乙、丙型肝炎病毒在慢性肝炎、肝硬化患者胃黏膜表达的临床研究

目的:探讨乙、丙型肝炎病毒(HBV、HCV)的泛嗜性.方法:选择慢性乙、丙型肝炎(慢肝组)28例、肝炎肝硬化(肝硬化组)44例,共72例作为研究对象.受检者常规胃镜检查,取胃窦幽门周围3cm以内活体组织两块,除普通病理检查外,分别做乙型肝炎病毒表面抗原(HBsAg)、乙型肝炎病毒核心抗原(HBcAg)、丙型肝炎病毒抗原(HCVAg)免疫组化法检测.结果:慢肝组有不同程度的胃黏膜慢性炎症者达92.9%(26/28)、肝硬化组达95.5%(42/44),排除年龄影响因素外,慢肝组以单纯慢性炎症为多,而肝硬化组以伴萎缩和肠化者为多.慢肝组与肝硬化组患者分别有53.6%(15/28)、81.8%(36/44)胃黏膜HBVAg阳性,其中HBsAg、HBcAg双阳性31例.在51例患者胃黏膜HCVAg检测中有33例(占64.7%)阳性表达、66.7%(22/33)与HBcAg同时表达.肝硬化组HBVAg及HBsAg、HBcAg双阳性者均高于慢肝组(P值均＜0.05).结论:HBV、HCV在慢性及肝硬化患者胃黏膜表达明显,应重视其在胃黏膜病变发病中的作用,并加强防护措施.     

慢性肝病胃粘膜乙型肝炎病毒表达及幽门螺杆菌感染

目的 探讨乙型肝炎病毒（HBV）的泛嗜性及与幽门螺杆菌（Hp）感染的关系。方法选择慢性乙型肝炎（慢肝）28例、乙型肝炎后肝硬化（肝硬化）44例,共72例作为观察组,无肝病的胃病患者30例作为对照组。受检者常规胃镜检查,取胃窦幽门周围3cm以内活体组织3块,除普通病理检查外,分别做乙型肝炎病毒表面抗原（HBsAg）、乙型肝炎病毒核心抗原（HBcAg）检测及快速尿素酶、品红染色和免疫组化法检测Hp。结果 慢肝组有不同程度的胃粘膜慢性炎症者达92.9％（26/28）、肝硬化组达95.5％（42/44）,其中慢肝组以单纯慢性炎症为多,而肝硬化组以伴萎缩和肠化者为多。72例慢性肝病者中有51例胃粘膜HBV阳性,其中HBsAg、HBcAg双阳性16例;肝硬化组HBV抗原表达高于慢肝组,而HBsAg、HBcAg双阳性者低于慢肝组（P均<0.05）。在慢肝和肝硬化组有炎症的胃粘膜中Hp阳性率分别为76.9％（20/26）、69.0％（29/42）,与对照组相比无显著差别。慢性肝病Hp阳性、阴性者胃粘膜HBV抗原表达率分别为69.8％（37/53）、73.7％（14/19）,亦无统计学差异（P>0.05）。结论 （1）HBV在慢肝及肝硬化患者胃粘膜表达明显,应重视其在胃粘膜病变中的作用,加强防护措施。（2）在胃粘膜中HBV与Hp表达未见相关关系。     

HCV/HBV重叠感染重症肝炎患者的临床与病理

探讨HCV／HBV重叠感染重症肝炎的发病机制。用直接酶标法检测肝组织内HCVAg，用PAP法检测肝组织内HBsAg、HBcAg。在264例肝病肝组织中共检出15例HCVAg阳性患者(5．7％)，肝内HCVAg阳性细胞表现为脑浆型9例、核浆型2例、核型4型。脑浆型HCVAg阳性患者肝组织内还检出HBsAg阳性5例、HBcAg阳性3例，脑浆型HCVAg阳性肝细胞疏松水肿，并可见淋巴细胞围绕。HCV／HBV重叠感染重症肝炎组与单纯HBV阳性重症肝炎组相比较，前者肝损害程度严重，结果提示HCV与HBV二者有相互促进作用，从而加重肝脏的损害。     

