人体胃内细菌数量相关因素分析

目的研究人体胃内细菌数量与胃内pH值、年龄、萎缩、幽门螺杆菌(Helicobacter pylori,H.pylori)感染及其他因素的关系。方法选择69例患者作为研究对象。胃镜下取胃液测胃液pH值,取胃组织做病理检查、检测H.pylori感染,并做需氧及厌氧细菌培养,计数胃组织细菌培养数量。结果需氧条件下,人体胃内细菌培养数量随胃内pH值的增高而升高(P=0.032),而与性别、年龄、糖尿病、H.pylori感染及萎缩性胃炎无关(P0.05)。厌氧条件下,细菌培养数量随胃内pH值增高(P=0.001)与糖尿病的加重(P=0.027)而增多,如伴有H.pylori感染(P=0.033),则胃内厌氧培养细菌数减少。结论需氧条件下,人体胃内细菌培养的数量与胃内pH值相关。厌氧条件下,细菌培养数与胃内pH值、糖尿病及H.pylori感染相关。     

125例2型糖尿病患者幽门螺杆菌感染现状及其对糖尿病胃轻瘫的影响

目的：探讨2型糖尿病患者 H ．pylori 感染现状及其对糖尿病胃轻瘫的影响。方法采用前瞻性临床病例对照研究方法,纳入2011年1月至2013年12月住院的125例2型糖尿病患者和同期的142名无消化不良症状的健康对照者。调查两组的 H ．pylori 感染状况及糖尿病患者胃轻瘫的发生率。将2型糖尿病患者按照病程进行分组,分析各组合并胃轻瘫和 H ．pylori 感染情况。对所有感染H ．pylori的2型糖尿病患者和健康对照者进行 H ．pylori 根除治疗,比较两组的根除率,并比较2型糖尿病患者治疗前后胃轻瘫症状的改善情况。统计学方法采用卡方检验。结果2型糖尿病组的H ．pylori感染率为66．4％（83／125）,高于健康对照组的51．4％（73／142）,差异有统计学意义（χ2＝5．549,P ＜0．05）。糖尿病病程＜10年,10～20年和＞20年患者的胃轻瘫发生率分别为33．8％（27／80）、47．1％（16／34）、8／11,差异有统计学意义（χ2＝6．554,P ＜0．05）;且合并胃轻瘫患者的H ．pylori感染率为78．4％（40／51）,高于未合并胃轻瘫患者的58．1％（43／74）,差异有统计学意义（χ2＝4．716,P ＜0．05）。2型糖尿病患者的 H ．pylori 根除率为68．7％（57／83）,低于健康对照组的87．8％（36／41）,差异有统计学意义（χ2＝4．385,P ＜0．05）。2型糖尿病患者 H ．pylori 根除治疗前的上腹胀痛、早饱和厌食的发生率分别为75．9％（63／83）、66．3％（55／83）和67．5％（56／83）,根除治疗后分别为44．6％（37／83）、37．3％（31／83）和39．8％（33／83）,差异均有统计学意义（χ2＝15．720、12．764、11．724, P 均＜0．01）。结论2型糖尿病患者 H ．pylori 感染率升高,且糖尿病胃轻瘫的发生与 H ．pylori 感染有关。2型糖尿病患者的 H ．pylori 根除率较低,H ．pylori 根除治疗可有效改善糖尿病胃轻瘫患者的消化不良症状。     

