Helicobacter pylori infection in gastric remnant cancer after gastrectomy

Patients who have undergone distal gastrectomy for peptic ulcer are at higher risk of developing gastric remnant cancer, and chronic bile reflux is believed to increase the risk of cancer in remnant stomach. In remnant stomach, carcinogenesis may be prevented by selecting the anastomosis method with a few reflux of intestinal juice including a bile acid. How Helicobacter pylori(H. pylori) infection participate in stomal gastritis and gastric remnant cancer, same as early gastric cancer in the intact stomach, is attended. H. pylori positive rate of remnant stomach is different by examination method and a report, but its rate is decreased every year after gastrectomy and in particular low in Billroth-II(B-II) anastomosis. B-II anastomosis is followed by a significantly lower rate than B-1. This may reflect the role of bile reflux because bile reflux interferes with colonization by H. pylori. Gastric cancer excision usual increase complicates gastric remnant stomach and H. pylori infection, but while H. pylori infection lasts after gastrectomy for gastric cancer, cell proliferation increase in remnant stomach. In remnant stomach after gastrectomy for gastric cancer, while H. pylori infection continues, H. pylori infection may cause remnant gastritis and a second cancer of remnant stomach. H. pylori infection and bile reflux seem to have a synergistic effect on cell proliferation in remnant stomach and may explain the increased risk of gastric remnant cancer. The cancer-causing dominant role might changed from H. pylori infection predominance to bile reflux every year after gastrectomy. Furthermore, a prophylactic effect to carcinogenesis by H. pylori eradication therapy is expected. Eradication of H. pylori after gastrectomy for gastric cancer has been recommended.     

Eradication of Helicobacter pylori in Japan]

Twenty five years has passed since the re-discovery of Helicobacter pylori. Many people have studied on this organism since that time. Some mechanisms about gastric mucosal inflammation have been clarified, and pathogenesis of peptic ulcer formation and gastric cancer have been solved. H. pylori infection is related to chronic gastritis, peptic ulcer, gastric carcinoma, and MALToma. In 1998, it was reported that gastric cancer occurred in H. pylori infected mongolian gerbils. In Japan, the prevalence of peptic ulcer and gastric cancer is very high. Therefore, the treatment for H. pylori infection is necessary to prevent occurrence of these diseases. To treat H. pylori infection, various regimen have been tried. Triple therapy with PPI and two antibiotics is recommended for cure of H. pylori infection in European and US guidelines. Some guidelines for management of H. pylori infection and regimen were shown in this part.     

白光胃镜下胃黏膜形态变化对幽门螺杆菌感染的诊断价值分析

目的探究白光胃镜下胃黏膜形态变化对幽门螺杆菌（H. pylori）感染相关性胃炎的诊断价值。 方法回顾性分析2018年7月至2020年7月在海南医学院第二附属医院进行白光胃镜检查和13-尿素呼气试验（¹³C-UBT）检查的1160例病例,依据¹³C-UBT检查结果分为2组：H. pylori感染组（812例）和无H. pylori感染组（348例）。比较2组白光胃镜下胃粘膜形态差异,进行Logistic回归分析筛选出H. pylori感染独立相关的胃黏膜形态特征,并应用受试者工作特征曲线（ROC）评价相关指标的预测价值。 结果H. pylori感染组白光胃镜下弥漫性胃黏膜充血、点状发红、胃黏膜肿胀、胃体皱襞肿大蛇形、胃体黏膜呈“龟纹样”等检出率均显著高于无H. pylori感染组。多因素Logistic回归分析显示,弥漫性胃黏膜充血（OR=116.280）、点状发红（OR=4.821）、胃黏膜肿胀（OR=3.432）、胃体皱襞肿大蛇形（OR=4.336）、胃体黏膜呈“龟纹样”（OR=9.346）是H. pylori感染的独立相关因子。ROC曲线分析显示,弥漫性胃黏膜充血、点状发红、胃黏膜肿胀、胃体皱襞肿大蛇形、胃体黏膜呈“龟纹样”预测H. pylori感染的曲线下面积分别为0.829（95%CI：0.796~0.859）、0.687（95%CI：0.648~0.725）、0.750（95%CI：0.713~0.785）、0.578（95%CI：0.537~0.619）、0.619（95%CI：0.578~0.619）,其中以弥漫性胃黏膜充血、胃黏膜肿胀较大,它们的敏感度和特异度分别为93.68%和72.17%、97.13%、52.96%。 结论白光胃镜下胃黏膜形态变化与H. pylori感染具有相关性,以弥漫性胃黏膜充血、胃黏膜肿胀对H. pylori感染的诊断价值较大。     

