尾型同源盒转录因子CDX1和CDX2在胃黏膜肠化生及胃癌组织中的表达

目的 研究尾型同源盒转录因子CDX1、CDX2在不同亚型胃黏膜肠化生及胃癌组织中的表达,探讨二者在胃黏膜肠化生进展及胃癌发生中的作用.方法 分别选取慢性浅表性胃炎40例,单纯慢性萎缩性胃炎(CAG)40例,CAG伴肠化生46例,胃癌40例,对应癌旁组织伴肠化生32例.分别用免疫组织化学和原位杂交方法观察CDX2蛋白及CDX1、CDX2 mRNA在上述胃黏膜病变中的表达情况.结果 癌旁组织伴肠化生中Ⅲ型肠化生的比例显著高于CAG伴肠化生(分别为56.25%和21074%,P<0.01);CDX1、CDX2 mRNA及CDX2蛋白在慢性浅表性胃炎及单纯CAG中均无表达,而在CAG伴肠化生、癌旁组织伴肠化生和胃癌中,CDX2蛋白及其mRNA表达阳性率分别为69.57%、53.12%、42.50%和63.04%、46.88%、35.00%,CDX1 mRNA表达阳性率分别为67.39%、50.00%、40.00%,胃癌中的表达阳性率均显著低于CAG伴肠化生(P<0.01),而与癌旁组织伴肠化生比较差异无统计学意义(P>0.05);CDX2蛋白在肠型胃癌中的表达阳性率(54.55%)显著高于弥漫型胃癌(27.78%)(P<0.05).Ⅲ型肠化生中CDX2蛋白表达阳性率及表达强度则显著低于Ⅰ型(P<0.05).结论 CDX1、CDX2在胃黏膜肠化生进展及胃癌发生中有重要作用,可能是新的胃癌相关基因.Ⅲ型肠化生与肠型胃癌有密切关系.     

不同亚型肠上皮化生黏膜mtp53和c-myc蛋白表达与幽门螺杆菌细胞毒素相关基因蛋白A的关系

目的 研究幽门螺杆菌(Hp)细胞毒素相关基因蛋白A(Hp-CagA)与肠上皮化生不同亚型中mtp53和c-myc蛋白表达的关系.方法 选取胃镜检查患者165例,其中慢性萎缩性胃炎伴肠上皮化生125例,非萎缩性胃炎40例.肠上皮化生分为完全型小肠上皮化生、不完全型小肠上皮化生、完全型结肠上皮化生和不完全型结肠上皮化生四种亚型.应用14C尿素呼气试验检测Hp；通过AB-PAS和HID-AB黏液染色区分肠上皮化生亚型；应用免疫组织化学染色Elivision法检测mtp53和c-myc蛋白的表达；采用间接ELISA法检测Hp-CagA.结果 不完全型结肠上皮化生45例,不完全型小肠上皮化生47例,完全型结肠上皮化生17例,完全型小肠上皮化生16例.肠上皮化生各亚型Hp-CagA阳性率均高于非萎缩性胃炎,但差异无统计学意义(P＞0.05).不完全型结肠上皮化生Hp-CagA阳性患者mtp53蛋白阳性表达率高于不完全型结肠上皮化生Hp-CagA阴性患者(x2=5.494,P＜0.05)；不完全型结肠上皮化生Hp-CagA阳性患者c-myc蛋白阳性表达率明显高于不完全型结肠上皮化生Hp-CagA阴性患者(x2=13.950,P＜0.01).结论 Hp-CagA阳性Hp是Hp的高毒力株,Hp-CagA阳性Hp具有较强的促进胃黏膜萎缩、肠上皮化生的作用,Hp-CagA阳性Hp可能通过癌基因激活实现胃黏膜肠上皮化生和癌变的过程.     

根除幽门螺杆菌对萎缩性胃炎病变转归的影响

目的 探讨根除幽门螺杆菌(Hp)后对萎缩性胃炎黏膜病变转归的影响.方法 入选患者均经胃镜和临床病理诊断为萎缩性胃炎伴肠上皮化生,并确定有Hp感染的状态;其中Hp根治组45例和Hp感染组38例,分别于入选时和随后1、4年行胃镜随访,在同一部位取活检,根据病理结果判断是否逆转.结果 根治Hp 1年后萎缩性胃炎和肠上皮化生均无明显逆转,4年后Hp根治组较Hp感染组肠上皮化生逆转率显著提高[42.22%(19/45)比7.89%(3/38),x2=17.28,P＜0.01],4年后Hp根治组肠上皮化生逆转率较1年后[15.56%(7/45)]显著提高(x2=7.78,P＜0.01),萎缩性胃炎病变无明显改变.结论 根除Hp后随时间推移对肠上皮化生有逆转作用,对萎缩性胃炎无逆转作用,有Hp感染的萎缩性胃炎伴肠上皮化生患者应及早根除Hp治疗.     