智能电子分光技术在判断幽门螺杆菌感染胃黏膜病变中的研究

目的通过智能电子分光技术（FICE）结合高分辨率放大内镜,描述正常及胃黏膜病变的特征性改变,并探讨其与幽门螺杆菌（H.pylori）及组织病理学的相关性。方法选择32例消化不良患者及5例正常志愿者,在内镜检查中分别于胃窦及胃体部行放大内镜及FICE观察,对胃黏膜按胃小凹形态做出相应分型（Ⅰ～Ⅲ型）,并行快速尿素酶^13C-尿素呼气试验及组织病理学检查。分析胃窦及胃体FICE下的分型对诊断H.pylori的价值,并对FICE观察部位的组织病理学改变（活动性、炎症度、萎缩、肠化）进行分级评估。结果对照组5例胃窦及胃体黏膜的FICE分型均为Ⅰ型,提示无H.pylori感染。研究组32例中,胃窦黏膜FICE分型为Ⅰ型14例,其中1例H.pylori感染（7．1％）;Ⅱ型13例中10例H.pylori感染（76．9％）,且9例同时有萎缩改变;Ⅲ型5例,均H.pylori感染,且3例同时有萎缩及肠化。胃窦黏膜各FICE分型间H.pylori感染情况的差异具有统计学意义（P〈0．01）;Ⅲ型结构与组织病理学诊断的一致性较好（kappa=0．890）。胃体黏膜FICE分型为Ⅰ型15例,其中1例H.pylori感染（6．7％）;Ⅱ型13例中11例（84．6％）H.pylori感染;Ⅲ型4例均存在H.pylori感染。胃体黏膜各FICE分型间H.pylori感染情况的差异具有统计学意义（P〈0．01）。组织病理学改变（炎症性、活动度、萎缩及肠化）的分级在无H.pylori感染组中显著低于H．pylori感染组（P〈0．01）。结论H.pylori感染与胃黏膜的炎症程度及萎缩、肠化生有明显相关性;FICE技术结合高分辨率放大内镜对预测H.pylori的存在及判断胃黏膜的病变具有一定临床价值。     

幽门螺杆菌相关上消化道疾病与复发性阿弗他溃疡相关性研究

目的探讨幽门螺杆菌（Helicobacter pylori，H．pylori）相关上消化道疾病与复发性阿弗他溃疡（recurrent aphthousulcer，RAU）的关系。方法运用聚合酶链反应技术和尿素酶试验对150例上消化道疾病患者的唾液和胃黏膜中的H．pylori检测，结合RAU的流行病学调查进行统计比较，并分析口腔和胃内H．pylori感染的相互影响及对龋齿的影响。结果胃黏膜H．pylori阳性患者中RAU的发病率为50．94％（27／53），明显高于阴性组13、40％（13／97）（P〈0．001）；口腔中H．pylori阳性和阴性两组患者的龋失补指数中位数分别为3．0和1．0，差异具有统计学意义（P〈0．05）；口腔中H．pylori阳性患者中RAU的发病率为24．72％（22／89），与阴性组29．51％（18／61）比较无明显差异（P〉0．05）；口腔内H．pylori感染与胃内H．pylori感染未见明显相关性（P〉0．05）。结论H．pylori相关上消化道疾病与RAU密切相关；口腔内H．pylori感染与龋齿发生有相关性。     

胃息肉发病机制相关因素研究

目的了解胃息肉伴随胃炎的相关表现及胃息肉的发病因素。方法对比182例（男60例，女122例，平均年龄56岁）胃息肉患者及110例（男45例，女65例，平均年龄54岁）不伴息肉的慢性胃炎患者的一些特征性表现如胃窦条状黏膜充血、幽门口胃黏膜流入、贲门口增宽等表现以及限pylori感染情况，以了解胃息肉发病的有关因素。结果①182例胃息肉包括胃底息肉156例（85．7％）、胃窦息肉26例（14．3％）。病理为淋巴瘤1例，管状腺瘤2例，增生性息肉29例，炎症性息肉150例。②出现贲门口松弛、胃窦条状黏膜充血及幽门口黏膜流入在各组比例：慢性胃炎组分别为28例（25．2％）、16例（14．4％），26例（23．4％），与慢性胃炎组相比，胃底体息肉组分别为61例（（39、1％，P〈0．05）、72例（46．2％，P〈0．001）及72例（46．2％，P〈0．001），胃窦息肉组分别为12例（46．2％，P〈0．05）、10例（38．5％，P〈0、01）、12例（46．2％，P〈0．05）。③合并食管炎：慢性胃炎组3例（2．7％），与之比较胃底体息肉组19例（12．2％，P〈0．001）。④合并限pylori感染：慢性胃炎组29例（26．4％）。胃底体息肉组显著较低为3例（1．9％，P〈0．001），胃窦息肉组显著较高为12例（46．2％，P〈0．05）。结论胃息肉患者更多合并贲门口松驰、胃窦条状黏膜充血及幽门口黏膜流入，提示与肠胃反流相关。胃底体息肉H．pylori感染率较低，其病因与H．pylori感染无关，胃窦息肉H．pylori感染率较高，其病因亦与H．pylori感染相关。     