幽门螺杆菌相关性胃溃疡与内皮素、降钙素相关基因肽的变化及临床意义

目的 为了探讨内皮素（ET）、降钙素相关基因肽（CGRP）在幽门螺杆菌（H．pylori）相关性胃溃疡发病中的作用。方法选择幽门螺杆菌感染（H．pylori）阳性胃溃疡患者50例，阴性组50例，健康人50例，用放射免疫法测定其血清降钙素相关基因肽（CGRP）内皮素（ET）水平。结果幽门螺杆菌阳性胃溃疡患者血清CGRP水平分别明显低于和ET高于阴性组和健康者，差异均有显著性（P〈0．01）．抗Hp治疗后血清CGRP上升，ET下降。结论提示血清CGRP水平下降，ET上升可能与幽门螺杆菌感染所致疡的发病有关.     

长春地区慢性胃病患者幽门螺杆菌感染状况调查

目的通过对本地区慢性胃病患者幽门螺杆菌（H.pylori）感染状况调查,了解本地区流行病学特点,为进一步阐明其与慢性胃病发生发展的关系提供理论依据。方法采用ELISA方法测定血清H.pyloriIgG抗体及CagA抗体;采取胃粘膜活检组织进行快速尿素酶试验,调查H.pylori感染情况,分析其与各种疾病的关系。结果1180例慢性胃病患者H.pylori感染率为67.11%,复合性溃疡、十二指肠溃疡、胃溃疡及慢性萎缩性胃炎感染率分别为90.9%、84.57%、83.96%和80.24%。与慢性浅表性胃炎相比差异有显著性。消化性溃疡、慢性萎缩性胃炎、胃癌和胃息肉患者血清Hp-CagA抗体的阳性率明显高于慢性浅表性胃炎（P〈0.05）。结论本地区慢性胃病患者H.pylori感染率高与多数地区的普通人群,H.pylori感染者尤其是CagA阳性者,更易发生慢性萎缩性胃炎、消化性溃疡及胃癌。     

幽门螺杆菌血清分型与上消化道疾病的关系

目的 探讨幽门螺杆菌(helicobacter pylori,Hp or H.pylori)分型与消化道不同疾病的关系。方法 入选198例Hp阳性的胃镜检查患者，采用免疫印迹法进行Hp的血清学分型，并取胃窦黏膜经HE染色观察胃窦黏膜病理组织学变化。结果 198例患者中检出HpI型菌株173例(87．4％)，Ⅱ型菌株25例(12．6％)。I型较II型Hp感染者胃镜下消化性溃疡、胃癌的比例更高，P=0.012；与胃炎组比较，十二指肠球部溃疡组、胃癌组的I型感染者更高（P值分别为0.026、0.048），而与胃溃疡组无显著差别(P=0.125)。病理组织学改变I型较II型Hp感染者的结果更为严重（P=0.038）。结论 临床上消化道疾病患者Hp感染以I型菌株最为多见。Hp感染的分型诊断有助于对胃、十二指肠疾病类型及病情的判断，I型菌株感染者需要更为积极的治疗。     

Causal relationship between Helicobacter pylori infection and upper gastroduodenal diseases

Helicobacter pylori infection causes chronic gastritis (nonatrophic gastritis), which progresses to atrophic gastritis and intestinal metaplasia over a period of decades. Atrophy may result from inflammation and apoptosis caused by H. pylori infection. H. pylori is an important risk factor for peptic ulcer disease. Duodenitis in the gastric metaplasia of the duodenum, hypergastrinemia, and impaired proximal duodenal mucosal bicarbonate secretion are considered causal factors for duodenal ulcer disease. Low-grade B-cell gastric lymphoma of mucosa-associated lymphoid tissue (MALT) develops in response to H. pylori infection. Studies of Mongolian gerbil model demonstrated that H. pylori had an initiator or promoter effect on gastric carcinogenesis.     

