幽门螺杆菌感染对老年消化性溃疡患者血清PGⅠ、PGⅡ、GS、PINP、TNF-α水平的影响

目的 探讨幽门螺杆菌感染对老年消化性溃疡患者血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)、胃泌素(GS)、Ⅰ型胶原氨基端前肽(PINP)、肿瘤坏死因子α(TNF-α)水平的影响。方法 本研究选取我院诊治的老年消化性溃疡患者200例,根据幽门螺杆菌感染状况分为阳性组(134例,其中胃溃疡82例、十二指肠溃疡52例)与阴性组(66例,其中胃溃疡40例、十二指肠溃疡26例),采用双抗体夹心酶联免疫吸附法检测血清PGⅠ、PGⅡ、GS、PINP、TNF-α水平。结果 幽门螺杆菌感染阳性消化性溃疡患者血清PGⅠ、PGⅡ、GS、TNF-α水平高于阴性患者(P<0.05),PINP低于阳性患者(P<0.05)。胃溃疡及十二指肠溃疡幽门螺杆菌感染阳性患者血清PGⅠ、PGⅡ、GS、TNF-α水平高于阴性患者(P<0.05),PINP低于阳性患者。十二指肠溃疡患者血清PGⅠ、GS高于胃溃疡患者(P<0.05),PINP低于胃溃疡患者(P<0.05),PGⅡ及TNF-α水平比较差异无统计学意义(P>0.05)。结论 幽门螺杆菌对老年消化性溃疡患者血清PGⅠ、PGⅡ、G...     

PG水平与抗幽门螺杆菌IgG水平在胃肠溃疡患者中的指导价值

目的探讨血清胃蛋白酶原(pepsinogen,PG)和抗幽门螺杆菌(Helicobacter pylori,H.pylori)免疫球蛋白G(immunoglobulin G,IgG)抗体胃肠溃疡患者中的诊断效果及价值.方法取2015-01/2016-07天津医科大学宝坻临床学院医学内科收治消化性溃疡250例,设为观察组,取同期入院健康体检者250例,设为对照组.采用化学发光微粒子免疫分析法测定2组血清PG水平,采用酶联免疫吸附法测定2组抗H.pylori IgG抗体水平,分析血清PG和H.pylori IgG抗体在消化性溃疡中的临床指导价值.结果观察组血清胃蛋白酶Ⅰ(pepsinogenⅠ,PGⅠ)、血清胃蛋白酶Ⅱ(pepsinogenⅡ,PGⅡ)及胃蛋白Ⅰ/Ⅱ比值(gastric proteinⅠ/Ⅱratio,PGR)水平,高于对照组(P0.05);观察组50例患者中31例H.pylori阳性,19例H.pylori阴性;H.pylori阳性患者血清PGⅠ、PGⅡ及PGR水平,显著高于H.pylori阴性患者(P0.05);PGⅠ、PGⅡ及PGR联合检测敏感性、特异性,显著高于单一PGⅠ、PGⅡ及PGR指标(P0.05).结论血清PG和H.pylori IgG抗体能对消化溃疡进行早期筛查,当二者异常时再行胃镜检查能提高诊断确诊率及检查依从性.     

胃息肉患者检测幽门螺杆菌及血清胃蛋白酶原的临床价值

目的探讨联合检测幽门螺杆菌(H.pylori)及血清胃蛋白酶原(PG)对胃息肉的临床价值。方法对249例接受内镜下治疗的胃息肉患者及100例对照组进行H.pylori感染测定,并检测空腹血清PGⅠ、PGⅡ水平,进行统计学分析。结果息肉组总体与对照组H.pylori感染率无明显差异,将息肉组分为炎性息肉组,增生性息肉组,腺瘤组三个亚组与对照组H.pylori感染率对比,显示腺瘤组及炎性息肉组H.pylori感染率明显高于对照及增生性息肉组。血清PGⅠ及PGⅠ/Ⅱ比值(PGR)息肉组明显低于对照组,以胃体及胃窦息肉亚组为著。结论联合检测H.pylori感染及血清PG浓度对胃息肉诊治有重要临床意义。     

