淮南地区幽门螺杆菌感染个体菌株基因多态性与感染结局的影响

目的:探讨淮南地区幽门螺杆菌感染个体菌株基因多态性及其与感染结局的影响。方法:选取125例幽门螺杆菌(H.pylori,HP)感染的慢性胃炎、消化性溃疡患者,常规获取胃窦、胃体部粘膜,进行HP分离、培养,提取HP基因组DNA,采用随机扩增多态性DNA(RAPD)指纹分析法检测菌株基因多态性;125例患者均给予质子泵抑制、H2受体拮抗剂、铋剂为基础的三联或四联疗法治疗,治疗后4~6周进行14C-尿素呼气试验评估Hp根除情况;获取HP根除失败患者的胃窦、胃体黏膜进行HP分离、培养、鉴定,并采用RAPD指纹分析法检测菌株来源,评估HP基因多态性对治疗结局的影响。结果:cagA、iceA1、iceA2、vacAs1、vacAm1、babA2阳性率分别为92.80%、36.00%、93.60%、93.60%、29.50%、53.50%,cagA、iceA2、vacAs阳性率均高于其他基因类型阳性率(P0.05或P0.01),其他基因类型阳性率比较差异无统计学意义(P0.05)。经治疗后HP根除率为86.4%(107/125),14.4%(18/125)根除失败;18例根除失败患者中,15例患者治疗前后的菌株具有相同的指纹图谱,证实为原菌株复发,其中cagA、iceA1、iceA2、vacAs1、vacAm1、babA2阳性率分别为93.33%、13.33%、86.67%、93.33%、6.67%、20.00%,cagA、iceA2、vacAs阳性率均高于其他基因类型阳性率(P0.05或P0.01)。结论:cagA+、vacAs+、iceA2+为淮南地区HP感染的优势基因型,该基因型易导致HP根除失败;未发现babA2与HP感染结局存在相关性。     

幽门螺旋杆菌感染与慢性胃炎患者IL-8、IL-10、CRP水平以及血脂指标的关系研究

目的:研究幽门螺旋杆菌(Hp)感染与慢性胃炎患者白细胞介素-8(IL-8)、白细胞介素-10(IL-10)、C反应蛋白(CRP)水平以及血脂指标的关系。方法:选择从2015年6月到2017年6月在我院接受治疗的慢性胃炎患者150例作为观察组,根据13C-尿素呼吸实验的结果将观察组患者分成HP阳性组71例和Hp阴性组79例,另选同期在我院进行健康体检的志愿者150例作为对照组,对比观察组以及对照组的炎症因子IL-8、IL-10、CRP及血脂指标[低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)、甘油三酯(TG)、总胆固醇(TC)]水平,并对比观察组不同HP感染情况的炎症因子及血脂指标水平,分析Hp感染与患者炎症因子及血脂指标水平的相关性。结果:观察组的IL-8、IL-10、CRP、LDL-C及TG水平均分别高于对照组,差异均有统计学意义(均P0.05)。Hp阳性组患者治疗前的IL-8、IL-10、CRP、LDL-C及TG水平均分别高于HP阴性组,但Hp阳性组患者治疗后的上述指标水平均分别低于HP阴性组,差异均有统计学意义(均P0.05)。两组治疗后的IL-10、CRP水平均分别低于治疗前,且Hp阳性组患者的IL-8、LDL-C及TG水平也低于治疗前,差异均有统计学意义(均P0.05),Spearman相关性分析结果显示,Hp感染与患者IL-8、IL-10、CRP、LDL-C及TG水平均呈正相关(均P0.05),但Hp感染与HDL-C和TC并无明显的相关性(P0.05)。结论:Hp感染与慢性胃炎患者的炎症指标及血脂指标关系紧密,临床上可考虑将此类指标作为存在Hp感染的慢性胃炎患者的监测指标,从而更好地辅助临床诊治。     