Current management of Helicobacter pylori infections in the elderly

Helicobacter pylori infection is a chronic gastric gram-negative infection that increases with age worldwide. However, the percentage age of H. pylori-positive elderly patients who are tested and treated for their infection remains very low. It is now demonstrated that H. pylori infection induces a whole cascade of events leading to gastric pathologies, such as peptic ulcer diseases, gastric precancerous lesions and gastric cancer. Recent data also demonstrated that H. pylori chronic infection can play a role in gastric aging, appetite regulation and extradigestive diseases, such as Alzheimer's disease, in the elderly. The diagnosis of H. pylori infection remains difficult to realize in the very old population, and the urea breath test obtains the best performance in this population. 1-week proton pump inhibitor-based triple therapy regimens are highly effective and well tolerated in elderly patients, and antibiotic resistance remains very low. Low compliance is the main factor related to treatment failure in this population.     

Helicobacter pylori infection and eradication

H. pylori infection is associated with various gastroduodenal diseases such as gastritis, peptic ulcer, gastric cancer, gastric MALT lymphoma. H. pylori infection is suggested that it plays a role as protective factor not promoting factor for reflux esophagitis and GERD. Epidemiological studies showed lower prevalence of H. pylori infection in reflux esophagitis and Barrett's esophagus comparing the control. Increased occurrence of reflux esophagitis after curing of H. pylori infection was reported. However, the relationship between H. pylori infection and reflux esophagitis has not been actually made clear. Also the mechanism of reflux esophagitis occurrence after H. pylori eradication is not obscure.     

端粒酶表达与幽门螺杆菌感染关系的临床观察

目的　探讨端粒酶表达与幽门螺杆菌 (HP)感染在胃癌发生发展过程中的关系及临床意义。方法　用PCR- EL ISA法、病理组织学方法及快速尿素酶试验检测 111例各种胃病变的胃粘膜活检标本中端粒酶活性和 HP感染情况。结果　胃癌组织中端粒酶表达阳性率为 85 % ,明显高于癌前病变 (2 1.2 % ) ,癌周正常组织 (10 % )及浅表性胃炎(0 ) ,差异非常显著 (P<0 .0 1)。 HP感染率在胃癌组为 5 5 % ,癌前病变组为 6 3.5 %。胃癌及癌前病变端粒酶阳性率在 HP阳性组 (90 .9%、2 4.2 % )高于 HP阴性组 (77.8%、15 .8% ) ,但统计学处理无显著性差异 (P>0 .0 5 )。结论　本研究结果显示 ,检测端粒酶活性有助于胃癌的早期诊断。胃癌及癌前病变组织端粒酶表达与幽门螺杆菌感染无关。     

Helicobacter pylori induces beta3GnT5 in human gastric cell lines, modulating expression of the SabA ligand sialyl-Lewis x

Chronic Helicobacter pylori infection is recognized as a cause of gastric cancer. H. pylori adhesion to gastric cells is mediated by bacterial adhesins such as sialic acid-binding adhesin (SabA), which binds the carbohydrate structure sialyl-Lewis x. Sialyl-Lewis x expression in the gastric epithelium is induced during persistent H. pylori infection, suggesting that H. pylori modulates host cell glycosylation patterns for enhanced adhesion. Here, we evaluate changes in the glycosylation-related gene expression profile of a human gastric carcinoma cell line following H. pylori infection. We observed that H. pylori significantly altered expression of 168 of the 1,031 human genes tested by microarray, and the extent of these alterations was associated with the pathogenicity of the H. pylori strain. A highly pathogenic strain altered expression of several genes involved in glycan biosynthesis, in particular that encoding beta3 GlcNAc T5 (beta3GnT5), a GlcNAc transferase essential for the biosynthesis of Lewis antigens. beta3GnT5 induction was specific to infection with highly pathogenic strains of H. pylori carrying a cluster of genes known as the cag pathogenicity island, and was dependent on CagA and CagE. Further, beta3GnT5 overexpression in human gastric carcinoma cell lines led to increased sialyl-Lewis x expression and H. pylori adhesion. This study identifies what we believe to be a novel mechanism by which H. pylori modulates the biosynthesis of the SabA ligand in gastric cells, thereby strengthening the epithelial attachment necessary to achieve successful colonization.     