隐匿性乙型肝炎病毒感染者临床特点和肝组织病理学检查

目的了解血清肝炎病毒标志物阴性、肝功能反复异常患者中HBV隐匿性感染的比例及其临床和病理学特点。方法对27例血清肝炎病毒标志物阴性、肝功能反复异常患者采用免疫组化法检测肝组织HBsAg、HBcAg和HCVAg，并进行常规的病理学检查。结果肝组织HBsAg和（或）HBcAg阳性9例（33．3％）；HBsAg和（或）HBcAg及HCVAg阳性10例（37．0％）；全阴性8例（29．6％）。在HBV隐匿性感染的19例患者中，慢性肝炎8例，肝硬化11例。结论HBV和HCV感染为血清肝炎病毒标志物阴性患者肝功能反复异常的主要原因之一，尤其是HBV感染。这种HBV隐匿性感染与慢性肝炎、肝硬化的发生关系密切，应引起重视。     

丁型肝炎患者肝组织HDAg和HBsAg/HBcAg的免疫组化检测

目的 探讨HDAg和HBsAg/HBcAg在丁型肝炎患者肝组织中表达及关系。方法 应用免疫组化双重染色,检测79例丁型肝炎患者肝组织HDAg、HBsAg和HBcAg表达,以52例乙型肝炎作对照。结果 丁型肝炎HBsAg、HBcAg检出率(81％、71％)较乙型肝炎(94％、92％)低(P<0.05或0.01)。HDAg以肝细胞核表达为主,HBsAg以肝细胞浆表达为主,HDAg和HBsAg表达强度及阳性细胞分布呈一致性,且均与肝组织的炎症活动和病理损害程度相关(P<0.01)。HBcAg以肝细胞核表达为主,阳性细胞主要呈单个细胞或点状分布,且HBcAg阳性细胞明显少于HDAg阳性细胞。结论 HDV感染会抑制HBV病毒抗原(HBcAg)表达;HDV致病机制中既有HDV的直接细胞毒性作用,也有HBV和HDV的协同作用。     

83例肝病患者临床与肝组织病理学分析

目的通过对83例肝病患者的临床与肝组织病理学检查的对比研究,以提高临床诊断的准确性。方法用全自动生化分析仪进行血清生化指标检测,ELISA法检测HBV血清标志物,同时进行肝组织病理检查,检测肝组织HBsAg和HBcAg的表达。结果51例血清HBsAg阳性者肝细胞中均有HBsAg和/或HBcAg表达,32例血清HB-sAg阴性者有9例(28.1%)肝组织中有HBsAg和/或HBcAg表达。75例慢性肝病患者中ALT在各炎症分级组间差异无统计学意义(P>0.05),AST和TBIL在不同的肝脏炎症分级组间差异有统计学意义(P<0.05),且炎症分级越高,AST和TBIL升高越明显;ALT、AST、TBIL值在肝脏纤维化S2期最高。以病理诊断为标准,临床慢性肝炎轻度和中度的诊断准确率分别为61.9%(13/21)和62.5%(20/32),肝硬化的临床诊断准确率为40%。结论以肝组织病理检查为金标准,肝病临床诊断的准确率仍较低。为提高慢性肝病的临床确诊率,应尽可能行肝组织病理学检查。     

HBsAg、HBcAg在慢性乙型肝炎肝细胞内的表达及临床意义

目的 探讨HBsAg、HBcAg在慢性乙型肝炎(CHB)患者肝细胞内的表达,及其与血浆HBVDNA定量、肝组织病理和临床间的关系。 方法 采用PCR检测351例CHB患者血浆HBV DNA定量,肝穿刺活检,采用免疫组织化学技术观察肝细胞内HBsAg、HBcAg的表达。 结果 在CHB患者肝细胞内HBsAg和HBcAg阳性表达率分别为92.3％和76.9％。HBcAg浆膜型(75.6％)和胞核型(24.4％)分别见于肝组织炎症较活跃和较静止期CHB。HBsAg表达强度与血浆HBV DNA定量呈较低正向关联(rp=0.24,P=0.0129)、与肝组织炎症和纤维化呈较低负向关联(rp=-0.22,P=0.0279和rp=-0.23,P=0.0186)。HBcAg的表达强度随着血浆HBV DNA定量的增加而增加,呈较强正向关联(rp=0.52,P<0.0001),随着肝组织炎症和纤维化程度的加重而减弱,呈较强的负向关联(rp=-0.33,P<0.0001和rp=-0.34,P<0.0001)。 结论 在CHB肝组织免疫损伤的免疫应答中,HBcAg是靶抗原,HBsAg不一定是靶抗原。HBsAg是筛查HBV感染的较敏感指标,HBcAg是评价HBV复制程度的较可靠指标。     