慢性多灶萎缩性胃炎患者胃酸分泌与Hp感染及血清胃泌素的关系

目的:探讨多灶萎缩性胃炎(BAG)患者胃酸分泌与幽门螺杆菌(HP)感染及血清胃泌素水平的关系。方法:根据病理结果将60例确诊的慢性BAG患者分为轻度、中度、重度BAG组,监测各组患者24小时胃内PH值的变化、血清胃泌素水平及HP感染情况。结果:随着萎缩程度的加重,HP阳性率、胃内中位PH值及算数均数p H值逐渐升高,血清胃泌素水平逐渐降低;轻度、中度、重度BAG组组间中位p H值、算数均数p H值及血清胃泌素水平比较有显著差异(均P0.05);重度BAG组HP感染与轻度组、中度组比较有统计学差异(均P0.05),而轻度组HP感染与中度组差异无统计学意义(P0.05)。结论:随着慢性BAG萎缩程度的加重,HP阳性率和p H值逐渐升高,血清胃泌素水平逐渐降低。HP感染、胃泌素水平及胃酸分泌水平三者相互影响,相互作用。     

幽门螺杆菌在口腔中的特征性分布

目的:研究幽门螺杆菌(Helicobacterpylori,Hp)在慢性胃炎患者口腔中的分布.方法:依据Hp尿素酶C基因和细胞毒素相关基因(cagA)设计引物建立PCR方法,从32例慢性胃炎患者口腔内多部位采集标本,检测和鉴定牙菌斑(每人采集6个牙的龈上和龈下菌斑)、含漱液、舌背黏膜、颊黏膜及腭黏膜表面中的Hp.结果:32例患者中有29例(90.6%)从口腔内牙菌斑、含漱液、舌背黏膜、颊黏膜及腭黏膜至少一处检测出Hp,其中28例(87.5%)从胃和口腔内同时检出Hp,口腔内各部位标本中Hp检出率依次为牙菌斑84.4%,口腔含漱液56.2%,舌背黏膜43.8%,颊黏膜28.1%,腭黏膜9.4%;在384份牙菌斑中,磨牙的牙菌斑Hp的检出率高于前牙(33.2%vs21.9%,P＜0.01);而上下牙的牙菌斑Hp的阳性率差异无显著性(29.7%vs29.2%,P＞0.05);在PD＞4 mm的牙周袋,菌斑Hp检出率显著高于PD＜4 mm的袋(P＜0.05),龈下菌班Hp的阳性率显著高于龈上菌斑(P＜0.01).结论:口腔多部位存在Hp,牙菌斑中居多,并呈一定的分布规律;口腔Hp可能是胃Hp感染的重要来源.     

幽门螺杆菌感染对慢性胃炎胃窦部EC细胞和CgA细胞的影响

目的探讨幽门螺杆菌（Helicobacter pylori Hp）感染与慢性胃炎（CG）患者胃窦粘膜内肠嗜铬细胞（Enterochromaffin,EC细胞）、嗜铬粒素A细胞（CgA细胞）变化的关系。方法采用免疫细胞化学方法,检测Hp相关性慢性胃炎胃窦部粘膜内EC细胞、CgA细胞的分布。结果1．Hp^＋组CgA^＋细胞数低,与Hp^＋组和正常组比较差异显著（P〈0．01）;2.EC细胞数随病理类型加重呈下降趋势,三组间的差异性极显著（P〈0．01）,慢性萎缩性胃炎组（CAG）CgA^＋细胞数与慢性非萎缩性胃炎（CNAG）组和正常组比较,差异极显著（P〈0．01）。结论Hp感染和慢性胃炎胃窦部EC细胞和CgA细胞之间存在密切关系。     

胃黏膜定植乳酸杆菌对幽门螺杆菌感染的影响

目的探讨胃黏膜定植乳酸杆菌对幽门螺杆菌感染及胃黏膜菌群数量的影响。方法收集130例慢性胃炎患者胃窦黏膜组织,病理学检测幽门螺杆菌,提取胃黏膜基因组DNA,采用荧光定量PCR法检测乳酸杆菌和总细菌数。结果幽门螺杆菌阳性组和阴性组的乳酸杆菌检出率和乳酸杆菌数(Log)差异均无统计学意义(P0.05);乳酸杆菌阳性者和阴性者之间胃黏膜总细菌数(Log)差异无统计学意义(P0.05);乳酸杆菌细菌数(Log)与胃黏膜总细菌数(Log)无显著相关性(P0.05);不同炎症程度胃炎患者乳酸杆菌检出率差异无统计学意义(P0.05);肠化组和未肠化组乳酸杆菌检出率差异无统计学意义(P0.05);但是重度胃炎组幽门螺杆菌感染率和总细菌数量均显著高于轻度(P0.05)和中度胃炎组(P0.05)。结论胃黏膜定植乳酸杆菌对幽门螺杆菌的感染无影响,其存在与否及细菌数量对胃黏膜总细菌数亦无明显影响,并与胃炎炎症程度及肠化无关。乳酸杆菌不能通过抑制幽门螺杆菌定植、调节胃黏膜菌群而减轻炎症反应。     