幽门螺杆菌感染相关慢性胃病患者血清MTL与胃泌素及胃蛋白酶原含量水平表达差异性

目的探讨幽门螺杆菌(Helicobacter pylori,H.pylori)感染相关慢性胃病患者胃黏膜肥大细胞数量、血浆胃动素及胃泌素水平差异性.方法选取2015-01/2017-01在绍兴市柯桥区齐贤医院和绍兴市中心医院接受治疗的H.pylori感染胃溃疡(gastric ulcer,GU)患者74例,H.pylori感染十二指肠溃疡(duodenal ulcer,DU)患者68例,H.pylori感染慢性萎缩性胃炎(chronic atrophic gastritis,CAG)患者76例,选取同一时间段内在绍兴市柯桥区齐贤医院和绍兴市中心医院接受体检的健康人80例作为对照组(无H.pylori感染),观察组4组对象肥大细胞(mast cell,MC)数量及血清内胃动素(motilin,MTL)、胃泌素、胃蛋白酶原含量状况.结果 CAG、GU、DU组MC数量均高于对照组(16.79个/HSP±2.64个/HSP),血清MTL含量均低于对照组(307.05ng/L±56.21 ng/L),差异有统计学意义(P0.05);血清G17在DU、GU、对照组及C A G组依次降低,GU组与DU组的胃蛋白酶原(pepsinogen,PG)Ⅰ、PGⅡ、PGⅠ/Ⅱ水平均高于对照组的(199.74mg/L±80.53mg/L)、(13.72mg/L±5.75mg/L)、(14.53±5.42),CAG组PGⅠ、PGⅠ/Ⅱ均低于对照组,差异均有统计学意义(P0.05).结论 H.pylori感染通过调节血清内MTL、胃泌素和胃蛋白酶原含量来促进GU、DU和CAG患者病情发展.     

功能性消化不良患者中幽门螺杆菌感染与胃蛋白酶原水平相关性研究

目的 探讨在功能性消化不良（functional dyspepsia,FD）患者中,胃蛋白酶原（Pepsinogen,PG）水平与幽门螺杆菌（Helicobacter pylori,H.pylori）感染相关性.方法 某部新兵FD患者按H.pylori感染分成H.pylori阳性组与H.pylori阴性组,采用ELISA法对其血清PGⅠ、PGⅡ含量进行检测,血清H.pylori-IgG抗体采用定性分析法.结果 在FD患者中,H.pylori阳性组PGⅠ、PGⅡ、PGⅠ/ PGⅡ水平分别为（137.93±27.73） μg/L、（7.05±3.92） μg/L、24.69±15.5,H.pylori阴性组PGⅠ、PGⅡ、PGⅠ/ PGⅡ水平分别为（131.17±＋26.38） μg/L、（2.85±2.11） μg/L、64.0±76.44,两组相比差异均有统计学意义（tⅠ=2.714,tⅡ=17.432,tⅠ/Ⅱ=5.270,P均〈0.05）.结论 在功能性消化不良患者中,H.pylori感染可能会引起胃蛋白酶原PGⅠ、PGⅡ水平升高,以PGⅡ为主.     