EB病毒潜伏膜蛋白1在慢性萎缩性胃炎伴肠上皮化生胃黏膜中的表达及意义

目的检测EB病毒（EBV）．潜伏膜蛋白1（LMPl）在作为癌前病变的慢性萎缩性胃炎（CAG）伴肠上皮化生胃黏膜中的表达,探讨其在胃癌发生、发展过程中的作用。方法应用免疫组织化学sP法检测经病理确诊的45例慢性浅表性胃炎（CSG）组织、63例CAG伴肠上皮化生组织、36例胃癌组织中EBV—LMP1的表达。结果45例CSG和36例胃癌组织中未见EBV-LMP1的表达,63例CAG伴肠上皮化生胃黏膜组织有23例阳性,阳性率为36．5％（23／63）,主要定位于细胞核,明显高于CSG及胃癌中的表达,差异有统计学意义（尸值均为0．000）。结论CAG伴肠上皮化生组织中存在EBV-LMP1表达,明显高于CSG及胃癌组织,提示EBV感染可能在胃癌发生的早期阶段起重要作用。     

慢性萎缩性胃炎胃镜下不同病理改变与幽门螺杆菌感染的关系

目的 探讨慢性萎缩性胃炎胃镜下不同病理改变与幽门螺杆菌感染的关系,为临床诊治提供借鉴.方法 对8012例行胃镜检查后诊断为慢性萎缩性胃炎患者的胃镜形态表现与幽门螺杆菌感染及病理结果进行回顾性分析.结果 胃镜下诊断为慢性萎缩性胃炎共1121例,其中A组(单纯萎缩性胃炎)共532例,B组(萎缩性胃炎伴增生)共589例；A组患者病理诊断为萎缩性胃炎385例,诊断符合率为72.37％；B组患者病理诊断为萎缩性胃炎505例,诊断符合率为85.74％,两组差异有统计学意义(P＜0.05)；A组患者病理结果肠上皮化生54例,不典型增生56例；B组患者病理结果肠上皮化生94例,不典型增生108例,两组差异有统计学意义(P＜0.05)；A组患者Hp感染307例,感染率为57.71％；B组患者Hp感染429例,感染率为72.84％,两组差异有统计学意义(P＜0.05).结论 内镜下以萎缩性胃炎伴增生诊断率高于单纯萎缩性胃炎,且其合并肠上皮化生、不典型增生及Hp感染率较高,临床上更应该重视其诊断、治疗和随访.     

Hp感染对胃癌组织中CD44和凋亡基因Survivin与MMP-9表达的影响

目的 探究幽门螺杆菌(Hp)感染对胃癌组织中CD44、凋亡基因Survivin以及基质金属蛋白酶-9(MMP-9)表达的影响。方法 收集2015年9月-2018年12月来厦门市长庚医院消化内科就诊的首次经胃镜及病理活检确诊为胃炎患者222例,其中慢性萎缩性胃炎78例,慢性非萎缩性胃炎69例,慢性萎缩性胃炎伴肠上皮化生75例;胃癌患者72例,检测Hp感染情况,免疫组织化学法检测CD44、Survivin以及MMP-9表达,分析CD44、Survivin以及MMP-9与Hp感染、临床病理指标以及患者预后的关系。结果 胃癌组织中Hp、CD44、Survivin以及MMP-9的阳性率高于慢性萎缩性胃炎、慢性非萎缩性胃炎、慢性萎缩性胃炎伴肠上皮化生组织(P<0.05)。Hp感染与胃癌患者肿瘤分化程度、TNM分期、淋巴结转移、CD44、Survival和MMP阳性有关(P<0.05)。胃癌患者中CD44阳性48例,Survivin阳性51例,MMP9阳性42例。CD44、Survivin、MMP-9的表达与患者肿瘤分化程度、TNM分期以及淋巴结转移有关(P<0.05),与患者性别...     