小儿消化性疾病的胃电图变化及与临床特点和胃镜特征的关联性

目的:分析小儿消化性疾病的胃电图变化及与临床病理特征和胃镜特征的关联性。方法:选取2018年1月至2019年5月我院儿科收治的经胃镜和病理学两种方式诊断为消化性疾病的患儿54例为观察组,另选取无胃肠道疾病的健康儿童40例为对照组。比较两组胃电图参数(频率均值和波幅均值),54例胃电图诊断后纤维胃镜检查结果,分析消化性疾病患儿HP感染与临床病理特征、溃疡面积的关系。结果:各组胃病患者胃电慢波频率均值各不相同(P0.05),三组患者胃电慢波波幅均值相比差异具有统计学意义(P0.05);且浅表性胃炎组、胆汁反流性胃炎组患者胃电慢波频率均值、胃电慢波波幅均显著低于胃溃疡组(P0.05);浅表性胃炎组患者胃电慢波频率均值显著低于胆汁反流性胃炎组(P0.05)。胆汁反流性胃炎组患者胃电慢波波幅显著低于浅表性胃炎组(P0.05)。胃镜检查结果显示,其中浅表性胃炎的诊断符合率较高,达90.00%,胃溃疡符合率为60.71%,胆汁反流性胃炎符合率为83.33%。HP检测结果显示,HP阳性患儿占总例数的77.78%(42/54),HP阴性患儿占总例数的22.22%(12/54);HP阳性组患儿淋巴滤泡形成、胃黏膜萎缩、胃黏膜炎性活动的发生率明显高于HP阴性组,差异具有统计学意义(P0.01);HP阳性组溃疡范围2 cm的患儿比例明显高于HP阴性患儿,差异具有统计学意义(P0.01)。结论:小儿消化性疾病胃电图存在餐后NSWP的下降及节律过缓的上升,胃电图检查和胃镜检查在诊断上有较高的符合率,HP感染科引起胃黏膜组织学改变,可作为小儿消化性疾病的靶向治疗。     

慢性胃病患者胃蛋白酶原I、II水平与幽门螺旋杆菌感染的关系研究

目的:探讨慢性胃病患者胃蛋白酶原(PG)Ⅰ、PG Ⅱ水平与幽门螺旋杆菌(HP)感染的关系。方法:选取2012年12月-2016年12月期间我院收治的慢性胃病患者64例作为研究对象,根据疾病类型分为慢性胃炎组23例、胃溃疡组22例以及胃癌组19例。另取同期于我院接受体检的健康志愿者30例作为对照组,应用免疫比浊法测定各组血清PG Ⅰ与PG Ⅱ水平,采用快速尿激酶法测定各组HP感染情况,分别对比各组研究对象HP感染发生情况,血清PG Ⅰ、PG Ⅱ、PG Ⅰ/PG Ⅱ水平,HP感染情况与血清PG Ⅰ、PG Ⅱ、PG Ⅰ/PG Ⅱ水平关系。结果:慢性胃炎组、胃溃疡组以及胃癌组患者HP阳性率分别为60.87%、63.64%、78.95%,均明显高于对照组的13.33%(P0.05)。慢性胃炎组、胃溃疡组以及胃癌组患者血清PG Ⅰ、PG Ⅰ/PG Ⅱ水平均低于对照组,且胃癌组低于慢性胃炎组与胃溃疡组(P0.05),慢性胃炎组和胃溃疡组血清PG Ⅰ、PG Ⅰ/PG Ⅱ水平比较差异无统计学意义(P0.05),各组血清PG Ⅱ比较无统计学差异(P0.05)。各组研究对象HP阳性血清PG Ⅰ、PG Ⅰ/PG Ⅱ水平均低于HP阴性(P0.05),而PG Ⅱ水平比较无统计学差异(P0.05),慢性胃炎组、胃溃疡组、胃癌组HP阳性血清PG Ⅰ水平低于对照组,且胃癌组低于慢性胃炎组、胃溃疡组(P0.05),胃溃疡组、胃癌组HP阳性血清PG Ⅰ/PG Ⅱ水平低于对照组,且胃癌组低于慢性胃炎组(P0.05)。结论:慢性胃病患者PG Ⅰ、PG Ⅱ水平异常降低,HP阳性患者PG Ⅰ、PG Ⅱ水平降低更为明显,随病变的程度增加,血清PG Ⅰ、PG Ⅰ/PG Ⅱ水平也呈现出下降的趋势。     