乙型肝炎相关性肝细胞癌HBV复制及其癌组织中HBsAg/HBcAg表达的研究

目的以慢性乙型肝炎(chronic hepatitisB,CHB)患者为对照,观察乙型肝炎相关性肝细胞癌(hepatocellular carcinoma,HCC)患者血清中HBVDNA水平的变化,以及HCC组织中HBsAg/HBcAg的表达情况,探讨HBV导致HCC的可能机制。方法 HCC组89例,CHB组120例。采用实时定量PCR法检测血清HBVDNA水平;分别留取肝脏穿刺组织标本(HCC组织均带有癌旁肝硬化组织),用免疫组化法检测组织中HBsAg/HBcAg的表达情况。结果 HCC组血清HBVDNA水平明显低于CHB组(P<0.05);在CHB组织、癌旁肝硬化组织和HCC组织中HBsAg表达阳性率分别为90%、51%和10%,HBcAg阳性率分别为78%、19%和3%,与CHB组织、癌旁肝硬化组织相比,HCC组织中2种抗原表达均明显较低(P均<0.05)。结论在HBV慢性感染不同疾病阶段,血清HBVDNA水平和HBsAg/HBcAg在肝组织内的表达具有显著差异;与CHB组相比,HCC组HBVDNA水平较低,HBsAg/HBcAg表达显著缺失,这可能与HCC患者HBVDNA复制水平降低有关,但也不排除其他因素导致HBsAg/HBcAg表达抑制。     

慢性乙型肝炎肝组织内HBsAg、HBcAg的表达及临床研究进展

一直以来临床将血清乙型肝炎e抗原(HBeAg)、乙肝病毒DNA(HBV DNA)阳性作为乙肝病毒复制的标志,随着肝穿活检及抗病毒治疗的研究进展,肝活检组织中乙肝表面抗原(HBsAg)和乙肝核心抗原(HBcAg)的表达模式与血清乙型肝炎病毒(HBV)DNA定量、肝组织炎症活动度分级及纤维化分期之间关系的临床研究日益增多,本文就HBsAg和HBcAg在肝组织的表达模式及临床研究进展综述如下.     

乙肝病毒感染对慢性乙肝肝硬化患者胃黏膜病变的影响

目的探讨乙肝病毒(HBV)感染对慢性乙肝、肝硬化患者胃黏膜病变的影响及其发病机制。方法2003-06～2004-02对河北医科大学第三医院感染科60例慢性乙肝、肝硬化患者同时行肝穿、胃镜、肝功能、血清肝炎病毒标志物检查,采用SP法检测肝及胃黏膜组织中HBsAg、HBcAg。结果(1)肝组织病理损害程度与胃黏膜病变程度成正比(r=0.483,P<0.01)。(2)56例中26例胃黏膜组织中可检测到HBsAg和(或)HBcAg,其病变以中重度为主。34例HBVM阴性患者中,病变以轻中度为主(P<0.01)。(3)肝组织与胃黏膜组织中HBsAg同时阳性17例;HBcAg同时阳性6例(P>0.05)。(4)血清及胃黏膜组织中HBsAg和(或)HBcAg同时阳性26例;HBVDNA同时阳性22例(P>0.05)。结论进一步证实了HBV可侵犯胃黏膜组织,并在其中复制,是导致慢性乙肝患者胃黏膜病变的重要因素。胃黏膜病变程度与胃黏膜组织HBV感染、肝组织病变程度密切相关;与血清及肝组织中HBV分布无关。     

乙型肝炎后肝硬化胃粘膜病变发病因素探讨

探讨乙型肝炎后肝硬化胃粘膜病变发病因素。102例肝病或非肝病因伴有胃病行胃镜检查的患者，取胃窦小弯距幽门周围(2—3)cm处粘膜3块，分别做快速尿素酶试验及嗜伊红、品红染色，并行免疫组化检测幽门螺旋杆菌HPlgG型抗原。发现肝硬化组(LC组)与慢性肝炎组(HB组)有不同程度胃粘膜炎症达95．5％(42／4)、53．6％(15／28)；前者萎缩、肠化多于后者(P＜0．05)。上述两组乙型肝炎病毒(HBV)抗原表达率分别为81．8％(36／44)、53．6％(15／28)；前者多于后者(P＜0．05)。与非肝病胃病患者30例相比，LC组、HB组HP阳性率无明显差别(P＞0．05)。说明门脉高压及HBV是LC胃粘膜病变的主要发病因素。     

