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.     

血清胃蛋白酶原Ⅰ、Ⅱ和G-17在功能性消化不良患者中的表达及其意义

目的:探讨功能性消化不良(FD)患者血清胃蛋白酶原(PG)Ⅰ、Ⅱ及胃泌素-17(G-17)的水平和意义.方法:根据罗马Ⅲ诊断标准,229例FD患者纳入本研究.均采用酶联免疫吸附试验(ELISA)定量测定血清PG Ⅰ、PGⅡ和G-17含量,计算PG Ⅰ/Ⅱ比值(PGR),血清幽门螺杆菌(H pylon)抗体滴度大于等于35EIU为阳性.结果:以≤40岁、41-50岁、51-60岁和≥61岁进行年龄分组.FD组年龄≥61岁组PGR低于≤40岁组(P=0.049).FD患者PGⅡ、G-17水平要明显高于对照组(P=0.000,0.000),PG Ⅰ没有明显变化(P=0.067),而PGR明显低于对照组(P=0.000).根据ROC曲线计算出诊断FD的PGⅡ和G-17的最佳界值分别为13.2μg/L(灵敏度51.5%,特异度96.2%,准确率65.5%),6.84μg/L(灵敏度52.8%,特异度100%,准确度67.5%).FD组男性在PG Ⅰ与PGⅡ水平均显著高于女性(P=0.003,0.004).FD组H pylori抗体阳性率高于对照组(P=0.028).结论:FD患者血清PGⅡ与G-17水平增加,胃窦与十二指肠近端黏膜可能存在功能学的改变.FD与Hpylori感染相关.     

老年功能性消化不良患者血清胃蛋白酶原Ⅰ、Ⅱ和胃泌素-17的水平及意义

功能性消化不良(FD)发病机制尚未完全明了,一般认为可能因胃肠动力学紊乱和胃肠内分泌失调所致.本研究旨在探讨老年FD患者血清胃蛋白酶原(PG)和胃泌素-17(G-17)水平及其临床意义.1对象与方法1.1 对象2011年1月至2011年6月我科门诊FD老年患者222例,人选标准:诊断符合罗马Ⅲ标准[1],患者知情同意.FD组男100例,年龄(67.9±4.6)岁,女122例,年龄(67.5±5.0)岁;对照组为在我院健康体检的40名老年人[男20例,女20例,年龄(66.9±4.7)岁],无上消化道症状,无腹部手术.     

血清胃蛋白酶原(PG)在胃相关疾病中的诊断价值

[目的]分析血清胃蛋白酶原(PG)在胃相关疾病中的水平变化,为疾病的鉴别诊断提供理论依据。[方法]选取2016-08—2017-08我院健康体检者50例(对照组)、胃癌患者30例(胃癌组)、胃炎患者40例(胃炎组)、出血性胃溃疡患者30例(胃溃疡出血组)、未出血性胃溃疡患者30例(胃溃疡未出血组),对所有参与人员进行血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)水平检测,并计算其比值(PGR=PGⅠ/PGⅡ)。[结果]与对照组比较:胃炎组、胃溃疡出血组和胃溃疡未出血组患者的PGⅠ、PGⅡ水平及其阳性率均明显升高,而PGR值则有所降低,差异有统计学意义(P<0.05);胃癌组的PGⅠ水平及PGR值明显降低,差异有统计学意义(P<0.05),而PGⅡ水平,与对照组比较,差异无统计学意义。胃溃疡患者中,出血组和未出血组的PGⅠ、PGⅡ水平、PGR值及其阳性率比较,差异无统计学意义。胃溃疡出血组和胃溃疡未出血组的PGⅠ、PGⅡ阳性率均高于胃炎组、胃癌组(均P<0.05)。胃癌组PGR阳性率明显高于胃炎组、胃溃疡出血组和胃溃疡未出血组(P<0.05)。[结论]血清PG能在胃相关疾病的诊断中提供帮助,尤其是胃癌的诊断。     

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。     

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。     

血清胃蛋白酶原测定对胃肠疾病诊断的意义

1836年schwann在胃液内发现一种能够分解蛋白质的物质，将其命名为胃蛋白酶。1886年lang-ley等人研究指出胃蛋白酶是以无活性的酶原形式分泌的，所以称其为胃蛋白酶原（peminogen，PG）。近年来随着科学技术的进步，分子生物学的快速发展，实验技术的改进，对胃蛋白酶原的产生、分子结构、特性等有了进一步的认识。尤其是其血清检测对胃部疾病的诊断和大量病例的筛查，减少患者x线检查、内窥镜检查的痛苦有重要意义。     

胃蛋白酶原亚群在胃癌及其术后血清含量变化的临床价值

人胃粘膜可分泌两种免疫活性不同的胃蛋白酶原亚群,即胃蛋白酶原Ⅰ、Ⅱ（ｐｅｐｓｉｎｏｇｅｎⅠ、Ⅱ,ＰＧⅠ、ＰＧⅡ）,国外学者的研究表明［１,２］,胃癌患者血清ＰＧⅠ、ＰＧⅡ含量下降。本文运用放免法,对胃癌及其手术前后、术后复发患者血清ＰＧⅠ、ＰＧⅡ含量...     