幽门螺杆菌对PCNA及HSP60在慢性胃炎中的表达的影响

目的研究HSP60与PCNA在幽门螺杆菌感染慢性胃炎组织中的表达及其意义。方法免疫细胞化学检测Hp 和Hp-慢性胃炎患者胃窦粘膜内的PCNA和HSP60。结果PCNA在浅表性胃炎以弱阳性或阳性表达为主,在萎缩性胃炎以阳性或强阳性表达为主。与Hp-患者相比,Hp 患者胃粘膜PCNA的表达显著增强,两者之间差异显著(P<0·05);HSP60在Hp 患者浅表性胃炎、萎缩性胃炎的阳性率分别为40·0%和76·9%,Hp 患者胃粘膜HSP60的表达比Hp-患者强(P<0·05)。结论幽门螺杆菌的感染增强了PCNA、HSP60在胃粘膜中的表达,与胃粘膜的病理特征有密切的关系,两者可能是胃粘膜病变趋势或临床病理特征的重要指标。     

白光胃镜下胃体黏膜形态与幽门螺杆菌感染的关系及其病理特征

目的探讨白光胃镜常规检查时根据不同的胃体黏膜形态判断幽门螺杆菌(H.pylori)感染的准确性及其病理表现,了解胃体黏膜形态变化的临床意义。方法选择2017年3月至2018年9月于本院行胃镜检查的520例患者为研究对象,对患者胃体和胃窦同时进行组织病理学和快速尿素酶检查及白光胃镜检查,根据白光胃镜检查结果分为胃体黏膜病变组(232例)和无胃体黏膜病变组(288例),分析胃镜下不同黏膜组织病变与H.pylori的感染情况,采用四格表分析白光胃镜检测对H.pylori感染的诊断价值。结果与无胃体黏膜病变组比较,胃体黏膜病变组患者H.pylori感染率显著升高,同时胃体黏膜黏液分泌增多、胃体黏膜广泛充血、胃体皱襞肥大、黏膜水肿、胃体黏膜"龟纹样"改变、胃体(单发或多发)息肉、胃体可见RAC。不同胃体黏膜病变患者H.pylori感染率差异有统计学意义(χ~2=62.711,P0.001)。胃体黏膜病变患者H.pylori感染率与十二指肠炎、十二指肠溃疡无关(均P0.05),与反流性食管炎、胃溃疡、胃窦糜烂有关(χ~2=7.087、6.230、17.934,P=0.008、0.013、0.001)。白光胃镜诊断H.pylori感染的灵敏度为71.43%,特异度为90.27%,准确度为79.62%,阳性预测值为90.52%,阴性预测值为70.83%。结论白光胃镜下胃体黏膜形态与H.pylori感染率及与炎症、肠化生、黏膜萎缩、非典型增生、反流性食管炎、胃溃疡、胃窦糜烂有关,白光胃镜检查可能对H.pylori感染有一定诊断价值。白光胃镜下较常见且易识别的胃体黏膜充血、水肿、"龟纹样"改变、胃体可见RAC等可能成为白光胃镜预测H.pylori感染的特异性表现。     

The pathological examinations of gastric mucosa in patients with Helicobacter pylori-positive and -negative pernicious anemia

