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...     

隆起糜烂性胃炎患者幽门螺杆菌感染与高胃泌素血症的关系

隆起糜烂性胃炎 (ｅｒｏｓｉｖｅｇａｓｔｒｉｔｉｓｐｒｏｔｕｂｅｒａｎｓ,ＥＧＰ)是由内镜诊断的一种特殊形态的隆起性病变。许多研究认为 ,幽门螺杆菌 (Ｈｐ)感染是ＥＧＰ的病因之一。我们对 6 2例ＥＧＰ患者进行Ｈｐ及血清胃泌素 (ＧＡＳ)水平检测 ,旨在观察其间的相互关系。材料和方法一、病例选择1999年 1月～ 12月间 ,经胃镜确诊为ＥＧＰ的门诊患者4例。入选条件 :按悉尼系统内镜下分类 ,主要表现为胃窦、胃体黏膜区出现多个疣状或丘疹样隆起 ,直径 5～ 10ｍｍ ,中央凹陷被覆暗褐色积血或白苔 ,周围潮红如天花样皮损。失访 2例 ,可…     

幽门螺杆菌感染引起高胃泌素血症机制的研究进展

胃泌素是重要的胃肠激素,不仅可以调节胃酸分泌,还可作为一种生长因子影响胃上皮细胞的增殖、分化,胃癌细胞的转移、浸润,及胃黏膜组织的重塑和血管再生.幽门螺杆菌(Hp)感染可引起胃泌素分泌异常增高,致胃黏膜癌变,对其具体机制的研究有助于从分子生物学角度寻找阻断Hp感染向胃泌素增高、胃癌转变进程的方法.此文就Hp感染引起胃泌素升高机制的研究进展作一综述.     

幽门螺杆菌与结肠腺瘤相关性的研究

目的探讨幽门螺杆菌感染（Helicobacter pylori, H.pylori）和结肠腺瘤的关系。 方法选取2014年1月至2015年5月就诊于我院有消化道症状或无症状体检患者,经结肠镜检查及病理证实为结肠腺瘤患者200例,无结肠腺瘤患者200例作为对照组,两组患者均行¹³C尿素呼气试验检查是否存在幽门螺杆菌感染,统计结果采用卡方检验,P<0.05时认为差异有统计学意义。 结果H.pylori感染合并结肠腺瘤的患者比例少于对照组,但两组数据比较差异无统计学意义。 结论H.pylori感染与结肠腺瘤的发生无明显相关性。     

十二指肠球部溃疡患者高胃泌素血症与幽门螺杆菌相关性的研究

本文报告我院１９９０年４月～１９９２年１０月期间经胃镜确诊的２６４例十二指肠球部溃疡患者胃窦部幽门螺杆菌检测和血清胃泌素测定结果。结果显示ＨＰ检出率球溃组高达８０．３％（２１２／２６４），与对照组２９．６３％（１６／５４）有显著差异（Ｐ＜０．００５）。ＨＰ阳性球溃组血清胃泌素水平１０３．０３±７２．４３（ｎｇ／Ｌ），较对照组６３．３３±３９．０４（ｎｇ／Ｌ）和ＨＰ阴性球溃组７４．３２±４９．７２（ｎｇ／Ｌ）明显增高（Ｐ均＜０．００５）。随访３８例治疗后ＨＰ阳性球溃患者，２６例溃疡愈合且ＨＰ转阴者血清胃泌素为７８．３２±４２５６（ｎｇ／Ｌ），较前明显下降（Ｐ＜０．０１）。表明球溃患者高胃泌素血症与ＨＰ感染有一定相关性。     

根治幽门螺杆菌对肝硬化高氨血症的影响

幽门螺杆菌（Helieobacter pylori,HP）由于其尿素酶活性较尿素酶阳性的肠杆菌强好多倍而产生大量氨。本研究旨在了解根除HP对肠菌群得以适当治疗的肝硬化患者高氨血症的影响。1. 对象和方法：(1)研究对象：1999年1月至2000年9月住院的100名肝硬化患者（男68例,女32例;年龄41～83岁,平均年龄62岁;肝功能以Childs-Pugh 分级：A级38例,B级36例,C级26例）。所有患者肾功能正常,未接受过抗HP治疗。肝硬化的诊断是通过病史、临床表现、实验室检查等方法确立,个别患者行肝活检证实。(2)研究方法：患者均在根治Hp治疗前口服卡那霉素…     