质子泵抑制剂在老年心血管病中的应用

<正>质子泵抑制剂(proton pump inhibitors,PPIs)是心血管内科临床工作中常用的保护胃黏膜药物,但是有关PPIs在有心血管疾病特别是有冠状动脉疾病病史的患者群体中的安全性一直存在争议。最近一些年来,医务工作者对此问题非常关注,发表了一系列与之相关的专家共识和建议,本文对PPIs在老年心血管病中的应用做一简要回顾。1心血管病抗凝/抗栓治疗与消化道损伤     

质子泵抑制剂在肝硬化治疗中的应用可能性

肝硬化是我国常见疾病和主要死亡病因之一，是一种以慢性肝损伤为原因，肝组织弥慢性纤维化，假小叶和再生结节形成为特征的慢性肝病。临床上有多系统受累，肝功能损害和门静脉高压为主要表现，晚期出现消化道出血、肝性脑病、肝癌等严重并发症。目前该病尚无特效治疗，一般只针对病因和加强一般治疗缓解病情和延长代偿期；     

Low yield of endoscopy in patients with persistent dyspepsia taking proton pump inhibitors

BACKGROUND: Options for the evaluation of dyspepsia include a Helicobacter pylori test-and-treat strategy, empiric acid suppression, and initial endoscopy. The aim of this study was to determine the yield of endoscopy in patients in whom empiric therapy is unsuccessful compared with patients who received no empiric therapy and to identify factors associated with endoscopic findings. METHODS: A total of 100 patients with dyspepsia referred for endoscopy completed a questionnaire that included a query concerning response to therapy. EGD findings were compared in patients taking an H2-receptor antagonist, patients taking a proton pump inhibitor, and those not receiving empiric therapy. RESULTS: There were fewer endoscopic findings in patients being treated with a proton pump inhibitor compared with those taking an H2-receptor antagonist or those not receiving therapy (p < 0.01). Fewer proton pump inhibitor recipients had esophagitis or ulcer compared with patients in the no therapy group. Lack of symptom relief (<20%) by acid suppression was highly associated with a normal endoscopy (17/17). CONCLUSIONS: Patients with persistent dyspepsia being treated with a proton pump inhibitor have fewer endoscopic abnormalities compared with patients with dyspepsia taking an H2-receptor antagonist and those receiving no therapy. For patients with partial symptom relief, proton pump inhibitor therapy may mask endoscopic findings, particularly esophagitis. Interruption of proton pump inhibitors before endoscopy may increase diagnostic yield. Endoscopy is unlikely to yield a positive finding in patients who experience no symptom relief while taking a proton pump inhibitor or H2-receptor antagonist.     

The efficacy of proton pump inhibitors in nonulcer dyspepsia: a systematic review and economic analysis

BACKGROUND AND AIMS: The evidence that proton pump inhibitor (PPI) therapy affects symptoms of nonulcer dyspepsia is conflicting. We conducted a systematic review to evaluate whether PPI therapy had any effect in nonulcer dyspepsia and constructed a health economic model to assess the cost-effectiveness of this approach. METHODS: Electronic searches were performed using the Cochrane Controlled Trials Register, MEDLINE, EMBASE, CINAHL, and SIGLE until September 2002. Dyspepsia outcomes were dichotomized into cured/improved versus same/worse. Results were incorporated into a Markov model comparing health service costs and benefits of PPI with antacid therapy over 1 year. RESULTS: Eight trials were identified that compared PPI therapy with placebo in 3293 patients. The relative risk of remaining dyspeptic with PPI therapy versus placebo was .86 (95% confidence interval, .78-.95; P = .003, random-effects model) with a number needed to treat of 9 (95% confidence interval, 5-25). There was statistically significant heterogeneity between trials (heterogeneity chi(2) = 30.05; df = 7; P < .001). The PPI strategy would cost an extra US dollar 278/month free from dyspepsia if the drug cost US dollar 90/month. If a generic price of US dollar 19.99 is used, then a PPI strategy costs an extra US dollar 57/month free from dyspepsia. A third-party payer would be 95% certain that PPI therapy would be cost-effective, provided they were willing to pay US dollar 94/month free from dyspepsia. CONCLUSIONS: PPI therapy may be a cost-effective therapy in nonulcer dyspepsia, provided generic prices are used.     

老年人质子泵抑制剂合理应用专家共识

<正>质子泵抑制剂(protonpump inhibitors,PPIs)自20世纪80年代问世至今已二十余年,显著改善了酸相关性疾病的临床结局,对酸相关性疾病的治疗具有里程碑式的意义。由于其突出的疗效和良好的安全性,在临床上的应用范围不断扩大,处方量与日俱增。但近年来,PPIs过度使用(超适应证、超剂量、超疗程)的问题日益突出~([1-2]),潜在的不良反应也备受重视~([3])。PPIs是老年人的常用药物之一,老年人     

Pharmacology of proton pump inhibitors

The gastric H,K-ATPase is the primary target for the treatment of acid-related diseases. Proton pump inhibitors (PPIs) are weak bases composed of two moieties, a substituted pyridine with a primary pK_a of about 4.0, which allows selective accumulation in the secretory canaliculus of the parietal cell, and a benzimidazole with a second pK_a of about 1.0. PPIs are acid-activated prodrugs that convert to sulfenic acids or sulfenamides that react covalently with one or more cysteines accessible from the luminal surface of the ATPase. Because of covalent binding, their inhibitory effects last much longer than their plasma half-life. However, the short half-life of the drug in the blood and the requirement for acid activation impair their efficacy in acid suppression, particularly at night. PPIs with longer half-life promise to improve acid suppression. All PPIs give excellent healing of peptic ulcers and produce good results in reflux esophagitis. PPIs combined with antibiotics eradicate Helicobacter pylori.