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。     

长期服用小剂量肠溶型阿司匹林对胃十二指肠黏膜损害的病例对照研究

背景：长期以来，因预防或治疗需要而长期服用小剂量肠溶型阿司匹林的安全性一直受到关注。目的：观察长期服用小剂量（≤100mg／d）肠溶型阿司匹林对胃十二指肠黏膜的损害情况。方法：纳入5年中服用小剂量肠溶型阿司匹林超过3个月且既往无消化性溃疡和消化道出血史、胃镜检查前2周未服用其他非甾体抗炎药（NSAID）、抑酸剂、抗生素、铋剂等药物、未接受过幽门螺杆菌（H.pytori）根除治疗而具有上消化道症状者行内镜检查。结果：92例人选患者中，40例（43．5％）发现轻度胃十二指肠黏膜损害，但无一例形成黏膜溃疡。黏膜损害组和无黏膜损害组患者的年龄、性别、吸烟、阿司匹林日平均用量和常见消化不良症状均无显著差异（P〉0．05）。黏膜损害组的H．pylori感染率显著高于无黏膜损害组（P〈0．05）。尽管吸烟、年龄的分层分析未能证实H．pytori感染在黏膜损害中的重要作用，但H．pylori的感染程度与黏膜损害程度呈正相关（rs=0．308，P〈0．05）。结论：长期服用小剂量肠溶型阿司匹林可引起轻度胃十二指肠黏膜损害，H．pytori感染、吸烟和年龄均是危险因素，但H．pytori感染的危险性可能更大。     

抗胆汁反流治疗对胃内幽门螺杆菌感染的影响

体外研究发现胆汁可抑制幽门螺杆菌（H.pylori)的生长，但人体内胆汁反流对H.pylori的作用尚不清楚。目的：探讨抗胆汁反流治疗对胃内H.pylori感染的影响。方法：50例经胃镜检查确诊有胆汁反流的慢性胃炎患者纳入本研究。取胃窦黏膜活检标本行组织病理学检查和快速尿素酶试验（RUT），用改良Giemsa染色、RUT或血清H.pylori-IgG检测H.pylori感染情况。患者接受铝碳酸镁治疗（1000mg.tid,4周），治疗结束后复查胃镜和H.pylori感染情况。结果：治疗前患者的H.pylori感染率为66．0％，H.pylori感染者在I、Ⅱ、Ⅲ级胆汁反流性胃炎中的分布无显著差异。治疗后共有48例患者接受胃镜复查，结果显示胃内胆汗反流程度较治疗前明显减轻，H.pylori感染率为64．6％，与治疗前相比无显著差异。合并H.pylori感染者的胃黏膜炎症细胞浸润较非H.pylori感染者为重，且肠化发生率（39．4％）与非H.pylori感染者（11．8％）相比有显著差异（P＜0．05）。结论：合并H.pylori感染胆汁反流患者的胃炎和肠化均较单纯胆汁反流者为重。抗胆汁反流治疗可有效缓解胆汁反流性胃炎，但未能改善胃黏膜的H.pylori感染情况。     

