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。     

萎缩性胃炎患者幽门螺杆菌感染与高胃泌素血症的关系

萎缩性胃炎患者幽门螺杆菌感染与高胃泌素血症的关系唐新华张虹程玲于澎作者对４０例萎缩性胃炎患者进行幽门螺杆菌（Ｈｐ）及血清胃泌素（ＧＡＳ）水平检测，旨在观察其间的相互关系。一、对象：４０例萎缩性胃炎患者为１９９６年６月～１９９６年１０月本院胃镜室受检病...     

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。     

血清胃蛋白酶原、胃泌素-17含量用于筛查慢性萎缩性胃炎的参考值

目的 探讨血清胃蛋白酶原I(PG I)、胃蛋白酶原I/胃蛋白酶原II(PG I/PG II)比值(PGR)和胃泌素-17与慢性萎缩性胃炎的关系,确立其筛查萎缩性胃炎的最佳界值.方法 选择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结果分为对照组(48例)和慢性萎缩性胃炎组(52例),以免疫放射和放射免疫法检测血清PG I、PG II和G-17水平.结果 慢件萎缩性胃炎组与对照组相比.血清PG I、PGR和G-17水平显著降低(P＜0.001).胃体萎缩组、全胃多灶性萎缩组的血清PG I、PGR显著低于胃窦萎缩组(P＜0.001),胃窦萎缩组、全胃多灶性萎缩组的血清G-17显著低于胃体萎缩组(P＜0.001).根据ROC曲线,PG I、PGR和G-17筛查慢性萎缩性胃炎的最佳界值分别为82.2μg/L(敏感性85%,特异性73%)、7.5(敏感性89%,特异性71%)和8.3 pmol/L(敏感性85%,特异性73%).结论 检测血清PG和G-17可以作为一种无创性的筛查慢性萎缩性胃炎的方法,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。     

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、血清胃泌素-17与抗幽门螺杆菌IgG抗体在萎缩性胃炎及胃癌筛查中的应用价值

近年来研究发现,血清胃蛋白酶原、血清胃泌素-17与抗幽门螺杆菌抗体在萎缩性胃炎及胃癌筛查中具有应用价值,甚至认为这些指标是胃黏膜血清学活检,现将有关进展简述如下。     

慢性萎缩性胃炎与幽门螺杆菌感染的生物学行为研究

目的 幽门螺杆菌与胃部疾病的关系已受到广泛关注。同认为，幽门螺杆菌（Ｈｐ）不仅是慢性活动性胃炎的致病因子，而且与胃窦部萎缩性胃炎、肠上皮化生、异型增生及胃癌的形成密切相关。本文检测上述疾病Ｈｐ的感染率，目的就是要明确Ｈｐ的污染率，目的就是要明确Ｈｐ与上述疾病的关系，为临床上述对以上疾病的诊断和治疗提供新的线索和方向。方法 对１９８你病例根据胃窦部胃镜及胃粘膜活检结果分为慢性活动性浅表性胃炎组，经度     

徐振盛治疗慢性萎缩性胃炎经验

本文介绍了徐振盛先生治疗慢性萎缩性胃炎的经验。强调急则治其标，务求其通；缓则治其本，务求其平。本病以脾胃本虚，吸收功能差，用药宜轻剂缓施，从量变到质变，若欲求速效而冒进大剂，只能是更伤脾胃，欲速而不达。     

幽门螺杆菌、胃泌素与慢性胃炎的关系

目的：对慢性浅表性胃炎（ＣＧＳ）患者行幽门螺杆菌（ＨＰ）及空腹血清胃泌素（ＳＧ）检测,对ＨＰ（＋）组和ＨＰ（－）组ＳＧ作对比,抗ＨＰ治疗前后ＳＧ、病理组织学作比较,探讨两者与ＣＳＧ的关系。方法：患者先行空腹作ＳＧ测定,再作胃镜检查,取胃罕粘膜３块,分另作快速尿素酶试验、Ｇｉｅｍｓａ染色及病理组织学检查。ＨＰ（＋）组抗ＨＰ治疗,１月后重复上述检查。结果：ＨＰ（＋）且ＳＧ明显高于ＨＰ（－）组（Ｐ〈０．     