幽门螺杆菌诱发肝硬化大鼠高氨血症的实验研究

幽门螺杆菌诱发肝硬化大鼠高氨血症的实验研究厉有名伊藤重二郡大裕石井靖黄怀德许多研究表明幽门螺杆菌（Ｈｐ）不仅能引起胃十二指肠粘膜病变，而且因其含有大量尿素酶，能分解尿素，从而与胃液中氨的产生有关［１，２］，然而，迄今为止，人们尚不了解Ｈｐ对肝脏疾病患...     

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．     

幽门螺杆菌感染与肝硬化高氨血症的关系

高血氨是引起肝硬化病人肝性脑病 (ｈｅｐａｔｉｃｅｎｃｅｐｈａｌｏｐａｔｈｙ ,ＨＥ)的重要原因 ,一直认为肠道内细菌产氨是其主要来源之一 ,近年有研究指出 ,胃腔中的幽门螺杆菌(Ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ,Ｈｐ)因富含尿素酶而成为血氨的另一主要来源。一、Ｈｐ引起肝硬化高氨血症的提出及实验研究1993年 ,Ｇｕｂｂｉｎｓ[1] 从其完成的多中心研究中发现 ,发生ＨＥ和未发生ＨＥ的酒精性肝病病人有Ｈｐ感染血清学表现分别者占 79%和 6 2 % ,差异十分显著 ,从而最早提出了Ｈｐ感染产生的氨可能是门体性ＨＥ高危因素的假说。此…     

Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

Both Zollinger-Ellison syndrome (ZES) and Helicobacter pylori infection are major etiologic factors for peptic ulcer. The aim of this study was to investigate the effect of H. pylori infection on ZES with special reference to acid secretion. Sixteen patients with ZES were selected (median age, 59 years; range, 39–66 years; M/F, 9/7), and H. pylori status, ulcer location, gastric acid secretion, serum pepsinogen (PG) I and II concentrations, and PG I/II ratio were determined. The seroprevalence of H. pylori infection was 50%, whereas active H. pylori infection was seen in only 25% of the patients. Thirteen patients had duodenal ulcer (DU), 1 had gastric ulcer (GU), and 2 had both GU and DU. DU was seen in both H. pylori-positive and H. pylori-negative patients, whereas GU was found only in H. pylori-positive patients. Both basal and maximal acid outputs were significantly lower in H. pylori-positive patients than in H. pylori-negative patients (P < 0.05). Moreover, both serum PG I and the PG I/II ratio were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. These results indicate that ZES is an independent risk factor for DU, but H. pylori infection may play some role in the development of GU in ZES. In patients with ZES, H. pylori infection may reduce both hypersecretion from parietal cells and PG I secretion from chief cells, and hyperacidity of the stomach in ZES may have eradicated H. pylori in some patients. Received: March 30, 2000 / Accepted: May 26, 2000     

410例患者结直肠腺瘤与幽门螺杆菌感染特征及相关性分析

目的　探讨结直肠腺瘤与幽门螺杆菌感染的关系。 方法　连续性收集在上海交通大学医学院附属仁济医院内镜中心同时行胃镜及结加肠镜的患者共410例患者的病例资料（其中结直肠腺瘤者74人,正常对照组336人）。比较结直肠腺瘤组和健康对照组幽门螺杆菌感染情况的差异。并将结直肠腺瘤组分别按腺瘤的数目、最大径、病理分型分亚组,比较各亚组与幽门螺杆菌感染情况。统计学分析采用t检验与卡方检验,P < 0.05 被认为具有统计学差异。 结果　结直肠腺瘤组和健康对照组幽门螺杆菌感染阳性率分别为29.73%和19.34%,前者高于后者,差异均有统计学意义（P＜0.05）。按腺瘤数目、最大径、病理分型分亚组,各亚组组内幽门螺杆菌感染阳性率差异均无统计学意义（P均＞0.05）,但按递进分层与对照组相比均有统计学差异（P均小于0.05）。 结论　结直肠腺瘤可能与幽门螺杆菌感染有直接相关,同时幽门螺杆菌对腺瘤的发展可能有促进作用。     

Helicobacter pylori infection

IS THERE ANYTHING NEW? Helicobacter pylori has been for many years a forgotten bacterium, since the first report on this spiral organism dated from the 19th century[1]. As early as in 1906, an association between a spiral organism and gastric carcinoma was suggested[2].Doenges reported in 1938 that on autopsy not less than 40% of human stomachs were found to be invaded by spiral organisms[3].     