中国上消化道疾病患者幽门螺杆菌感染根除前后胃粘膜病理改变与空泡毒素活性的关系

目的：观察幽门螺杆菌（H.pylori)阳性消化性溃疡病和慢性胃炎患者H.pylori根除前后胃粘膜病理改变与空泡毒素（VacA)活性的关系。方法：功能性消化不良伴H.pylori感染的中国患者74例,于H.pylori根除前和4－6周后作胃镜检查,根据新悉尼病理分级法按半定量记分对治疗前后的胃粘膜病理变化程度进行分级。结果：VacA^ 菌检出率为80％（59／74）,消化性溃疡病患者的检出率与慢性胃炎患者无明显差别;VacA^ 和VacA^-组患者的H.pylori根除率亦无明显差别。根除治疗前,VacA^ 和VacA^-组患者的胃粘膜慢性炎症、活动性、表面上皮损伤、萎缩、肠化和淋巴滤泡数量无显著差别;治疗后4－6周,两组患者的胃窦粘膜炎症活动性、表面上皮损伤和慢性炎症程度均明显减轻,尤以前者为著（P＜0．0001）,VacA^ 组患者的胃窦部淋巴滤泡数量减少亦稍较VacA^-组明显（P＝0．051）,两组患者的胃粘膜萎缩和肠化程度均无明显好转。结论：中国上消化道疾病患者H.pylori感染根除前后的胃粘膜病理改变与VacA活性无明显关系。成功根除H.pylori感染并不引起萎缩和肠化的逆转。     

胃息肉的临床病理特征及其与癌变和幽门螺杆菌感染关系的研究

目前对胃息肉的研究远不及结肠息肉,胃息肉与癌变以及幽门螺杆菌（H．pylori）感染的关系存在较多争议。目的：总结胃息肉的临床病理特征,并分析不同类型胃息肉与癌变和H．pylori感染的关系。方法：回顾性分析北京大学第三医院2003年1月～2008年12月经病理检查证实的胃息肉患者,分析不同类型胃息肉与肠化生、异型增生和癌变以及H．pylori感染的关系。结果：共检出1825例胃息肉患者,检出率4.3％。男女之比为l：2.3,663％为单发性息肉;胃底腺息肉、增生性息肉、腺瘤性息肉、炎性息肉和并发息肉（2种息肉同时发生于同一病例）分别占62．5％、32．2％、0．8％、1．7％和2．8％。贲门、胃底体和胃窦是增生性息肉较常见的发生部位。增生性息肉肠化生率和异型增生率均显著高于胃底腺息肉（5．3％对0．2％,7．2％对0．4％,P〈0．001）。2例增生性息肉发生癌变,癌变率0.3％。增生性息肉H．pylori感染率显著高于胃底腺息肉（36．5％对8．0％,P〈0．001）。结论：胃息肉检出率较低,以胃底腺和增生性息肉多见,并发息肉并非罕见。增生性息肉的肠化生率、异型增生率和H．pylori感染率均高于胃底腺息肉．且其可发生癌变。增生性息肉的发生可能与H．pylori感染有关。     

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。     

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.     

以胃黏膜胆汁酸浓度评估胆汁反流对胃黏膜组织的作用

背景:胃黏膜胆汁酸水平可直接反映胃黏膜细胞胆汁酸暴露的程度,并体现胆汁酸对胃黏膜的损伤程度。目的:探讨以胃黏膜组织胆汁酸浓度评估胆汁反流对胃黏膜病理改变的影响。方法:选取经内镜检查和黏膜胆汁酸浓度确诊的40例胆汁反流性胃炎患者和20例无胆汁反流性胃炎患者,评估幽门螺杆菌(H.pylori)检出率,行组织病理学评分,并分析胃黏膜胆汁酸浓度与组织病理学评分的相关性。结果:与无胆汁反流性胃炎患者相比,胆汁反流性胃炎患者H.pylori检出率无明显差异;胃窦、胃体黏膜组织胆汁酸含量显著升高(P0.05);胃窦黏膜慢性炎症和肠化生评分显著升高(P0.05),胃体黏膜慢性炎症、炎症活动性、萎缩和肠化生评分均显著升高(P0.05)。胆汁反流性胃炎患者胃窦、胃体组织病理学改变均与胆汁酸浓度相关(P0.05)。结论:以胃黏膜胆汁酸浓度评估的胆汁反流与胃黏膜病理损伤严重程度呈正相关。与无胆汁反流性胃炎相比,胃内胆汁反流主要加重胃体部组织病理学损伤。     

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

Comparison of He/icobacter py/ori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylineosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