慢性萎缩性胃炎患者幽门螺杆菌根除后胃黏膜G细胞数量和血清胃泌素含量的变化

背景:幽门螺杆菌(H.pylori)感染是慢性萎缩性胃炎(CAG)最重要的致病因素,根除H.pylori能否阻止或逆转胃黏膜萎缩目前尚不清楚.目的:通过观察CAG患者H.pylori根除前后胃黏膜G细胞数量和血清胃泌素含量的变化,探讨H.pylori感染对胃黏膜G细胞数量及其分泌功能的影响.方法:60例H.pylori阳性的CAG患者进行了根除治疗,在治疗前和治疗结束3个月后分别行胃镜检查.采用免疫组织化学法和放射免疫分析法测定H.pylori根除前后胃窦黏膜G细胞数量和血清胃泌素含量.结果:31例H.pylori感染的CAG患者在根除治疗3个月后进行了复查,根除率为77.4%.G细胞数量和血清胃泌素含量随胃黏膜萎缩程度的加重而逐渐显著减少(P<0.01).轻度萎缩组H.pylori根除后G细胞数量与治疗前相比无显著差异(P<0.05),而升高的血清胃泌素含量显著降低(P<0.01);中、重度萎缩组H.pylori根除后减少的G细胞数量显著增加(P<0.05),血清胃泌素含量呈上升趋势(P<0.05).结论:CAG患者根除H.pylori后胃黏膜G细胞数量及其合成、分泌胃泌素的功能可出现恢复性变化,可能有助于阻断CAG的进一步发展.     

慢性萎缩性胃炎幽门螺杆菌检出量与氧自由基关系的研究

检测71例不同程度感染幽门螺杆菌(HP)的慢性萎缩性胃炎患者(患者组)和70例健康成人(对照组)血浆-一氧化氮(P-NO)、血浆维生素C(P-VC)、血浆维生素E(P-VE)、血浆β-胡萝卜素(P-β-CAR)、血浆过氧化脂质(P-LPO)含量及红细胞超氧化物歧化酶(E-SOD)、红细胞过氧化氢酶(E-CAT)、红细胞谷胱甘肽过氧化物酶(E-GSH-PX)活性和红细胞过氧化脂质(E-LPO)含量。结果与对照组比较,患者组的P-VC、P-VE、P-β-CAR、E-SOD、E-CAT和E-GSH-PX水平均值均显著降低(P<0.001),且随HP增多而降低;P-NO、P-LPO和E-LPO平均值均显著升高(P<0.001),且随HP增多而升高。并均呈一定程度的直线回归和相关(P<0.001)。提示慢性萎缩性胃炎患者体内的NO代谢异常,氧化和抗氧化平衡严重失调,氧自由基反应和脂质过氧化反应病理性加剧,且与HP检出量呈正相关。     

Atrophic Gastritis Serum Levels of Amidated Gastrin-17 and Pepsinogen I in Atrophic Gastritis: An Observational Case-Control Study

Background: Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed nonendoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing. Methods: The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method. Results: A low S-PGI (<25 μg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori -associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori -related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; CI 95%: 81%-97%) had a low SPGI and/or a low S-G-17prand with positive H. pylori serology. Such low values were found in 3 of the 44 control patients (7%; CI 95%: 0%-14%). Conclusions: Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori .     

Serum Gastrin and Mucosal Somatostatin in Helicobacter pylori-Associated Gastritis

Aims: The aims were to study serum gastrin concentrations and gastric mucosal somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter pylori infection. Methods: We measured basal serum gastrin concentrations and somatostatin and gastrin concentrations in antral mucosal biopsy specimens and somatostatin concentrations in corpus biopsy specimens in 88 consecutive dyspeptic subjects undergoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pangastritis, H. pylori-positive antral gastritis with normal body histology, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test. Results: Basal serum gastrin concentrations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with controls (mean ± SEM: 72 ± 7, 46 ± 10, and 42 ± 7ng/l, respectively). Subjects with pangastritis or antral gastritis had significantly lower antral somatostatin concentrations than controls (mean ± SEM: 0.80 ± 0.07, 1.03 ± 0.15, and 2.40 ± 0.31 μg/g(protein), respectively). We also found significantly lower antral mucosal gastrin concentrations in subjects with pangastritis and in those with antral gastritis only as compared with controls (mean ± SEM: 62 ± 13, 78 ± 16, and 165 ± 25 μg/g(protein), respectively). In subjects with pangastritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis only and controls. Conclusion: These results suggest that hypergastrinemia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a key role in the origin of hypergastrinemia. Furthermore, in patients with pangastritis a corpus mucosal somatostatin deficiency was found.     