Background. The basic histopathological finding in gastric mucosa is chronic atrophic gastritis in patients with pernicious anemia.
Materials and Methods. We evaluated the frequency of Helicobacter pylori and pathological examinations of gastric mucosa in pernicious anemia (n = 30) by endoscopical findings and biopsy. The results were compared with gastric mucosa specimens of patients with H. pylori –positive nonulcer dyspepsia (n = 36) and H. pylori –negative nonulcer dyspepsia (n = 21).
Results. H. pylori was diagnosed in 12 patients (40%) with pernicious anemia. Fundal biopsy examinations showed atrophic gastritis in 30 patients (100%), intestinal metaplasia in 13 patients (43.3%), lymphoid follicle in 15 patients (50%), and dysplasia in 6 patients (20%). Antral biopsy examinations showed atrophic gastritis in 8 patients (26.6%), intestinal metaplasia in 8 patients (26.6%), lymphoid follicle in 8 patients (26.6%), and dysplasia in 3 patients (10%). The frequency of fundal inflammation, atrophy, intestinal metaplasia, lymphoid follicle, and dysplasia and antral intestinal metaplasia and mild antral dysplasia were found to be higher in those in the pernicious anemia group than in the nonulcer dyspeptic patients. Antral inflammation, atrophy, and moderate and severe antral dysplasia were found to be higher in those in the nonulcer dyspeptic group.
Conclusions. Particularly, fundal precancerous lesions were found to be more frequent in patients with pernicious anemia independent of H. pylori.     

Genetic factors in the development of gastric precancerous lesions--a role of Helicobacter pylori ?

Helicobacter pylori is believed to predispose to gastric cancer by inducing gastric precancerous alterations. There is a well known predisposition to gastric cancer and the risk of developing it is greater in relatives of patients with familial cases of this malignancy. The aim of this study was to determine the prevalence of gastric precancerous lesions (atrophy and intestinal metaplasia) and their association with Hp infection in first-degree relatives in patients with noncardia gastric cancer. METHODS: Hp status and gastric histology assessed by upper gastrointestinal endoscopy, biopsies from the antral and body region, the rapid urease test and staining for Hp, inflammation, activity, atrophy and intestinal metaplasia (prevalence and grading) were studied in 108 first-degree relatives of patients with noncardia gastric cancer and compared with 73 controls with mild non-ulcer dyspepsia who had no cancer relatives and were examined in the same way. RESULTS: subjects with and without cancer relatives had a similar prevalence of Hp infection (49 vs. 47%). Endoscopy revealed a few asymptomatic duodenal ulcers and small hiatus hernias in Hp positive subjects of both groups. Hp positive relatives of gastric cancer had a markedly higher prevalence of atrophy than those with Hp negativity without cancer relatives (29 vs. 9%) and those with Hp negativity and cancer relatives (29 vs. 3%. Prevalence of intestinal metaplasia was also higher in those with Hp positivity and cancer relatives than in those without cancer relatives (15 vs. 5% and was not present in Hp negative subjects with cancer relatives. Inflammation and activity showed similar scores in subjects with and without cancer relatives with higher scores in both Hp positive groups. The prevalence of precancerous lesions in the relatives of gastric cancer was nearly always confined to those with Hp positivity. One year after eradication the prevalence of atrophy in cancer relatives decreased from 29 to 14%; prevalence of intestinal metaplasia remained without substantial changes. Scores for inflammation and activity were also lower after eradication. CONCLUSIONS: First-degree relatives of patients with gastric cancer have an increased prevalence of gastric precancerous abnormalities which are strongly confined to those with Hp infection. Eradication of Hp in these subjects with cancer relatives reduces the prevalence of precancerous lesions (atrophy) and grades of inflammation and activity. In view of these results, eradication of Hp should be offered to such subjects.     