Helicobacter pylori infection

Summary The present report describes two patients with fasting hypergastrinemia, gastric acid hypersecretion, andHelicobacter pylori gastritis. Provocative testing for Zollinger-Ellison syndrome was negative and imaging studies did not demonstrate an intra-abdominal mass. Following eradication of theHelicobacter pylori infection, the fasting hypergastrinemia resolved in both patients and in one patient the gastric acid hypersecretion also resolved. The implications of this case on the differential diagnosis of Zollinger-Ellison syndrome are discussed.     

Helicobacter pylori infection increases the risk of colorectal adenoma and adenocarcinoma, especially in women

Background Recent reports suggest that Helicobacter pylori infection can potentially increase the risk of colorectal cancer. The purpose of this study was to assess the association between H. pylori infection and the risk of colorectal adenoma and adenocarcinoma, and to evaluate any differences on the basis of sex. Methods The subjects were 669 (40- to 80-year-old) patients who underwent both barium enema examination and total colonoscopy, and who were evaluated for H. pylori infection by ¹³C-urea breath test, urease test, or histological diagnosis of biopsied gastric specimens. There were 142 H. pylori-negative and 527-positive patients. The odds ratios (ORs) for H. pylori-positive patients with colorectal adenoma and adenocarcinoma, and for tumor patients with either adenoma or adenocarcinoma were calculated. Results Among the H. pylori-negative patients, there were 52 patients without tumor, 63 with adenoma, 27 with adenocarcinoma, and 90 with tumor. Among the H. pylori-positive patients, there were 136, 264, 127, and 391 patients respectively. Pooling all subjects, those infected with H. pylori had a significantly increased OR for adenoma, adenocarcinoma, or tumor, compared to H. pylori-free patients (OR, 1.60, 1.80, and 1.66, respectively). For female H. pylori-positive subjects, the risk of having adenocarcinoma or tumor was significantly higher than that for their H. pylori-free counterparts, while for male H. pylori-positive and -negative subjects, there was no such significant difference. Conclusions The results therefore suggest that, in patients aged 40–80 years, H. pylori infection increased the risk of colorectal adenoma and adenocarcinoma, with significantly higher risks for female patients.     

Extreme hypergastrinemia caused by atrophic gastritis and Helicobacter pylori infection--a case report

We present a case with extremely high serum gastrin induced by atrophic gastritis and Helicobacter pylori infection. The patient, a 95-year-old male, was diagnosed with idiopathic chronic diarrhea. During diagnostic work-up, his fasting serum gastrin was up to 2078 pg/mL. The secretin test was negative for gastrinoma. Octreotide scan showed no suspicious lesion except for diffuse faint uptake over the gastric antrum on the 48-hour-delay film. Gastric acidity test revealed achlorhydria. On histology examination, atrophic gastritis with Helicobacter pylori infection was found in the gastric body, but the antral mucus was normal with a slight increase in gastrin-secreting cells. To our knowledge, such extremely high serum gastrin induced by atrophic gastritis and Helicobacter pylori infection has never been reported before.     

