoms were enrolled for the study. Of these, 41 patients were confirmed to become negative for H. pylori after therapy to eradicate the infection. The other 28 patients were diagnosed as positive for H. pylori infection. Blood samples were collected from all the patients after 12 hours of fasting, before upper gastrointestinal endoscopy was performed. The plasma levels of total and active ghrelin, as well as the serum levels of pepsinogen I (PGI) and pepsinogen II (PGII) were measured by radioimmunoassay. Based on endoscopic assessment, the atrophic changes in the gastric mucosa were classified as open-type atrophy or closed-type atrophy. RESULTS: There were no significant differences in the plasma total and active ghrelin levels between H. pylori-positive and H. pylori-eradicated (negative) patients. The serum levels of PGI correlated well with the plasma levels of total ghrelin (p<0.01, r=0.38) and active ghrelin (p<0.05, r=0.29). The ratio of serum PGI to PGII level (PG I/II ratio) also correlated well with the plasma level of total ghrelin (p<0.05. r=0.31) and active ghrelin (p<0.05, r=0.27). The plasma levels of total as well as active ghrelin were significantly decreased in patients with low PG levels as compared with those in patients with high PG levels (PGI > 70 ng/mL or PGI/II >3.0). The plasma levels of total as well as active ghrelin were also significantly decreased in patients with endoscopically diagnosed open-type atrophy as compared with those in patients with endoscopically diagnosed closed-type atrophy (p < 0.01), especially in the H. pylori-eradicated cohorts. CONCLUSIONS: The plasma levels of ghrelin, which correlated well with the serum levels of PGI as well as the PGI/II ratio, decreased with increasing extent of gastric mucosal atrophy, suggesting that it could be a potentially useful non-invasive marker for chronic atrophic gastritis.     

血清胃蛋白酶原对胃癌的诊断价值

目的探讨血清胃蛋白酶原对胃癌的诊断价值。方法收集我院2011年6月-2011年11月经胃镜活检病理诊断浅表性胃炎27例,癌前状态51例,癌前病变8例,胃癌17例,晨起空腹采静脉血3 mL,收集血清,以酶联免疫吸附测定(ELISA)定量检测血清胃蛋白酶原Ⅰ(PGⅠ)、PGⅡ水平,计算PGⅠ/PGⅡ(PGR)值。结果在浅表性胃炎、癌前状态、癌前病变、胃癌中血清PGⅠ水平及PGR逐渐降低,而血清PGⅡ水平逐渐升高;血清PGⅠ、PGR在胃癌与浅表性胃炎、癌前状态比较差异有统计学意义,与癌前病变比较差异无统计学意义;血清PGⅡ在胃癌与浅表性胃炎、癌前状态、癌前病变比较差异均有统计学意义;胃癌与癌前疾病ROC曲线下面积PGⅠAUCROC=0.782,PGⅡAUCROC=0.919,PGR AUCROC=0.989,PGⅠ为93.53 g/L时诊断胃癌的敏感性76.47%,特异性76.27%;PGⅡ为58.85 g/L时诊断胃癌的敏感性82.35%,特异性89.83%;PGR为1.88时诊断胃癌的敏感性94.12%,特异性89.83%。结论血清PGⅠ、PGⅡ水平及PGR值对诊断胃癌有较高的敏感性和特异性,可用于胃癌筛查和早期诊断。     

胃癌与十二指肠溃疡患者血清胃蛋白酶原比较

目的 比较胃癌患者与十二指肠溃疡患者血清胃蛋白酶原水平的差异及探讨其与H．pylori感染的关系。方法 采用时间分辨荧光免疫分析方法检测108例胃癌和96例十二指肠溃疡患者血清胃蛋白酶原Ⅰ、Ⅱ（PGⅠ，PGⅡ），ELISA方法检测血清H．pylori抗体。结果 胃癌和十二指肠溃疡患者之间PGⅠ水平有显著性差异，胃癌组和十二指肠溃疡组中H．pylori阳性和阴性间PGⅠ、PGⅡ、PGⅠ，PGⅡ水平等无显著性差异。结论 胃癌患者血清PGⅠ水平显著低于十二指肠溃疡患者，H．pylori感染对胃癌和十二指肠溃疡患者血清胃蛋白酶原水平和PGⅠ，PGⅡ比值均无影响。     

"Familial hyperpepsinogenemia" and Helicobacter pylori infection

OBJECTIVE: Pepsinogen 1 (PG1) is a proenzyme precursor to pepsin, a protease secreted by the gastric chief cell. PG1 levels correlate with maximal gastric acid output. In 1979, Rotter et al. reported two pedigrees in which elevated PG1 levels and duodenal ulcers were prevalent. They proposed autosomal dominant inheritance of elevated PG1 and suggested that it was a risk factor for duodenal ulcer disease. In 1982, Helicobacter pylori (Hp) was discovered and was shown to be an important factor in peptic ulcer disease. Hp infection is also associated with increased PGI levels. We tested serum from one of the original pedigrees for Hp antibodies to determine whether Hp infection could explain the ulcers and elevated PG1 levels. METHODS: ELISA tests were performed using the urease fraction of a crushed Hp extract. Banked serum from one of the original families was thawed and tested. RESULTS: Of the subjects, 90% (nine of 10) with elevated PG1 were seropositive for Hp, compared to only 31% (17 of 55) of those with normal PG1 levels (p < 0.001). The mean PG1 level was higher in the seropositive (94.1+/-13.3 ng/ml) than the seronegative subjects (54.8+/-3.6, p < 0.05). Three of the four subjects with ulcers were Hp-seropositive. The prevalence of Hp-seropositivity and elevated PG1 declined in parallel in each successive generation. When neither parent was seropositive, children were seronegative. CONCLUSIONS: The etiology of elevated PG1 levels in this pedigree is more likely due to Helicobacter pylori infection than to a genetic predisposition.     