Oxidative damage of the gastric mucosa in Helicobacter pylori positive chronic atrophic and nonatrophic gastritis, before and after eradication

Background. Helicobacter pylori is the main cause of gastritis and a primary carcinogen. The aim of this study was to assess oxidative damage in mucosal compartments of gastric mucosa in H. pylori positive and negative atrophic and nonatrophic gastritis. Materials and methods. Five groups of 10 patients each were identified according to H. pylori positive or negative chronic atrophic (Hp‐CAG and CAG, respectively) and nonatrophic gastritis (Hp‐CG and CG, respectively), and H. pylori negative normal mucosa (controls). Oxidative damage was evaluated by nitrotyrosine immunohistochemistry in the whole mucosa and in each compartment at baseline and at 2 and 12 months after eradication. Types of intestinal metaplasia were classified by histochemistry. Results. Total nitrotyrosine levels appeared significantly higher in H. pylori positive than in negative patients, and in Hp‐CAG than in Hp‐CG (p < .001); no differences were found between H. pylori negative gastritis and normal mucosa. Nitrotyrosine were found in foveolae and intestinal metaplasia only in Hp‐CAG. At 12 months after H. pylori eradication, total nitrotyrosine levels showed a trend toward a decrease in Hp‐CG and decreased significantly in Hp‐CAG (p = .002), disappearing from the foveolae (p = .002), but remaining unchanged in intestinal metaplasia. Type I and II of intestinal metaplasia were present with the same prevalence in Hp‐CAG and CAG, and did not change after H. pylori eradication. Conclusions. Oxidative damage of the gastric mucosa increases from Hp‐CG to Hp‐CAG, involving the foveolae and intestinal metaplasia. H. pylori eradication induces a complete healing of foveolae but not of intestinal metaplasia, reducing the overall oxidative damage in the mucosa.     

树突状细胞对胃癌前病变的免疫保护分析

摘要 目的：探究树突状细胞(Dendritic cells,DC)对胃癌的免疫保护作用。方法：选择2016年1月至2018年1月于我院接受治疗的145例胃癌、39例慢性萎缩性胃炎、21例不典型增生、27例肠上皮化生以及20例正常对照组患者为研究对象,分别采集其胃粘膜标本进行染色,记录和比较其胃粘膜中S100⁺、CD4⁺和CD8⁺细胞的数量、平均面积以及平均吸光度,并将胃癌患者分为中分化腺癌(49例)、低分化腺癌(53例)和未分化癌(43例)进行对比。结果：(1)胃癌组、慢性萎缩性胃炎组、不典型增生、肠上皮化生组的胃粘膜S100⁺阳性细胞计数明显高于正常对照组（P<0.05）,胃癌组平均吸光度低于对照组,其他3组平均吸光度显著高于对照组,(P<0.05);胃癌组平均面积与正常对照组相比无差异(P>0.05),其他三组平均面积显著高于对照组（P<0.05）;(2)慢性萎缩性胃炎组、肠上皮化生组、不典型增生组患者CD4⁺细胞数均低于对照组(P<0.05);胃癌组、慢性萎缩性胃炎组、肠上皮化生组患者平均面积均低于对照组(P<0.05);胃癌组、慢性萎缩性胃炎组、不典型增生、肠上皮化生组平均吸光度均低于对照组(P<0.05);(3)慢性萎缩性胃炎组、肠上皮化生组、不典型增生组患者CD8⁺细胞数明显高于对照组(P<0.05),胃癌组稍低于对照组(P>0.05);胃癌组患者平均面积低于对照组(P<0.05);胃癌组患者平均吸光值低于对照组,慢性萎缩性胃炎组、肠上皮化生组患者高于对照组(P均<0.05);(4)随着胃癌分化程度的降低,胃癌患者DC细胞数有降低趋势。结论：胃癌前病变患者胃粘膜中DC数量会显著增多,免疫功能加强,DC细胞数量会随胃癌分化程度的降低而减少,分析其原因与DC细胞能够抑制癌前病变有关。     

Helicobacter pylori associated gastric pathology.