儿童牙垢幽门螺杆菌抗原检测的临床研究

目的探讨牙垢幽门螺杆菌抗原检测在诊断儿童幽门螺杆菌感染及治疗后复查的价值。方法采用天津瑞爱金生物科技有限公司幽门螺杆菌快速检定卡对56例有消化道症状的患儿牙垢幽门螺杆菌抗原检测,并同时进行胃黏膜抗原检测,以胃黏膜幽门螺杆菌抗原为标准,对牙垢幽门螺杆菌抗原检测方法进行评价。结果胃黏膜幽门螺杆菌抗原检测阳性47例、阴性9例,牙垢幽门螺杆菌抗原检测阳性50例。阴性6例。胃黏膜幽门螺杆菌抗原阳性中有1例牙垢幽门螺杆菌抗原阴性,胃黏膜幽门螺杆菌抗原阴性中有4例牙垢幽门螺杆菌抗原阳性。牙垢幽门螺杆菌抗原检测HP感染的敏感度97．9％（46／47）,阳性预测值为92％（46／50）,阴性预测值为83．3％（5／6）,检测的准确性为91．1％（51／56）。结论牙垢幽门螺旋杆菌抗原检测法可提供一种非侵人性的Hp检测法,具有取材方便、操作简单、快捷,多次重复获取牙垢标本,患儿无痛苦,又经济,是儿童HP感染的诊断及治疗后复查最好的方法。     

Diagnosis of H. pylori infection by PCR

Because of its high sensitivity, polymerase chain reaction (PCR) method can be used to detect the presence of very few numbers of H. pylori organisms in gastric biopsy materials or gastric juice samples. PCR has also been applied to the detection of H. pylori organisms in the oral cavity, in stools, and in the environment. RT-PCR is useful to study the expression of H. pylori pathogenic genes and gene expression of gastric mucosal cells in response to H. pylori infection. Other PCR-based techniques, such as PCR-RFLP or real-time quantitative PCR, are now providing important information on H. pylori and pathophysiology of H. pylori infection.     

Antibiotic therapy for Helicobacter pylori

Helicobacter pylori is one of the most common bacterial infections in the world. H pylori infection of the gastric mucosa is the most common cause of peptic ulcers and is believed to be responsible for 50% to 60% of all gastric carcinomas. This infection is difficult to treat because the bacterium is located within the gastric lumen in the mucus and not within the gastric tissue. Antimicrobial therapy for H pylori includes two or three antibiotics plus either a proton pump inhibitor or a histamine receptor antagonist. H pylori readily develops resistance to antibiotics; therefore, if the initial treatment is unsuccessful, repeat treatment should include different antibiotics.     

EGF在幽门螺杆菌感染同时长期饮酒引起胃黏膜癌相关性病变中的作用

目的探讨幽门螺杆菌感染同时长期饮酒引起胃黏膜癌相关性病变与EGF之间的关系。方法 2007年1月～2010年12月对符合条件的幽门螺杆菌合并长期饮酒56例和长期饮酒64例患者进行内镜下胃黏膜活检组织的病理学观察,同时抽静脉血及胃液用ELISA法检测EGF浓度。结果 (1)幽门螺杆菌合并长期饮酒组中胃黏膜轻度和中重度萎缩亚组患者血清EGF浓度均分别明显高于长期饮酒组中胃黏膜轻度和中重度萎缩亚组患者血清EGF浓度,P均=0.00。(2)幽门螺杆菌合并长期饮酒组中胃黏膜轻度和中重度肠化亚组患者血清EGF浓度均分别明显高于长期饮酒组中胃黏膜轻度和中重度肠化亚组患者血清EGF浓度,P均=0.00。(3)幽门螺杆菌合并长期饮酒组中胃黏膜有或无不典型增生亚组患者血清EGF浓度均分别明显高于长期饮酒组中胃黏膜有或无不典型增生亚组患者血清EGF浓度,P=0.02或0.00。(4)两组各亚组患者之间胃液EGF浓度对比,P均>0.05。结论幽门螺杆菌感染合并长期饮酒患者血液中EGF参与胃黏膜癌相关性病变的发生和发展,胃液EGF与胃黏膜癌相关性病变的之间关系有待于进一步探讨。     