消化性溃疡患者血清胃蛋白酶原、胃泌素、Ⅰ型胶原氨基端前肽和肿瘤坏死因子-α的变化与幽门螺杆菌感染的关系

目的探讨消化性溃疡患者血清胃蛋白酶原Ⅰ(PGⅠ)、PGⅡ、胃泌素(GS)、Ⅰ型胶原氨基端前肽(PINP)和肿瘤坏死因子-α(TNF-α)的变化及其与幽门螺杆菌(Hp)感染的关系。方法选取2015年10月至2017年10月间在青海仁济医院消化内科经消化内镜确诊的194例消化性溃疡患者,其中胃溃疡患者105例(胃溃疡组)、十二指肠溃疡患者89例(十二指肠溃疡组),检测两组患者的血清PGⅠ、PGⅡ、GS、PINP及TNF-α水平并进行比较,然后按照Hp感染结果进行分层分析。结果十二指肠溃疡组的血清PGⅠ、GS表达水平高于胃溃疡组,血清PINP表达水平低于胃溃疡组,差异均有统计学意义(P均0.05);十二指肠溃疡组的血清PGⅡ、TNF-α水平与胃溃疡组相比较,差异无统计学意义(P0.05)。Hp感染阳性的胃溃疡组的血清PGⅠ、GS、TNF-α表达水平显著高于Hp感染阴性组,血清PINP水平低于Hp感染阴性组,差异均有统计学意义(P均0.05);Hp感染阳性的胃溃疡组的血清PGⅡ表达水平与阴性组比较,差异无统计学意义(P0.05)。Hp感染阳性的十二指肠溃疡组的血清PGⅠ、PGⅡ、GS、TNF-α表达水平高于阴性组,血清PINP表达水平低于阴性组,差异均有统计学意义(P均0.05)。结论血清PGⅠ、PGⅡ、PINP、GS、TNF-α水平变化与溃疡的部位及Hp感染有关。     

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。     

早期与进展期胃癌患者胃黏膜“血清学活检”指标差异比较

目的探讨血清胃蛋白酶原(PG)、胃泌素17(G17)水平在胃癌进展不同阶段的差异。方法本研究共纳入早期及进展期胃癌患者168例,应用酶联免疫吸附测定法(ELISA)检测血清PG、G17水平以及幽门螺杆菌(H.pylori-Ig G)滴度。结果年龄≤60岁胃癌患者与60岁者相比,PGⅠ水平升高,而PGⅡ水平降低;PGⅠ/PGⅡ比值高于60岁以上者(P=0.026)。H.pylori阳性胃癌患者的PGⅠ(P=0.001)、PGⅡ(P=0.000)水平显著高于阴性者,PGⅠ/PGⅡ比值(P=0.045)水平则显著低于阴性者。此外,女性胃癌患者血清G17水平普遍高于男性(P=0.004)。早期胃癌和进展期胃癌的血清PG、G17水平在总体上相比,差异无统计学意义(P0.05);在分层分析者中,早期胃癌PGⅠ/PGⅡ比值在男性患者中显著高于进展期胃癌患者(P=0.031);早期胃癌患者血清G17水平在年龄≤60岁组(P=0.015)、H.pylori感染阳性组(P=0.041)和胃体癌组(P=0.035)中均低于进展期胃癌。结论更低水平的PGⅠ/PGⅡ比值和高的G17水平在特定人群中可能提示更高阶段的胃癌。     

血清PGⅡ水平与胃疾病及幽门螺杆菌感染关系研究

目的探讨血清胃蛋白酶原Ⅱ(PGⅡ)在不同疾病中的血清表达水平及其与幽门螺杆菌(H.pylori)感染的关系。方法本研究共纳入2004年于庄河市中心医院就诊的患者565例,应用酶联免疫吸附测定法(ELISA)检测血清PGⅡ水平以及H.pyloriIg G抗体(H.pylori-Ig G)滴度。结果在≤60岁人群、H.pylori-Ig G阴性人群及浅表性胃炎(SG)组中,女性患者血清PGⅡ水平均显著低于男性(P0.05);在萎缩性胃炎(AG)组中,女性患者血清PGⅡ水平与男性相比存在升高的趋势(P0.05)。在SG组、胃糜烂溃疡(GEU)组、AG组及胃癌(GC)组中,H.pylori阳性患者血清PGⅡ水平均显著高于H.pylori阴性患者(P0.0005)。在总人群中,与SG组相比,GEU组血清PGⅡ水平显著升高(P=0.010)。在H.pylori阳性人群中,与SG组相比,GEU组血清PGⅡ水平显著升高(P=0.006);与GEU组相比,AG组PGⅡ水平显著降低(P=0.029)。结论血清PGⅡ水平受患者性别及H.pylori感染等相关因素的影响,在从浅表性胃炎、胃糜烂溃疡、萎缩性胃炎到胃癌的动态变化过程中呈现先升高后降低的趋势。血清PGⅡ作为胃黏膜分化成熟的标志物,其表达水平有望成为胃疾病筛查及早期诊断的一个重要检测指标,尤其是对于H.pylori感染相关胃疾病具有较好的提示作用。     