胃粘膜萎缩与Hp感染淋巴组织增生的关系

目的研究幽门螺杆菌（Ｈｐ）诱生的胃粘膜相关淋巴组织（ＭＡＬＴ）增生与萎缩关系及Ｈｐ根除后淋巴滤泡（ＬＦ）消失情况．方法光镜观察２５８例Ｈｐ阳性的慢性胃炎三联（奥美拉唑、克拉霉素、痢特灵，７ｄ）药治疗前后（１ｍｏ及１ａ）及正常胃粘膜２５例的ＬＦ检出率和聚集强度．结果慢性胃炎ＬＦ总检出率为７２５％；萎缩性胃炎＞浅表性胃炎，而正常胃粘膜ＬＦ检出率为４％；慢性胃炎ＬＦ聚集强度与粘膜炎症程度呈正相关（ｒ＝０６５，Ｐ＜００１）；但与粘膜萎缩程度呈负相关（ｒ＝－０６９，Ｐ＜００１）；治疗后慢性胃炎ＬＦ检出率和聚集强度明显减低（Ｐ＜００１）；腺上皮萎缩与ＬＦ形成关系密切．结论胃ＭＡＬＴ增生及相伴的免疫反应，可能是引起Ｈｐ相关性胃炎出现胃粘膜萎缩的重要原因之一．     

影响慢性胃炎患者幽门螺杆菌根除的临床因素分析

背景:幽门螺杆菌(H.pylori)感染与慢性胃炎和消化性溃疡密切相关,然而,目前临床普遍采用的三联疗法对相当一部分患者的H.pylori根除无效。目的:探讨影响慢性胃炎患者H.Pylori根除的主要临床因素。方法:取128例H.pylori阳性的慢性胃炎患者的内镜活检标本行H.pylori培养和药敏试验,以奥美拉唑+克拉霉素+甲硝唑的7 d三联疗法行H.pylori根除治疗,以PCR-RFLP法检测CYP2C19基因型。分析不同因素对H.pylori根除率的影响。结果:共123例完成治疗,H.pylori根除率按ITT和按PP分析分别为66.4%和69.1%。H.pylori对甲硝唑和克拉霉素的耐药率分别为48.4%和14.1%。有吸烟史者的H.pylori根除率显著低于无吸烟史者(37.0%对88.3%,P0.01)。甲硝唑敏感菌株和克拉霉素敏感菌株的根除率均显著高于相应的耐药菌株(90.5%对46.7%,P0.01;76.6%对18.8%,P0.01)。CYP2C19强代谢型的根除率显著低于弱代谢型(63.4%对 86.7%,P0.05)。不同性别、年龄以及是否饮酒的患者之间H.pylori根除率差异均无统计学意义(P0.05)。结论:H.pylori对抗生素耐药和宿主CYP2C19强代谢型是导致H.pylori根除失败的主要原因,吸烟史对根除失败亦具有一定的意义。     

Expression of cell-cycle related proteins in Helicobacter pylori gastritis and association with gastric carcinoma

Helicobacter pylori (H. pylori) infection is associated with changes in epithelial turnover, through their significance of these in gastric carcinogenesis is still controversial. The purpose of this study was to determine the influence of H. pylori infection on cell proliferation and the relation with the cell-cycle regulators, and finally to provide insights into the mechanism by which H. pylori may lead to gastric carcinogenesis. We investigated Ki-67, p53, p21(Waf1/Cip1), cyclin D1 expression in 55 patients with H. pylori gastritis, and compared the results with patients those of non-H. pylori gastritis patients (n=21), gastric adenocarcinoma patients (n=8) and samples with normal gastric mucosa (n=12). Gastric biopsies were histologically evaluated for inflammatory reaction, intestinal metaplasia and atrophy according to the Sydney system. Overexpression of Ki-67, p53, p21(Waf1/Cip1) and cyclin D1 was found in H. pylori gastritis patients (32.7%, 10.9%, 20.0% and 7.3%, respectively), whereas only scattered expression in cells in the neck region of the crypts, but no overexpression was found in gastric antral epithelial cells in biopsy specimens from patients with non-H. pylori gastritis and noninflammed mucosa. A significant relationship was found between the grade of H. pylori colonization and Ki-67, p53, p21(Waf1/Cip1) and cyclin D1 expression. Expression was significantly higher in patients with intestinal metaplasia with atrophy, whereas no overexpression was found in patients without intestinal metaplasia with atrophy (p=0.05). H. pylori infection is associated with increased cell proliferation, increased epithelial DNA damage, and atrophy, which might contribute to the development of gastric cancer. Even if the exact mechanism has not been elucidated yet, our results suggest that H. pylori infection acts as a cofactor in gastric carcinogenesis.     