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。     

幽门螺杆菌相关性慢性胃炎中医辨证分型与胃泌素的关系

目的:研究幽门螺杆菌(Hp)相关性慢性胃炎中医辨证分型与空腹血清胃泌素(GAS)的关系.方法:将中医辨证为脾胃湿热型、脾胃虚弱型的42例慢性胃炎患者进行电子胃镜、病理组织学检查,并检测Hp及血清GAS.结果:Hp相关性慢性胃炎中脾胃湿热型占62.96%(P<0.05);空腹血清GAS(125.35 ng/L)高于脾胃虚弱型(96.59 ng/L,P<0.01).结论:高GAS血症可能是Hp相关性慢性胃炎脾胃湿热证型重要病理生理基础之一.     

Serum Pepsinogen and Gastrin Levels: Reliable Markers to Predict Small Intestinal Bacterial Overgrowth

BackgroundSerum pepsinogen, a useful indicator of gastric acidity, could reflect small intestinal bacterial overgrowth. The aim of this study is to evaluate the relationship between small intestinal bacterial overgrowth and profiles including pepsinogen or gastrin.MethodsWe conducted a prospective study with 62 patients with a functional gastrointestinal disorder. All patients underwent glucose breath test for small intestinal bacterial overgrowth, immediately followed by upper endoscopy to survey gastric injury and Campylobacter-like organism test for Helicobacter pylori and serum laboratory tests including gastrin, pepsinogen I and II.ResultsThe positivity to small intestinal bacterial overgrowth was 17.7%. Significantly, low total hydrogen concentration during a glucose breath test, low prevalence for gastric injury, and high H. pylori positivity rate were shown in groups with pepsinogen I/II ratio ≤ 3.5 compared to those with pepsinogen I/II ratio > 3.5 or in groups with serum gastrin > 35.4 pg/mL comparing to those with serum ≤ 35.4 pg/mL, respectively. A high gastrin level was independently associated with H. pylori infection. A proportionally correlated tendency between pepsinogen I/II ratio and total hydrogen concentration was shown, whereas that of inverse proportion between H₂ and gastrin was observed. Old age was solely independent predicting factor for small intestinal bacterial overgrowth (P = .03) in the multivariate analysis.ConclusionOld age was significantly related to the presence of small intestinal bacterial overgrowth in functional gastrointestinal disorder patients. Although pepsinogen and small intestinal bacterial overgrowth seem irrelevant, elevated gastrin level may cautiously indicate a decreased breath hydrogen concentration. Further studies should consider the function of intestinal motility and gastric acidity in patients with hydrogen-producing small intestinal bacterial overgrowth.     

Serum biomarker tests are useful in delineating between patients with gastric atrophy and normal, healthy stomach

AIM： TO study the value of serum biomarker tests to differentiate between patients with healthy or diseased stomach mucosa： i.e. those with Helicobacter pylori （H pylori） gastritis or atrophic gastritis, who have a high risk of gastric cancer or peptic ulcer diseases. METHODS： Among 162 Japanese outpatients, pepsinogen Ⅰ （Pg Ⅰ） and Ⅱ （Pg Ⅱ） were measured using a conventional Japanese technique, and the European GastroPanel examination （Pg Ⅰ and Pg Ⅱ, gastrin-17 and H pylori antibodies）. Gastroscopy with gastric biopsies was performed to classify the patients into those with healthy stomach mucosa, Hpylori nonatrophic gastritis or atrophic gastritis. RESULTS： Pg Ⅰ and Pg Ⅱ assays with the GastroPanel and the Japanese method showed a highly significant correlation. For methodological reasons, however, serum Pg Ⅰ, but not Pg Ⅱ, was twice as high with the GastroPanel test as with the Japanese test. The biomarker assays revealed that 5% of subjects had advanced atrophic corpus gastritis which was also verified by endoscopic biopsies. GastroPanel examination revealed an additional seven patients who had either advanced atrophic gastritis limited to the antrum or antrum-predominant H pylori gastritis. When compared to the endoscopic biopsy findings, the GastroPanel examination classified the patients into groups with ＂healthy＂ or ＂diseased＂ stomach mucosa with 94% accuracy, 95% sensitivity and 93% specificity. CONCLUSION： Serum biomarker tests can be used to differentiate between subjects with healthy and diseased gastric mucosa with high accuracy.