胃癌及癌前状态MG7表达的动态观察及分析

目的：探讨在胃癌发生发展过程中MG7抗原表达的动态变化及意义。方法：采用免疫组化技术及组化技术检测406例胃黏膜MG7抗原的表达情况及肠上皮化生类型。结果：从组织学角度观察，正常胃黏膜→肠上皮化生及异型增生→胃癌；Ⅰ、Ⅱ型肠上皮化生→Ⅲ型肠上皮化生，MG7抗原阳性表达率依次上升(P＜0．01)。从临床疾病角度观察，浅表性胃炎→萎缩性胃炎→胃癌，MG7抗原阳性表达率依次上升(P＜0．01)。结论：MG7抗原与胃癌发生发展有良好的相关性，对胃癌具有较高的特异性；对萎缩性胃炎，Ⅲ型肠上皮化生与异型增生进行严密监测有可能提高早期胃癌的检出率，MG7在胃癌前疾病动态随访中具有重要应用价值。     

幽门螺杆菌vacA s1m2基因型与胃黏膜肠上皮化生关系

目的探讨幽门螺杆菌(H.pylori)vacA s1m2基因型与胃黏膜肠上皮化生(IM)的关系,为萎缩性胃炎治疗及胃癌预防提供依据。方法选取H.pylori阳性胃镜活检的石蜡包埋标本271例,包括浅表性胃炎76例(伴IM 18例)、萎缩性胃炎56例(伴IM 37例)和胃溃疡139例(伴IM 30例);提取标本中DNA,经巢式PCR方法及琼脂糖凝胶电泳对H.pylori的细胞空泡毒素基因(vacA)基因型进行检测。结果萎缩性胃炎组中vacA s1m2亚型的检出率为53.6%(30/56),明显高于浅表性胃炎组和胃溃疡组;在271例H.pylori阳性病例中,伴IM组vacA s1m2亚型检出率为62.4%(53/85),明显高于无IM组;萎缩性胃炎病例中伴IM组vacA s1m2亚型检出率为75.7%(28/37),明显高于无IM组,同时高于浅表性胃炎伴IM组和胃溃疡伴IM组。结论幽门螺杆菌vacA s1m2基因型与胃黏膜肠上皮化生密切相关,vacA s1m2基因型幽门螺杆菌为萎缩性胃炎相关高致病性菌株。     

胃癌及癌前病变组织中Hp感染与C-myc基因蛋白表达及相关性研究

目的探讨胃癌及及癌前病变组织中幽门螺杆菌(Hp)感染及C-myc基因蛋白表达情况。方法采用W-S染色法观察52例胃癌、37例胃粘膜癌前病变及18例慢性浅表性胃炎组织中Hp的感染情况;采用免疫组织化学S-P法检测上述组织中C-myc基因蛋白表达的情况。结果胃癌及癌前病变各组Hp感染阳性率均显著高于慢性浅表性胃炎组(P<0.01);胃癌各组间、肠上皮化生及异型增生组间Hp感染阳性率差异均无显著性。胃癌、癌前病变各组C-myc阳性率显著高于中~高分化腺癌组(P<0.05)。Hp感染阳性胃癌、癌前病变组C-myc阳性率均显著高于各自Hp感染阴性组(P<0.01)。结论Hp感染与C-myc基因过表达密切相关,Hp感染可能是通过激活C-myc基因而诱发胃黏膜癌变。     

根除幽门螺杆菌对胃窦部黏膜萎缩和肠上皮化生的影响

目的比较幽门螺杆菌（Hp）根除前后胃窦部黏膜的病理变化,探讨根除Hp是否可以减少黏膜萎缩和肠上皮化生程度。方法将因上腹痛进行胃镜检查的病人180例随机分为Hp根除组98例和对照组82例,对Hp根除组给予抗Hp治疗,对照组仅给予对症治疗。再次进行胃镜检查,观察两组患者胃窦部病理变化。Hp检测采用Giemsa染色法和快速尿素酶试验,萎缩和肠上皮化生诊断采用HE染色。结果对病人两次胃镜检查的胃黏膜萎缩和肠上皮化生程度进行比较,Hp根除组黏膜萎缩程度减轻（P〈0.05）,对照组无变化（P〉0.05）;Hp根除组肠上皮化生程度减轻（P〈0.05）,对照组加重（P〈0.05）。结论根除Hp能够使胃窦黏膜萎缩程度和肠上皮化生程度减轻。     