Incidence of Gastric Metaplasia and Helicobacter pylori Infection in Duodenal Bulb - With Specific Reference to Patients With Duodenal Ulcers

We determined the incidence of gastric metaplasia in the duodenal bulb of duodenal ulcer patients and the Helicobacter pylori (H. pylori) infection rate at sites with gastric metaplasia. Biopsy of the duodenal bulb showed the presence of gastric metaplasia in 61 of 86 patients (71%) overall and in 18 of 47 patients (38.3%) who had gastrectomy at an early gastric cancer. The histological diagnosis of H. pylori infection showed good agreement (83.3%) with the result of the rapid urease test, indicating that H. pylori occurs in regions with gastric metaplasia. This finding suggests that H. pylori infects gastric metaplasia in the duodenal bulb, causing mucosal injury, which is then transformed into duodenal ulcers. The exact mechanism by which gastric metaplasia is caused is unknown, but it is believed to occur in the transitional zone in the duodenal mucosa.     

Molecular markers in Helicobacter pylori-associated gastric carcinogenesis

Helicobacter pylori infection is a known risk factor of gastric carcino-genesis. This article presents early molecular alterations associated with H. pylori chronic gastritis and advances in the molecular characterization of preneoplastic intestinal metaplasia (IM) and premalignant gastric mucosal lesions. H. pylori infection induces changes in gene expression, genomic instability and accumulation of gene mutations in the stomach epithelium. Mutations, including LOH and microsatellite instability, and gene hypermethylation are seen not only in gastric cancer, but are already detectable in IM and gastric dysplasia/adenoma. Recent reports using microarray expression analysis identified several gastric epithelial genes that are regulated by H. pylori. Among the many genes showing altered epithelial expression in response to H. pylori, some might be useful as markers to assess gastric cancer risk. Profiles of mutagenesis and gene expression in IM and dysplasia/adenoma have been characterized and represent potential markers of preneoplastic and premalignant lesions during gastric carcinogenesis.     

幽门螺杆菌传播和定植机制研究进展

幽门螺杆菌是一种定植于宿主胃黏膜上皮细胞层的微需氧、螺旋状革兰阴性杆菌。幽门螺杆菌感染会持续数十年,可致胃肠道疾病,甚至引发胃癌。世界卫生组织将幽门螺杆菌定义为Ⅰ类致癌因子,其感染率非常高,我国部分地区感染率甚至超过80%,且呈逐年上升的趋势。幽门螺杆菌感染影响因素较多,但传播和定植是关键。文章就幽门螺杆菌在传播和定植方面的研究进展作一综述。     

中国幽门螺杆菌感染的现状

我国是幽门螺杆菌（HP）高感染地区，HP感染相关疾病负担（尤其是胃癌）较重，国内学术界应尽快统一认识，重视HP感染的危害，建立有效的胃癌一、二级预防体系；同时，随着近年来抗生素耐药率的不断上升，传统方案根除率逐年下降，临床医师应参照最新共识，规范HP感染的诊治，重视提高初次HP根除率。     

A case of Helicobacter pylori infection complicated with gastric cancer, gastric mucosa-associated lymphoid tissue lymphoma, and idiopathic thrombocytopenic purpura successfully treated with laparoscopy-assisted total gastrectomy and splenectomy

Helicobacter pylori infection plays a key role in the pathogenesis of H. pylori-associated diseases, including gastroduodenal and non-gastroduodenal diseases. A 71-year-old man was evaluated for a positive fecal occult blood test by upper gastrointestinal endoscopy, which revealed H. pylori infection, two adenocarcinomas and two gastric mucosa-associated lymphoid tissue lymphomas. Hematological examination revealed low platelet-count, elevated platelet-associated immunoglobulin G and anti-H. pylori immunoglobulin G antibodies. We diagnosed H. pylori infection complicated by simultaneous occurrence of gastric cancer, gastric mucosa-associated lymphoid tissue lymphoma, and idiopathic thrombocytopenic purpura. These diseases were successfully treated with laparoscopy-assisted total gastrectomy and splenectomy, and there was no evidence of recurrence for about 2 years. This is the first reported case of H. pylori infection complicated by these three diseases and cured with laparoscopic surgery.