云南哈尼族彝族幽门螺杆菌感染人群胃癌易感基因研究

胃癌的发生是生物、环境、宿主等因素共同作用的结果．宿主遗传因素与幽门螺杆菌（H．pylori）感染后的不同临床结局有关。目的：筛选云南红河州哈尼族彝族Hpylori感染人群的胃癌易感基因,探讨不同基因型和等位基因与H．pylori感染宿主胃癌发病风险的相关性。方法：通过PubMed、CNKI和HapMap数据筛选出12个中国人群胃癌易感相关单核苷酸多态性（SNP）位点,以芯片技术对哈尼族彝族H．pylori感染慢性胃炎和胃癌患者的这些SNP位点进行分型。结果：IL-1β-3IC／T和IL-1β-511C/T位点存在完全连锁不平衡．其基因型（P=0．014）和等位基因频率（P=0．049）在胃癌和胃炎组中有显著差异,-511CT／-31CT（OR=2．256,95％CI：1．048～4．855）和-511TT/-31CC（OR=3．312,95％CI：1．462～7．502）基因型胃癌发病风险显著高于-511CC／-31TT基因型。COX-2．899C／G位点基因型频率在胃癌和胃炎组中有显著差异（P=0．033）,GG基因型胃癌发病风险显著高于CG基因型（OR=2．796,95％CI：1．053～7．423）。TNF—α-238A／G位点基因型频率在胃癌和胃炎组中有显著差异（P=0．037）．AA、AG基因型胃癌发病风险显著高于GG基因型（OR=2．600．95％CI：1．130～5．985）。结论：IL-1β-31C、IL-1β-511T等位基因和COX-2—899GG基因型可增高云南红河州哈尼族彝族Hpylori感染人群的胃癌发病风险,TNF-α-238GG基因型对上述人群的胃癌发生具有保护作用。     

Helicobacter pyloriin gastric corpus of patients 20 years after partial gastric resection

AIM:To determine the long-term prevalence of Helicobacterpylori(H pylori)gastritis in patients after partial gastricresection due to peptic ulcer,and to compare the severityof Hpylori-positive gastritis in the corpus mucosa betweenpartial gastrectomy patients and matched controls.METHODS:Endoscopic biopsies were obtained from 57patients after partial gastric resection for histologicalexamination using hematoxylin/eosin and Warthin-Starrystaining.Gastritis was graded according to the updatedSydney system.Severity of corpus gastritis was comparedbetween Hpylori-positive partial gastrectomy patients andHpylori-positive duodenal ulcer patients matched for ageand gender.RESULTS:In partial gastrectomy patients,surgery wasperformed 20 years(median)prior to evaluation.In 25patients(43.8%)Hpyloriwas detected histologically inthe gastric remnant.Gastric atrophy was more common inH pylori-positive compared to H pylori-negative partialgastrectomy patients(P<0.05).The severity of corpusgastritis was significantly lower in Hpylori-positive partialgastrectomy patients compared to duodenal ulcer patients(P<0.01).There were no significant differences in theactivity of gastritis,atrophy and intestinal metaplasiabetween the two groups.CONCLUSION:The long-term prevalence of Hpylorigastritisin the gastric corpus of patients who underwent partialgastric resection due to peptic ulcer disease is comparableto the general population.The expression of Hpylorigastritisin the gastric remnant does not resemble the gastric cancerphenotype.