血清胃蛋白酶原在慢性胃部病变中变化的临床研究

目的分析不同胃部病变发生情况下血清胃蛋白酶原(pepsinogen,PG)表达水平,为消化系统疾病的临床诊断提供一定帮助。方法收集2015年7月至2017年4月武汉大学人民医院住院患者372例,包括312例胃部病变患者和60例无胃部病变者(对照组)。根据胃部病变不同可分为幽门螺旋杆菌(Helicobacter pylori,H. pylori)感染、胃炎、消化性溃疡、胃癌前病变、胃癌,其中胃炎包括浅表性胃炎组、糜烂性胃炎组、萎缩性胃炎组;消化性溃疡包括胃溃疡组、十二指肠球部溃疡组、复合溃疡组;胃癌前病变包括胃息肉组及残胃吻合口炎组。采用全自动生化分析仪检验血清PG(PGⅠ和PGⅡ)表达情况,并求PGⅠ与PGⅡ的比值(PGR),采用t检验及方差分析对各组的PG水平差异进行分析比较。结果 H. pylori感染组与对照组比较,PGⅠ、PGⅡ水平及PGR值明显升高,差异有统计学意义(P 0. 05)。在胃炎各组中,浅表性胃炎组PGⅠ、PGⅡ水平及PGR值与对照组相比,差异无统计学意义(P 0. 05);糜烂性胃炎组与对照组比较,PGⅠ水平、PGR值明显升高,差异有统计学意义(P 0. 05),PGⅡ水平升高,但差异无统计学意义(P 0. 05);萎缩性胃炎组PGⅠ、PGⅡ水平及PGR值与对照组相比均明显下降(P 0. 05)。在消化性溃疡各组中,胃溃疡组患者与对照组进行比较,PGⅠ、PGⅡ水平均明显升高(P 0. 05),PGR值变化不大差异无统计学意义(P 0. 05);与对照组比较,十二指肠球部溃疡组及复合溃疡组PGⅠ、PGⅡ水平及PGR值明显升高(P 0. 05)。在癌前病变中,胃息肉组与对照组相比,PGⅠ水平及PGR值均显著升高(P 0. 05),PGⅡ水平也升高,但差异无统计学意义(P 0. 05);残胃吻合口炎组PGⅠ、PGⅡ水平和PGR值与对照组相比均明显下降(P 0. 05)。胃癌组与对照组比较,PGⅠ水平、PGR值均明显下降(P 0. 05),PGⅡ水平升高,但差异无统计学意义(P 0. 05)。结论血清PGⅠ、PGⅡ水平和PGR值的联合运用可有助于慢性胃部疾病的筛查、诊断及鉴别,具有较为显著的临床意义。     

Noninvasive evaluation of Helicobacter pylori therapy: role of fasting or postprandial gastrin, Pepsinogen I, Pepsinogen II, or serum IgG antibodies

OBJECTIVE: We evaluated the potential value of a change in serum IgG antibodies, fasting or meal-stimulated gastrin levels, and pepsinogen I (PGI) or pepsinogen II (PGII) levels for identifying Helicobacter pylori (H. pylori) status after antibiotic therapy. METHODS: A total of 32 men and one woman with peptic ulcer disease and documented H. pylori infection were enrolled. Fasting and 30-min postprandial blood samples were obtained at 0, 2, 7, 11, 17, 23, 27, and 39 wk of the study and were analyzed for the factors evaluated. RESULTS: Treatment was successful in 25 patients and failed in seven. Serum IgG antibodies, meal-stimulated gastrin, and both fasting and meal-stimulated pepsinogen I and II levels fell throughout the study, and pepsinogen I:II ratios increased in those whose infection was cured. The mean levels at wk 0 versus wk 7 were: fasting gastrin (fmol/ml) 12.4 and 11, meal-stimulated gastrin 26.5 and 15.4, PGI (ng/ml) 83.7 and 59, PGII (ng/ml) 24.5 and 13.6, PGI/PGII 3.5 and 4.7, and enzyme-linked immunosorbent assay value 4.8 and 4.55. The sensitivity, specificity, and positive and negative predictive values for the data analyzed using different percent changes (e.g., 80%, 50%, and 20%) were calculated. The specificity and sensitivity remained <80% at all time points. CONCLUSIONS: Despite a significant fall in serum markers of H. pylori infection in groups of individuals, no marker tested could be used to reliably determine posttherapy H. pylori status for individual patients.     