Location and Type of Gastric Carcinoma in Relation to Pepsinogen I Level in Blood

Chang FY, Lai KH, Wang TF, Lee SD, Tsai YT, Tsay SH. Location and type of gastric carcinoma in relation to pepsinogen 1 level in blood. Scand J Gastroenterol 1992;27:884-888.

Serum pepsinogen I (PGI) levels were measured in 192 gastric carcinoma (GC) patients and 70 controls. Among GC patients serum PGI levels were not influenced by the following variables: age, sex, smoking, Borrmann's or Lauren's classification, tumor size, cellular differentiation, and layer of invasion. The mean scrum PGI levels of tumors restricted to the body, antrum, or involving both areas were 64.8 ± 37.6ng/ml, 76.0 ± 47.0ng/ml, and 51.1 ±25.5ng/ml, respectively (P< 0.005). Odds ratios of GC patients from the quartile of 262 serum PGI levels in the limits s 100 ng/ml, 70-99.9 ng/ml, 45-69.9 ng/ml, and <45 ng/ml were 1.00, 0.76, 3.44, and 37.1, respectively (F < 0.001). The lower serum PGI levels of Chinese GC patients seem to be related to disease location rather than other characters of the tumor.     

Follow-up study on a high risk population of gastric cancer in north China by serum pepsinogen assay

OBJECTIVE: To explore the features and clinical significance of serum pepsinogen (PG) assay in a follow-up study on a high-risk gastric cancer (GC) population. METHODS: A total of 444 participants from a high-risk area of GC in north China were enrolled in this follow-up study from April 1997 to December 1999. Serum PG was measured by enzyme-linked immunosorbent assay (ELISA), and the percentage changes in PG were calculated with 'PG( follow-up)/PG (first test)' thrice from the beginning to the end of these 30 months. Stomach diseases were diagnosed by a gastroscopy with biopsy examination. Helicobacter pylori (H. pylori) status was assessed by histopathological examination and serum H. pylori-immunoglobulin (Ig)G antibody assay with ELISA. RESULTS: In all groups except for the 51-60-year olds no significant differences of percentage changes in PGII and the PGI/II ratio were observed during 30-month follow-up period. In the superficial gastritis (SG) group the percentage change in PGI of group A (after 6 months' follow up) was significantly lower than that of group B (after 12 months' follow up) (0.69 vs 0.97, P = 0.002) in SG-->SG; while in SG-->normal (NOR), it was significantly higher than that in SG-->atrophic gastritis (AG) (0.94 vs 0.79, P = 0.022). In the AG group the percentage change in the PGI/II ratio of group A was significantly higher than that of group C (after 30 months' follow up) (1.13 vs 0.75, P = 0.042) in AG-->AG; and the percentage changes in PGI and PGII in AG-->NOR were significantly lower than those in AG-->SG (0.43 vs 0.87, P = 0.000; 0.60 vs 1.11, P = 0.010, respectively). In the H. pylori(-) (Hp(-)) group, the percentage change in PG of Hp(-)-->Hp(+) was significantly higher than that of Hp(-)-->Hp(-) (0.94 vs 0.81, P = 0.026). Percentage changes in PGI and PGII of Hp(+)-->Hp(-) were significantly lower than those of Hp(+)-->Hp(+) (0.74 vs 0.93, P = 0.000; 0.86 vs 1.15, P = 0.000, respectively), while the percentage change in the PGI/II ratio was higher than that the group of Hp(+)-->Hp(-) (0.90 vs 0.70, P = 0.022). CONCLUSION: The serum PG levels were influenced by the physiopathologic status of gastric mucosa and H. pylori infection, but they altered during the period of follow up. Serum PG assay might be a feasible and appropriate procedure to use in following up on a high-risk GC population.     

Location and type of gastric carcinoma in relation to pepsinogen I level in blood.

Serum pepsinogen I (PGI) levels were measured in 192 gastric carcinoma (GC) patients and 70 controls. Among GC patients serum PGI levels were not influenced by the following variables: age, sex, smoking, Borrmann's or Lauren's classification, tumor size, cellular differentiation, and layer of invasion. The mean serum PGI levels of tumors restricted to the body, antrum, or involving both areas were 64.8 +/- 37.6 ng/ml, 76.0 +/- 47.0 ng/ml, and 51.1 +/- 25.5 ng/ml, respectively (P < 0.005). Odds ratios of GC patients from the quartile of 262 serum PGI levels in the limits > or = 100 ng/ml, 70-99.9 ng/ml, 45-69.9 ng/ml, and < 45 ng/ml were 1.00, 0.76, 3.44, and 37.1, respectively (P < 0.001). The lower serum PGI levels of Chinese GC patients seem to be related to disease location rather than other characters of the tumor.