人β3-防御素-2在消化性溃疡中的表达及作用

目的 探讨胃窦黏膜炎性反应、人β3-防御素(HBD)-2、幽门螺杆菌(Hp)之间的相互作用及临床意义.方法 将所有溃疡组(43例)及对照组(30例)活检的胃窦黏膜进行电镜下组织病理学分析及HBD-2免疫组织化学检测.对于23例Hp阳性消化性溃疡患者进行统一的抗Hp感染治疗及消化性溃疡治疗后,再次进行电镜下组织病理学分析及HBD-2免疫组织化学检测.结果Hp感染程度与胃窦黏膜慢性炎性反应、活动性、萎缩、肠化相关性分析显示:Hp感染程度与活动度、萎缩有相关性(r =0.574、0.640,P＜ 0.01).无论是溃疡组还是对照组,HBD-2表达都与Hp感染呈正相关(r＝0.533、0.577,P＜0.01),组间比较差异无统计学意义(P＞0.05).Hp阳性的消化性溃疡患者抗Hp治疗后显示:胃窦黏膜慢性炎性反应及萎缩、肠化无明显改变,炎性反应活动性显著性降低(P＜ 0.01);HBD-2表达则显著下降(P＜0.01),而Hp治疗失败患者HBD-2表达无显著降低(P＞0.05).结论 当消化道上皮细胞受到Hp感染后,HBD-2在炎性反应细胞及因子的作用下大量表达,参与胃窦黏膜炎性反应过程,起到抑制或灭活细菌的作用;HBD-2的缺失可能加速Hp感染相关的胃炎进程,加重胃窦黏膜炎性反应.     

Effect of Helicobacter pylori infection and eradication on proliferative kinetics of the gastric mucosa

Helicobacter pylori infection is associated with an increased cell proliferation activity, however the exact mechanisms have not been elucidated. Our aim was to study the effect of Helicobacter pylori infection on normal gastric epithelia, gastritis, intestinal metaplasia and carcinoma by the expression of proliferating cell nuclear antigen and nucleolus organizer regions. Antral biopsies were taken from 121 patients (61 women, 60 men; mean age 58.5 y.). Sections were scored for normal epithelia (n = 15), gastritis without intestinal metaplasia (n = 74), gastritis with intestinal metaplasia (n = 24) and gastric carcinoma (n = 8). 52 patients had H. pylori positive gastritis, and success of eradication therapy was controlled in 34 cases. To characterize cell proliferation immunohistochemistry (PCNA) and histochemistry methods (AgNOR) were used. Results of PCNA and AgNOR significantly correlated except of that in the intestinal metaplasia group. PCNA LI and AgNOR counts were not significant higher in H. pylori positive compared to the H. pylori negative gastritis. Presence of H. pylori caused higher proliferation rate in intestinal metaplasia group measured by PCNA. In the group of intestinal metaplasia the proliferation activity decreased to the activity of the normal epithelia after the successful eradication, but remained high if eradication therapy was failed. Our results suggest, that H. pylori infection plays only as a co-factor in gastric carcinogenesis. Results were controversial in the intestinal metaplasia group, that can be explained by the heterogeneity of the bacteria.     

慢性萎缩性胃炎的胃黏膜保护机制的研究进展

慢性萎缩性胃炎是慢性胃炎的一种类型,其胃黏膜组织学病理表现为黏膜炎症、腺体萎缩、肠上皮化生和异型增生,而肠上皮化生被认为是萎缩的典型标志以及胃癌的前兆。胃黏膜保护机制可能与抑制胃酸分泌、抵抗H.pylori感染及热休克蛋白的启动等胃黏膜保护因子有关,热休克蛋白在抵御黏膜损害中起重要作用。     

Determination of cagA, vacA genotypes of Helicobacter pylori with real-time PCR-method