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.     

Serum pepsinogen I and pepsinogen II, and the ratio of pepsinogen I pepsinogen II in peptic ulcer diseases: With special emphasis on the influence of the location of the ulcer crater

To investigate the effect of the location of the ulcer crater on the serum levels of pepsinogen I (PGI), pepsinogen II (PGII) and the ratio of PGI/PGII, these parameters were determined in 161 healthy controls, 29 patients with gastric ulcer in the gastric body (GU-I), 65 with coexistent gastroduodenal ulcer (GU-II), 104 with gastric ulcer in the prepyloric region (GU-III), and 116 with duodenal ulcer (DU). Serum PGI levels were significantly higher (P<0.01) in patients with GU-III (110.6 ± 65.1 ng/mL), GU-II (100.0 ± 46.6 ng/mL), and DU (92.2 ± 35.2 ng/mL) than in the controls (77.4 ± 31.4 ng/mL), while there were no significant differencs between GU-I (82.5 ± 36.3 ng/mL) and the controls. Patients with gastric ulcer in any region had significantly higher (P<0.01) serum PGII levels (GU-I, 20.0 ± 15.7 ng/mL; GU-II, 15.5 ± 10.9 ng/mL; GU-III, 14.3 ± 10.0 ng/mL) than the controls (10.6 ± 6.0 ng/mL) and the patients with DU (10.0 ± 5.5 ng/mL), whereas no significant differences existed between the latter two. The ratio of PGI/PGII in GU-I (5.86 ± 3.90) was significantly lower (P<0.01) than any other group (controls, 8.83 ± 4.70; GU-II, 8.33 ± 4.99; GU-III; 9.64 ± 6.13; DU, 10.45 ± 4.49), while patients with DU it was significantly higher (P<0.01) than any other groups. These findings indicate that peptic ulcer is comprised of a heterogeneous group of diseases. A normal level of serum PGI, an increased level of PGII, and a decreased ratio of PGI/PGII in GU-I patients reflected extensive atrophic gastritis, while an elevated level of PGI, a normal level of PGII, and an increased ratio of PGI/PGII in DU patients implicated hypersecretory status coexistent with superficial fundic gastritis. These findings suggest functional heterogeneity of the gastric mucosa according to the different locations of the ulcer crater.     

Th response to Helicobacter pylori differs between patients with gastric ulcer and duodenal ulcer

OBJECTIVE: Helicobacter pylori (H. pylori) infection induces both gastric (GU) and duodenal ulcers (DU). We examined whether host immunological response to H. pylori determines different disease outcomes. MATERIAL AND METHODS: Thirty-two GU and 28 DU patients infected with H. pylori, and 24 dyspeptic patients without infection were enrolled. The constituents of cellular infiltrates in biopsies from each patient were determined and lymphokines secreted by stimulated T cells were measured. Serum concentrations of IgG subclasses specific to H. pylori were measured. RESULTS: Low pepsinogen I and high pepsinogen II levels were observed in GU patients, while a high pepsinogen I level was found in DU patients. T cells predominate over other cell types in both GU and DU patients. GU patients had a higher number of T cells (p < 0.01) and lower plasma cells (p < 0.05) than those in DU patients. T cells from GU patients produced greater amounts of IFN-gamma and less IL-4 than those in DU patients (p < 0.01). GU patients had a higher serum level of IgG2 specific to H. pylori than that in DU patients (p < 0.01). CONCLUSIONS: Th response by gastric T cells in GU patient was more polarized to Th1 as compared with that in DU patients, suggesting that a distinct immune response to H. pylori induces different disease outcomes.     