Chronic inflammation at the gastroesophageal junction (carditis) appears to be a specific finding related to Helicobacter pylori infection and gastroesophageal reflux disease. The Central Finland Endoscopy Study Group

OBJECTIVE: The clinical significance of chronic inflammation at the gastroesophageal junction (carditis) is unknown: it may be associated with Helicobacter pylori (H. pylori) gastritis or with gastroesophageal reflux disease (GERD). We aimed to examine the association between carditis and H. pylori gastritis and endoscopic erosive esophagitis. METHODS: One thousand and fifty-three patients undergoing gastroscopy were enrolled in the study. Biopsy specimens were obtained from gastric antrum and corpus, immediately distal to normal-appearing squamocolumnar junction and distal esophagus. RESULTS: Chronic inflammation at the gastroesophageal junctional mucosa (carditis) was detected in 790 (75%) of 1053 patients. The male:female ratio of the carditis group was 1:1.5 and of the noncarditis group 1:1.6 (p = 0.6). The mean age of the carditis group was 58.7 yr (95% confidence interval [CI], 57.6-59.9) and of the noncarditis group, 52.6 yr (95% CI, 50.7-54.6, p < 0.001). Of the carditis group (N = 790), 549 (69%) had chronic gastritis (70% H. pylori positive) and 241 (31%) had normal gastric histology. In multivariate analyses, the only risk factor for carditis in subjects with chronic gastritis was H. pylori infection (odds ratio [OR], 2.9; 95% CI, 1.6-5.0), whereas the independent risk factor for carditis in subjects with histologically normal stomach was endoscopic erosive esophagitis (OR, 1.8; 95% CI, 1.1-3.1). The prevalence of complete intestinal metaplasia (IM) in the gastric cardia mucosa was 7% in the noncarditis group, 19% (p < 0.001) in the carditis group with chronic gastritis, and 10% (p = 0.3) in the carditis group with normal stomach. The respective prevalences of incomplete IM were 3%, 12% (p < 0.001), and 12% (p < 0.001). Among carditis patients with normal stomach histologically (N = 241), those with complete and/or incomplete IM (N = 49) were older than those with carditis only (63.6 yr [95% CI, 59.9-67.2] vs 51.4 yr [95% CI, 48.9-53.9]; p < 0.001). CONCLUSIONS: Two dissimilar types of chronic inflammation of the gastric cardia mucosa seem to occur, one existing in conjunction with chronic H. pylori gastritis and the other with normal stomach and erosive GERD. Most cases of chronic gastric cardia inflammation and intestinal metaplasia are detected in patients with chronic H. pylori gastritis.     

幽门螺杆菌感染对胃黏膜病理变化的影响

背景：幽门螺杆菌(H．pylori)感染已被公认为慢性胃炎和消化性溃疡的重要危险因素，根除H．pylori能加速消化性溃疡的愈合，但其对胃黏膜病理变化的影响尚有待进一步探索。目的：了解根除H．pylori对慢性胃炎胃黏膜病理变化和癌前状态的影响。方法：采用多中心随机对照临床试验和回顾性队列研究，样本选自胃癌高发区：上海郊区的金山区和奉贤区。共纳入360例经内镜检查证实有H．pylori感染的慢性胃炎伴或不伴十二指肠溃疡患者，随机分为两组。治疗组用三联疗法(质子泵抑制剂或Hz受体阻滞剂加两种抗生素)治疗，对照组单纯慢性胃炎患者予西沙必利、十二指肠溃疡患者予西米替丁治疗。在第1年和第4年末随访胃镜，根据H．pylori是否根除将患者分为两组：H．pylori阳性组和H．pylori阴性组。所有胃黏膜活检标本由两位病理科医师统一复读。结果：至第4年末，有120例患者完成全部随访，其中H．pylori持续根除组54例，阳转组5例；H．pylori持续未根除组45例，阴转组16例。持续根除组第1年随访时，活动性炎症比例减少(P＜O．05)；第4年随访时，慢性炎症和肠化程度以及活动性炎症比例减少(P＜O．05)。持续未根除组第1年随访时，慢性炎症程度增加(P＜O．05)；第4年随访时，慢性炎症和肠化程度以及活动性炎症比例增加(P＜O．05)，萎缩程度较第1年随访时增加(P＜O．05)。结论：根除H．pylori可以减轻慢性胃炎的炎症程度，防止肠化的发生和发展。     