Helicobacter pylori (HP), undoubtedly, the most common world-wide infection plays an important role in pathogenesis of peptic ulcer. Proof for a causal role for HP in peptic ulcer rests in two major points; 1) the majority of ulcer patients are HP infected and the prevalence of this infection for both gastric ulcer (GU) and duodenal ulcer (DU) is much higher than for gender- and age-adjusted controls and 2) the cure of HP infection dramatically reduces ulcer recurrence. Conclusions regarding the mechanisms by which HP induces peptic ulcer are restricted mainly to studies observing the consequences of its eradication by antibiotics combined with gastric inhibitors or bismuth agents. Several specific virulence factors such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) as well as other noxious substances including ammonia, lipopolysaccharide (endotoxin), platelet activating factor (PAF), nitric oxide (NO) and others have been implicated in gastritis and were found to be significantly more frequent in gastric cancer than in gender- and age-matched controls, especially in younger generation. Chronic inflammation, atrophic gastritis, intestinal metaplasia, impaired defense mechanisms combined with hypergastrinemia, deficiency of vitamin C in the stomach , excessive oxygen metabolites and epithelial cell proliferation have been associated with gastric cancer. This multi-step pathway originally proposed by Correa and his colleagues, long before the HP was discovered in the stomach, leads to cancer but may be reversed by eradication of HP. This is, however, a controversial issue because gastric atrophy and intestinal metaplasia may be also caused by other factors such as bile reflux, dietary irritants, and autoimmunity. The implication of HP in MALT-lymphoma is based on the observations that eradication of HP in early stage of low-grade of this tumor leads to complete remission. The significance of HP in non-ulcer dyspepsia remains questionable and requires further studies.     

胃癌病理特征改变与幽门螺旋杆菌感染的相关性分析

目的:探究HP感染与胃癌患者病理特征性改变的相关性。方法:选取我院消化内科收治并确诊为胃癌的患者50例,作为胃癌组;确诊为慢性浅表性胃炎的患者50例,作为胃炎组;选取同期进行健康体检未发现胃部异常的患者50例,作为对照组。对三组患者进行快速尿素氮试验、13C尿素呼气试验以及血清抗HPCag A等检查,比较患者HP感染等情况。结果:胃癌组及胃炎组患者HP感染阳性率及抗HPCag A阳性率显著高于对照组,且胃癌组较胃炎组明显增高,差异有统计学意义(P0.05)。胃癌早期及进展期患者HP感染率高于对照组,差异有统计学意义(P0.05)。胃癌组患者非贲门部HP感染率显著高于贲门部及对照组,差异有统计学意义(P0.05)。结论:HP感染是导致胃癌的主要因素,明确HP感染与胃癌病理分期及病变部位的相关性对胃癌的治疗及预防有重要的临床意义。     

Effect of Helicobacter pylori infection and eradication on gastric epithelial cell proliferation and apoptosis.

OBJECTIVES: the effect of Helicobacter pylori infection on gastric epithelial cell proliferation and apoptosis is still controversial. Our aim was to evaluate the effect of H. pylori infection on cell kinetic parameters in normal gastric epithelium, gastritis with/without intestinal metaplasia and gastric cancer. PATIENTS AND METHODS: antral biopsies were taken from 121 patients (61 women, 60 men, mean age 58.5+/-14.3 years of age) who underwent routine gastroscopy for upper gastrointestinal symptoms. Sections were scored for normal epithelia (n=15), gastritis without intestinal metaplasia (n=74), gastritis with intestinal metaplasia (n=24), and gastric adenocarcinoma (n=8). Fifty-two patients had H. pylori positive gastritis, and success of H. pylori eradication therapy was controlled in 12 cases, all with intestinal metaplasia. To characterize cell proliferation and assess apoptosis, immunohistochemistry [Proliferating Cell Nuclear Antigen (PCNA)], histochemistry [Argyrophil Nucleolar Organizer Regions (AgNOR)], and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridinetriphosphate (dUTP) nick end-labeling (TUNEL) were used, respectively. RESULTS: both cell proliferation and apoptosis is was higher in chronic gastritis when compared with normal epithelia, but neither PCNA LI (54.79+/-19.1 vs. 53.20+/-20.7) nor AgNOR counts (291.43+/-44.3 vs. 277.8+/-57.54) were different in H. pylori positive versus negative chronic gastritis. A significant positive correlation (P<0.05) was found in this group between PCNA and AgNOR techniques. Apoptosis was significantly higher (P<0.05) in H. pylori positive cases only when intestinal metaplasia was not present. Cell proliferation in intestinal metaplasia decreased to the activity of normal epithelium after successful eradication of H. pylori but remained high if eradication therapy failed. CONCLUSIONS: epithelial cell proliferation does not depend on H. pylori status in chronic gastritis. H. pylori increases apoptosis only in the absence of intestinal metaplasia.