Basal and stimulated gastrin and pepsinogen levels after eradication of Helicobacter pylori: a 1-year follow-up study

AIM: A decrease in gastrin and pepsinogen (PG) levels 1 month after Helicobacter pylori eradication has been described repeatedly, but the long-term progression of such a decrease has been scarcely studied. We therefore studied the effect of H. pylori eradication on basal and stimulated gastrin and PG levels for 1 year. Initially, the usefulness of measuring these parameters for the noninvasive diagnosis of H. pylori eradication was validated. Furthermore, an assessment was made of the association between H. pylori reinfection and a re-increase in gastrin and PG values. Finally, an evaluation was made of the variables influencing gastrin and PG concentration, with particular attention to H. pylori infection and histological lesions of gastric mucosa. METHODS: Two-hundred and twenty-two patients with duodenal ulcer were studied prospectively. Exclusion criteria were the administration of antibiotics, H2 antagonists, omeprazole or bismuth prior to endoscopy. In all patients serum basal levels of gastrin, PGI, and PGII were measured before and 1 month after completing eradication therapy. In the successfully eradicated patients, gastrin, PGI, and PGII were also measured at 6 and 12 months. In 80 patients stimulated measurements of gastrin (after ingestion of two beef cubes) and PGI (after injection of pentagastrin) were also performed. H. pylori-negative patients after therapy underwent a urea breath test at 6 and 12 months, and patients who had stimulated gastrin and PG concentration measured had also an endoscopy performed at 6 months. RESULTS: H. pylori was eradicated in 73% of patients. A histological improvement was observed 1 month after completing H. pylori eradication therapy, both at gastric antrum and body (P < 0.001), while a further improvement at antrum was demonstrated at 6 months (P < 0.01). With regard to the different cut-off points for decreased basal and stimulated measurements for diagnosing H. pylori eradication, the best results were obtained, respectively, with PGII (sensitivity of 90% and specificity of 76%) and PGI 30 min after stimulation (sensitivity and specificity of 82%), with an area under the ROC curve of 0.87 in both cases. In the multiple regressions analysis H. pylori status correlated with gastrin, PGI and PGII after therapy (P < 0.001), while histological lesions correlated only with gastrin levels (P < 0.05). A decrease in basal and stimulated serum parameters was demonstrated immediately after eradication (Wilcoxon test, P < 0.001), and an additional decrease (at 6 months) was observed just in PGI (Friedman test, P < 0.01). However, gastrin and PGII values remained unchanged after the first month post-eradication. Seven patients were reinfected with H. pylori during follow-up. Quantitation of basal and stimulated gastrin and PGI levels was not reliable as a reinfection marker. Regarding basal PGII, the parallelism was strong at 6 months (re-increase in all four reinfected patients), although only in one out of three with reinfection at 1 year did PGII rise at that stage. CONCLUSIONS: (1) Measurement of gastrin and PG levels (especially basal PGII values) is a useful non-invasive method to confirm H. pylori eradication after therapy. (2) H. pylori eradication is associated with a significant decrease in basal and stimulated gastrin levels and in basal PGII levels that is detected immediately (1 month) after finishing treatment, and remains unchanged for 1 year. However, the decrease in basal and stimulated PGI levels occurs progressively for 6 months, although such levels remain also unchanged afterwards. (3) Measurement of gastrin and PGI concentrations has a limited usefulness in the diagnosis of H. pylori reinfections after successful eradication, although PGII determination could be more useful in this situation.     

Barrett's esophagus is characterized by the absence of Helicobacter pylori infection and high levels of serum pepsinogen I concentration in Japan