Prevalence of Helicobacter pylori infection and gastric cancer precursor lesions in patients with dyspepsia

BACKGROUND: Helicobacter pylori infection has been considered to play significant role in gastric carcinogenesis, but only a minority of people who harbor this organism will develop gastric cancer. H. pylori infection first causes chronic non atrophic gastritis. Chronic non atrophic gastritis may evolve to atrophic gastritis and intestinal metaplasia and finally to dysplasia and adenocarcinoma. AIMS: To estimate the prevalence of H. pylori infection and the precancerous gastric lesions and their relationship, in patients with dyspeptic symptoms who underwent upper gastrointestinal endoscopy at a reference center in the central region of Rio Grande do Sul state, Brazil. METHODS: We analyzed gastric biopsies taken from corpus and antrum of patients who underwent upper gastrointestinal endoscopy for H. pylori detection, between 1994 and 2003. According to Sydney system, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed by histological examination (H-E stain). The histological diagnoses were related to H. pylori infection status. RESULTS: Biopsies from 2,019 patients were included in the study. Patients mean age was 52 (+/-15) and 59% were female. Seventy six percent had H. pylori infection. Normal mucosa, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed in 5%, 77%, 3% and 15%, respectively. The OR for any degree of gastric mucosa lesion in infected patients was 10 (CI95% 6.50 - 17%). The OR for infected patients had chronic non atrophic gastritis was 3 (CI95% 2,2 - 3,4). The OR for infected patients had atrophic gastritis or intestinal metaplasia was less than 1. CONCLUSIONS: The prevalence of H. pylori infection in this population was high (76%) and infected individuals had the probability 10 folds greater than non infected individuals to have any lesion of gastric mucosa. The prevalence of precancerous lesions was 77% for non atrophic chronic gastritis, 3% for atrophic gastritis and 15% for intestinal metaplasia. Infected patients had risk 3 folds greater than non-infected for the occurrence of non atrophic chronic gastritis. H. pylori infection did not show risk for occurrence of atrophic gastritis and intestinal metaplasia, suggesting that other risk factors should be involved in the carcinogenesis process.     

Gastric metaplasia and chronic inflammation at the duodenal bulb mucosa

BACKGROUND: Chronic inflammation and gastric metaplasia are often observed in biopsy specimens from the duodenal bulb of Heliobacter pylori positive patients with duodenal ulcer disease (DU). AIMS: We set out to investigate the prevalence of these lesions and their associations with other gastric and duodenal histopathological lesions. PATIENTS: A total of 1255 consecutive patients who underwent upper gastrointestinal endoscopy were recruited into the present study. METHODS: Two biopsy specimens were obtained from each of the following sites: duodenal bulb, gastric antrum, gastric body, and distal to the superior duodenal angle. These specimens were stained with hematoxylin-eosin, alcian blue periodic acid Schiff (pH 2.5) and modified Giemsa (Heliobacter pylori infection was determined only by histology). RESULTS: The mean age of the study population was 57 years, and male:female ratio 1:1.6. Overall, 235 (19%) had gastric metaplasia and/or chronic inflammation in the duodenal bulb mucosa, and H. pylori organisms could be found in 17 (1%). In univariate analyses, gastric metaplasia and/or chronic duodenal bulb inflammation positively associated with male sex (p = 0.046), Heliobacter pylori-positive chronic gastritis (p = 0.033), villous atrophy of distal duodenal mucosa, i.e., coeliac disease (p < 0.001), duodenal ulcer (p < 0.001), and duodenal bulb deformity and scarring in endoscopy (p < 0.001), but not with age (p = 0.7) nor use of nonsteroidal anti-inflammatory drugs (p = 0.055). Multivariate analysis revealed that independent risk factors for gastric metaplasia and chronic inflammation in duodenal bulb were duodenal Heliobacter pylori infection (odds ratio 1.6, 95% confidence interval CI 1.1-2.1), and villous atrophy of the distal duodenal mucosa (odds ratio 12.7, 95% CI 4.4-36.5), while chronic atrophic gastritis was protective against them (odds ratio 0.5, 95% CI 0.3-0.8). CONCLUSIONS: In addition to Heliobacter pylori infection, duodenal bulb gastric metaplasia and chronic inflammation may result from predisposition to toxic dietary components in gluten-sensitive subjects.     