Presence of cagA gene of Helicobacter pylori (H. pylori) increases proliferation of stomach mucosa and it is an index of raised virulence of the bacteria. The vacA gene of H. pylori induces a serious inflammation of stomach. The purpose of this study was to determine cagA and vacA genotypes of H. pylori using real-time polymerase chain reaction (PCR) method with the double strain DNA-(dsDNA) binding SYBR Green I. dye. Results were compared with those of two immunohistochemical methods. 43 patients' paraffin embedded biopsy tissue samples were examined by histology, epidermal growth factor receptor (EGFR), proliferating cell nuclear antigen (PCNA) immunohistochemistry and melting curve analysis of real-time PCR using LightCycler instrument. Results of histology and real-time PCR from gastric biopsies correlated in 57% of cag acases and in 58% of vac cases. Significant difference was detected between normal and gastritis cases in the presence of cagA gene (p = 0.003) and between normal epithelial and intestinal metaplasia cases in the presence of vacA gene (p = 0.045) by investigation of association of histology and genotype of bacterium. Statistically significant difference (p = 0.02) was found between increased cell proliferation and the presence of gastritis. Significant correlation was found between the presence of cagA gene and EGFR expression in intestinal metaplasia cases (p = 0.0418). Results underlie the statistics that infection with cagA positive H. pylori strain increases the cell proliferation on the stomach mucosa and raises the chance of development of intestinal metaplasia. Infection with vacA positive H. pylori inhibits the signal-transduction pathway of EGFR, which influences mechanisms of mucosa repair. The role of EGFR and H. pylori infection is yet unclear in intestinal metaplasia and cancer. The authors' method seem to be suitable for determination of genotypes of H. pylori.     

PTEN基因在胃癌组织中的表达及临床意义

目的研究正常胃粘膜、慢性萎缩性胃炎（伴肠化）、胃癌组织中抑癌基因PTEN的ⅢRNA和蛋白的表达情况,探讨其在在胃癌发生、发展中的作用及临床意义。方法（1）收集2011年11月--2012年11月期间内蒙古医学院第三附属医院病理和内窥镜结合确诊的正常胃组织30例、慢性萎缩性胃炎（伴肠化）30例．手术切除的45例胃癌标本并经病理确诊。（2）所有患者术前均未接受放、化疗和其他针对性抗肿瘤治疗,无其它肿瘤病史。（3）通过实时荧光定量PCR及Western印迹技术检测PTENmRNA及其蛋白在胃粘膜不同组织中的相对表达,所有数据采用SPSSl3．0统计软件包进行处理,统计学方法采用单因素方差分析及t检验,以P〈O．05为差异有统计学意义。结果（1）PTENmRNA在正常胃粘膜、慢性萎缩性胃炎（伴肠化）、胃癌中表达量分别为（1．902±0．981、1．158±0．241、0．740±0．221）,三组相比差异有统计学意义（F=3．292,P=O．041）。胃癌组织中PTENmRNA表达量分别与正常胃粘膜组织、慢性萎缩性胃炎（伴肠化）组相比,差别均有统计学意义（t=4．451,P=O．001;t=3．007,P=O．041）;（2）PTEN蛋白在正常胃粘膜、慢性萎缩性胃炎（伴肠化）、胃癌中表达量分别为（2．001i0．67I、1．141±0．326、0．599±0．220）,三组相比差异有统计学意义（F=4．122,P=O．030）。胃癌组织中PTEN蛋白的表达量与正常胃粘膜、慢性萎缩性胃炎（伴肠化）组相比,差别均有统计学意义（t=4．301,P=O．001;t=3．123,p-0．040）。结论PTEN基因在胃癌组织中表达降低和缺失与胃癌的发生密切相关,提示PTEN基因的表达可能为临床早期诊断胃癌提供新的指标。     

Helicobacter pylori-associated gastritis and the ascorbic acid concentration in gastric juice

Patients infected with Helicobacter pylori have abnormally low ascorbic acid concentration in gastric juice. Low vitamin C intake and Helicobacter pylori infection have been related to an increased risk of gastric carcinoma. This report examines the association between ascorbic acid and Helicobacter pylori in patients referred for upper gastrointestinal endoscopy. Elevated gastric pH and the damage to the gastric surface epithelium were inversely associated with the ascorbic acid concentration in gastric juice. We postulate that these two factors mediate the ascorbic acid-decreasing effect of Helicobacter pylori. Patients with nonpremalignant conditions (normal gastric histology, diffuse antral gastritis, or duodenal ulcer) had lower gastric pH, less damage to the gastric epithelium, and higher levels of ascorbic acid in gastric juice than patients with atrophic gastritis, intestinal metaplasia, or dysplasia.     