Background and Aim:  It has been reported that patients with Barrett's esophagus (BE) may have gastric acid hypersecretion. Serological markers such as serum pepsinogen or gastrin have been used to estimate the gastric secretory function. The aim of this study was to compare the serum pepsinogen and gastrin concentrations in view of Helicobacter pylori infection status between BE patients and the controls.
Methods:  Thirty-six patients with long-segment BE were enrolled in this study. Three age- and sex-matched controls were assigned to each patient. Serum pepsinogen and gastrin concentrations were measured by radioimmunoassay and H. pylori infection was determined by histology and serum IgG antibodies.
Results:  Helicobacter pylori infection was present in 4 of 36 patients (11%) with BE and in 80 of 108 controls (74%), being less prevalent in BE patients than in the controls ( P  < 0.0001). When examined in the H. pylori -negative subjects, both the serum pepsinogen I and pepsinogen II concentrations in BE patients were significantly higher than those in the controls (mean pepsinogen I:BE 51.0 ± 14.0 ng/mL vs control 38.9 ± 13.5 ng/mL, P  = 0.0012; mean pepsinogen II:BE 10.8 ± 4.0 ng/mL vs control 7.9 ± 2.0 ng/mL, P  = 0.0097). There was no significant difference in the serum gastrin levels between BE patients and the controls irrespective of the H. pylori infection status.
Conclusions:  Most of the Japanese BE patients are characterized by the absence of H. pylori infection and high levels of serum pepsinogen. Determination of the serum pepsinogen level in combination with the H. pylori infection status could be a useful serological marker for BE screening.     

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.     

Relationship between Helicobacter pylori status and serum pepsinogens as serologic markers in atrophic gastritis.

BACKGROUND/AIMS: Serum pepsinogen levels are considered as a non-endoscopic blood test in the diagnosis of atrophic gastritis. The objective of the present study was to investigate whether there is any difference between pepsinogen levels in Helicobacter pylori-positive and -negative patients with atrophic gastritis, and to analyze the relationship between histopathology and pepsinogen levels after treatment in H. pylori-positive patients with atrophic gastritis. METHODS: The study enrolled a total of 30 cases with atrophic gastritis (18 H. pylori-positive and 12 H. pylori-negative). The H. pylori-positive cases received a one-week eradication treatment. Initially for all and after the treatment for H. pylori-positive cases, serum pepsinogen I and II levels, anti-H. pylori IgG titration and histopathologic analysis were carried out. RESULTS: In the H. pylori-positive patients with atrophic gastritis, the levels of pepsinogen I and pepsinogen I/II ratio were lower while the levels of pepsinogen II were higher compared to the H. pylori-negative patients (p<0.05 for all). The post-treatment serum pepsinogen I levels and pepsinogen I/II ratios did not change in the H. pylori-positive group, while the levels of pepsinogen II, H. pylori antibody titration and gastric atrophy degree remarkably decreased (p<0.05 for all). CONCLUSIONS: In atrophic gastritis, the levels of serum pepsinogen and pepsinogen I/II ratio show a difference in H. pylori-negative versus -positive cases. Additionally, the usage of pepsinogen II as a serum marker in predicting the eradication of H. pylori with atrophic gastritis could be more reliable than pepsinogen I or the I/II ratio.     

Serological comparison of serum pepsinogen and anti-parietal cell antibody levels between Japanese and German patients

BACKGROUND: Atrophic gastritis is more common in Japan than in Germany. The expression of anti-parietal cell antibody has been implicated in the genesis of atrophic gastritis associated with Helicobacter pylori infection. OBJECTIVE: We investigated the difference in serum levels of pepsinogens and in anti-parietal cell antibody expression between Japanese and German patients. METHODS: We recruited 102 Japanese and 46 German patients with dyspepsia. Endoscopic examination detected no localized lesions in the upper gastrointestinal tract of any patients. Anti-parietal cell antibody was investigated by enzyme-linked immunosorbent assay with the purified porcine H+,K+-ATPase fraction and immunohistochemistry. H. pylori infection was diagnosed by the presence of anti-H. pylori antibody, by using the urease test and by histological examination. Serum levels of pepsinogen I and II and of gastrin were measured by a modified radioimmunoassay. RESULTS: Seventy-one Japanese (70%) and 17 Germans (37%) were positive for H. pylori. Serum levels of anti-parietal cell antibody were not significantly different between Japanese and Germans in both H. pylori negative and positive groups. The serum pepsinogen I/II ratio and gastrin levels were altered by H. pylori infection in both populations. Moreover, anti-parietal cell antibody levels were higher in H. pylori-positive patients with low pepsinogen levels than in those with high pepsinogen levels in both populations. CONCLUSIONS: The levels of anti-parietal cell antibody do not differ statistically between Japanese and Germans. Anti-parietal cell antibody might play a role in the progression of atrophic gastritis in both Japanese and German patients.