口腔幽门螺杆菌感染与胃幽门螺杆菌感染的相关性探讨

目的 分析口腔和胃幽门螺杆菌(Hp)感染的检测结果,探讨口腔Hp感染与胃Hp感染的相关性,及口腔Hp感染对Hp根除治疗的影响.方法 采用唾液测定螺旋杆菌抗原技术(HPS)和13C/14C尿素呼气试验(UBT)同步检测的方法,对114例有上消化道症状的初诊患者(第1组),129例确诊为胃Hp感染经根除治疗后4周复查的患者(第2组)和33例无消化道症状的健康志愿者(第3组),进行口腔和胃Hp检测.结果 第1组、第2组和第3组HPS阳性检出率分别为77.19%、75.97%和81.82%,3组比较差异无统计学意义(χ2=0.47,P值均>0.05);UBT阳性检出率第1组(52.63%)比第2组(34.11%)和第3组(21.21%)高,第1组与第2组和第3组比较,差异有统计学意义(χ2=8.48和10.19,P均<0.05),第2组与第3组之间差异无统计学意义(χ2=2.03,P>0.05);在UBT阳性者中,HPS阳性检出率差异无统计学意义(3组分别为81.67%、88.64%和100%,χ2=2.25,P值均>0.05).结论 唾液中存在高Hp抗原检出现象,口腔可能是Hp在胃以外的"第二定居地".口服药物治疗对口腔Hp感染几乎无效,口腔Hp的存在可能是胃病发病和复发的一个重要和直接的原因.

Abstract：

Objective To explore association between Helicobacter pylori (Hp) infection in oral cavity and gastric Hp infection through oral cavity and gastric Hp infection testing results analysis, and also to study the effect of Hp infection in oral cavity on Hp eradication treatment. Methods Through Hp saliva test (HPS) and 13C/14C urea breath test (UBT) method, the Hp in oral cavity and stomach were tested in 114 first-visit patients with upper gastrointestinal symptoms (group 1), 129 re-visiting patients who were diagnosed gastric Hp infection with eradication treatment for four weeks (group 2) and 33 volunteers without gastrointestinal symptoms. Results The positive rates of Hp infection by HPS method were 77.19%, 75.97% and 81.82% in group 1, group 2 and group 3 respectively. There was no significant difference between these three groups (χ2=0.47, P>0.05). The positive rate of Hp infection by UBT method in group 1 (52.63%) was higher than those of group 2 (34.11%) and group 3 (21.21%). Compared group 1 with group 2 or group 3, there was significant difference (χ2=8.848, 10.19, P<0.05). There was no significant difference between group 2 and 3 (χ2=2.03, P>0.05). In positive individuals of these three groups tested by UBT method, there was no significant difference of positive rate tested by HPS method (81.67%, 88.64% and 100% of three groups respectively, χ2=2.25, P>0.05). Conclusions The High detection of Hp antigen in saliva indicates that the oral cavity may be the "second settlement" of Hp beside stomach. The oral medicine haslittle effect on oral cavity Hp infection. The existence of oral Hp may be an important and direct factor of incidence and recurrent of gastric diseases.     

Helicobacter pylori infection and infertility

OBJECTIVE: To determine (1) the prevalence of Helicobacter pylori infection in male and female patients with reproductive disorders and controls; (2) the presence of anti-H. pylori antibodies in samples of follicular fluid, vaginal secretions and sperm; and (3) the existence of a structural homology between a major spermatozoa protein, tubulin, and H. pylori proteins. PATIENTS AND METHODS: Serum samples from 167 patients with infertility and 837 age- and gender-matched controls (blood donors) were examined by enzyme-linked immunosorbent assay (ELISA) and Western blotting to determine the seropositivity for H. pylori infection. The presence of anti-H. pylori antibodies in samples of follicular fluid, vaginal secretions and sperm was determined using the same techniques. The possible cross-reactivity with spermatozoa of anti-H. pylori hyperimmune sera and human antibodies was studied by immunofluorescence. The N-acid homology of human tubulin with the principal H. pylori proteins was assayed by the WU-blastp program available on the Internet. RESULTS: The prevalence of infection was significantly higher in patients than controls (49.1% v. 33.5%, P < 0.001). Follicular fluids from infected patients contained specific antibodies in all cases, sperm samples in about 50% of cases, and vaginal secretions in a minority of cases. Sera to H. pylori whole antigens and VacA reacted with the tails and the pericentriolar area of human spermatozoa (which are rich in tubulin); sera to urease and heat-shock protein (Hsp) did not. Follicular fluids with anti-H. pylori antibodies immune reacted with spermatozoa. A linear homology was found between beta-tubulin and three H. pylori proteins, flagellin, VacA and CagA. CONCLUSIONS: H. pylori infection may increase the risk of developing reproductive disorders or worsen the clinical expression of this syndrome.