胃癌及胃癌前疾病患者血清及组织癌胚抗原检测的意义

目的 检测胃癌、胃癌前疾病患者血清与胃组织癌胚抗原(CEA),为胃癌及胃癌前疾病的诊断、监测提供参考指标.方法 采用放射免疫法测定胃癌(111例)、胃癌前疾病(167例,其中慢性萎缩性胃炎104例,胃溃疡31例,胃黏膜肠上皮化生32例)患者血清CEA,免疫组化SP法测定胃组织CEA,并与浅表性胃炎(31例)对照.结果 胃癌组织中CEA阳性率(89.2%,99/111)明显高于胃癌前疾病[慢性萎缩性胃炎52.9%(55/104),胃黏膜肠上皮化生53.1%(17,32),胃溃疡48.4%(15/31)]及浅表性胃炎组织(19.4%,6/31),P＜0.01;胃癌与胃癌前疾病及浅表性胃炎的血清CEA阳性率比较差异有统计学意义(分别为19.8%、1.9%、0),P＜0.01;胃癌前疾病与浅表性胃炎的血清CEA阳性率比较差异无统计学意义,P＞0.05.结论 胃组织中CEA阳性有助于胃癌的诊断.并可作为监测胃癌前疾病的指标之一;血清CEA水平对胃癌有一定的诊断价值,对胃癌前疾病的诊断价值不大.     

慢性萎缩性胃炎胃镜下不同病理改变及幽门螺杆菌感染情况研究

目的 探讨慢性萎缩性胃炎胃镜下不同病理改变与幽门螺杆菌(Hp)感染的关系.方法 对1623例行胃镜检查后诊断为慢性萎缩性胃炎患者的胃镜形态表现与Hp感染及病理结果进行回顾性分析,探讨不同胃镜表现患者Hp感染的差异及病理表现.结果 胃镜下诊断为慢性萎缩性胃炎482例,其中A组239例(胃镜表现黏膜红白相间以白为主,皱襞变平甚至消失,血管显露),B组243例(胃镜表现黏膜呈颗粒状或结节状).A组患者病理诊断为萎缩性胃炎173例,诊断符合率为72.4%(173/239);B组患者病理诊断为萎缩性胃炎206例,诊断符合率为84.8%(206/243),两组诊断符合率比较差异有统计学意义(P<0.05).A组患者病理结果肠上皮化生24例(10.0%,24/239),不典型增生25例(10.5%,25/239);B组患者病理结果肠上皮化生45例(18.5%,45/243),不典型增生57例(23.5%,57/243).两组肠上皮化生与不典型增生的发生率比较差异有统计学意义(P<0.05).A组患者Hp感染138例,感染率为57.7%(138/239),B组患者Hp感染177例,感染率为72.8%(177/243),两组Hp感染率比较差异有统计学意义(P<0.05).结论 内镜下以黏膜呈颗粒状或结节状为主要表现的慢性萎缩性胃炎合并肠化生、不典型增生及Hp感染率较高,临床上更应该重视其诊断、治疗和随访.

Abstract：

Objective To investigate the relationship between different appearance and pathology change under gastroseope in chronic atrophic gastritis and Helicobacter pylori (Hp) infection. Method The performance of endoscopic morphology, Hp infection and pathology results of patients diagnosed as chronic atrophic gastritis by endoscopy were analyzed retrospectively in 1623 cases and the relationship between different gastroscope forms of change in chronic atrophic gastritis and Hp infection were investigated and the pathological diagnosis results were analyzed retrospectively. Results Four hundred and eighty-two eases were diagnosed as chronic atrophic gastritis in 1623 cases. Group A included 239 patients (endoscopic features were red and white to white-based mucosal, or even flattened folds disappeared, mucosal blood revealed), group B included 243 patients (endoscopic features were granular or nodular mucosa). In group A, 173 eases (72.4%) were diagnosed as atrophic gastritis. In group B, 206 eases (84.8%) were diagnosed as atrophic gastritis. The diagnosis accordance rate of the two groups had significant difference (P < 0.05). In group A, 24 cases (10.0%) showed intestinal metaplasia,and 25 cases( 10.5% ) showed atypical hyperplasia.In group B, 45 cases (18.5%) showed intestinal metaplasia ,and 57 cases (23.5%) showed atypical hyperplasia. The occurrence rates of intestinal metaplasia and atypical hyperplasia had significant difference between the two groups (P< 0.05). The Hp infection rate of group A and group B was 57.7% (138/239) and 72.8% (177/243) respectively, and there was significant difference (P <0.05). Conclusions The incidences of intestinal metaplasia, dysplasia and Hp infection in chronic atrophic gastritis with endoscopic mucosal rough as the main manifestation are higher than those in other forms of chronic atrophic gastritis.More attention should be paid to clinical diagnosis, treatment and follow-up.