幽门螺杆菌感染者胃粘膜癌前病变与Fas抗原表达的关系

目的研究幽门螺杆菌(Hp)感染后胃粘膜癌前病变中 Fas 抗原表达的情况,了解 Hp 在胃癌发生过程中的作用。方法采用免疫组织化学等方法检测83例经病理证实为慢性胃炎病人胃粘膜上皮细胞中 Fas 抗原的表达情况。结果在浅表性胃炎、萎缩性胃炎、肠化生及异型增生中,Fas 抗原表达率分别为20.00%、36.36%、73.33%、43.75%,Fas 抗原在肠化生中的表达率显著高于浅表性胃炎、萎缩性胃炎及异型增生(P<0.01及P<0.05)。Hp 感染者 Fas 抗原表达率为60.71%,显著高于 Hp 阴性者的22.22%(P<0.01)。在萎缩、肠化生及异型增生等癌前病变中,Hp 感染者与未感染者表达率分别为65.96%及28.57%(P<0.01)。结论 Hp 感染对 Fas 抗原表达有一定的影响,Hp 感染可促进 Fas 抗原表达增加,这可能是 Hp 感染诱导胃粘膜上皮细胞凋亡的机制之一。     

幽门螺杆菌及胃粘膜肠上皮化生与CD_(44)V_6表达的关系

目的　探讨幽门螺杆菌 (Hp)感染及慢性萎缩性胃窦炎伴肠上皮化生与CD4 4V6表达程度之间的关系。方法　以单克隆抗体及免疫组化技术等方法对Hp阴性单纯慢性胃炎、Hp阴性萎缩性胃炎伴肠上皮化生、Hp阳性萎缩性胃窦炎伴肠上皮化生、胃窦腺癌的胃镜下活检组织标本进行测定分析。结果　在Hp阴性单纯性胃炎组粘膜上皮未见CD4 4V6表达 ,Hp阴性萎缩性胃窦炎伴肠上皮化生、Hp阳性萎缩性胃窦炎伴肠上皮化生、胃窦腺癌各组CD4 4V6表达程度依次逐渐升高 ,各组之间比较差异有显著性 (P <0 .0 5 )。结论　CD4 4V6的表达可能是上皮细胞癌前病变出现的早期生物学信号 ,肠上皮化生细胞可能诱导CD4 4V6的表达 ,而Hp感染则有促进这种诱导表达的作用。     

Effects of bile reflux on gastric mucosal lesions in patients with dyspepsia or chronic gastritis

AIM: To investigate the influences of bile reflux on profiles of gastric mucosal lesions in patients with dyspepsia or chronic gastritis. METHODS: A total of 49 patients diagnosed with dyspepsia and chronic gastritis underwent 24-h ambulatory and simultaneous monitoring of intragastric bilirubin absorbance and pH values, and then they were divided into bile reflux positive group and bile reflux negative group. Severity of pathological changes in gastric mucosa including active inflammation, chronic inflammation, intestinal metaplasia, atrophy and dysplasia as well as Helicobacter pylori (H pylori) infection at the corpus, incisura and antrum were determined respectively according to update Sydney system criteria. The profiles of gastric mucosal lesions in the two groups were compared, and correlations between time-percentage of gastric bilirubin absorbance >0.14 and severity of gastric mucosal lesions as well as time-percentage of gastric pH >4 were analyzed respectively. RESULTS: Thirty-eight patients (21 men and 17 women, mean age 44.2 years, range 25-61 years) were found existing with bile reflux (gastric bilirubin absorbance >0.14) and 11 patients (7 men and 4 women, mean age 46.2 years, range 29-54 years) were bile reflux negative. In dyspepsia patients with bile reflux, the mucosal lesions such as active inflammation, chronic inflammation, intestinal metaplasia, atrophy or H pylori infection in the whole stomach, especially in the corpus and incisura, were significantly more severe than those in dyspepsia patients without bile reflux. Moreover, the bile reflux time was well correlated with the severity of pathological changes of gastric mucosa as well as H pylori colonization in the near-end stomach, especially in the corpus region. No relevance was found between the time of bile reflux and pH >4 in gastric cavity. CONCLUSION: Bile reflux contributes a lot to mucosal lesions in the whole stomach, may facilitate H pylori colonization in the corpus region, and has no influence on acid-exposing status of gastric mucosa in patients with dyspepsia or chronic gastritis.