幽门螺杆菌感染的胃黏膜上皮细皮细胞环氧合酶-2表达及意义

目的探讨幽门螺杆菌(Hp)感染的胃黏膜上皮细胞环氧合酶-2(COX-2)的表达及其在胃黏膜癌变过程中的意义.方法采用快速尿素酶试验和组织学碱性品红染色法检测胃黏膜Hp 感染状况;应用免疫组化法检测胃黏膜上皮细胞COX-2表达状况.结果 32例胃癌中,COX-2表达阳性22例(68.7%).12例Hp阴性的胃黏膜中,有1例(8.3%)COX-2低表达;10例Hp阳性正常胃黏膜中,仅1例(10.0%)COX-2低表达;9例Hp阳性的胃黏膜充血水肿糜烂者中,有5例(55.6%)COX-2表达阳性,与Hp阴性者和Hp阳性正常胃黏膜者比较,差异有统计学意义(P<0.05);10例Hp阳性的轻度萎缩性胃炎伴轻度肠化生者中,COX-2表达阳性5例(50.0%);10例Hp阳性的中重度萎缩性胃炎伴中重度肠化生者中,COX-2表达阳性8例(80.0%);8例Hp阳性的中重度不典型增生者中,COX-2表达阳性6例(75.0%).中重度萎缩性胃炎伴中重度肠化生和不典型增生者的COX-2表达高于轻度萎缩性胃炎伴轻度肠化生者(P<0.05).结论 Hp感染诱导慢性浅表性胃炎黏膜上皮细胞的COX-2表达与黏膜损伤形成有关;根据胃癌发生模式,COX-2表达上调与Hp感染胃黏膜癌变发生相关,且可能在癌前病变形成早期阶段起作用.     

ERK2在胃黏膜病变中的表达及其与Hp感染的关系

目的探讨胃癌前病变及胃癌组织中细胞外调节蛋白激酶2(extracellular regulated protein kinases 2,ERK2)表达与幽门螺旋杆菌(helicobacter pylori,Hp)感染的相关性,及Hp感染与胃癌发生的关系。方法收集慢性浅表性胃炎(chronic superficial gastritis,CSG)、慢性萎缩性胃炎伴中重度肠上皮化生(intestinal metaplasia,IM)、慢性萎缩性胃炎伴中重度不典型增生(dysplasia,Dys)各30例及胃癌(gastric cancer,GC)40例,采用SP免疫组化法,检测4组中ERK2蛋白的表达。结果 CSG、IM、Dys、GC组织中,Hp感染患者胃黏膜组织中ERK2表达水平高于无Hp感染患者(P<0.05)。结论 Hp感染可能通过上调ERK2表达水平,从而在胃癌发生、发展过程中发挥重要作用。     

幽门螺杆菌感染和环氧合酶-2表达在胃癌发生中的作用

目的探讨幽门螺杆菌 (Hp) 感染和环氧合酶-2(COX-2)表达在胃癌发生中的作用.方法 138例胃镜活检标本包括慢性非萎缩性胃炎30例,慢性萎缩性胃炎85例(其中伴有中度以上肠化生45例,中、重度异型增生12例),和胃癌23例.快速尿素酶试验和组织学改良Giemsa染色联合检测Hp,免疫组化检查COX-1和COX-2表达.结果胃癌的Hp阳性率为69.6%,显著高于慢性非萎缩性胃炎的36.7%(P<0.05).慢性非萎缩性胃炎、慢性萎缩性胃炎、肠化生、异型增生和胃癌的COX-2表达率分别为10.0%、37.6%、37.8%、41.7%和69.6%,而不同胃黏膜病变中COX-1表达无明显差异.慢性萎缩性胃炎、肠化生和异型增生中Hp阳性病例的COX-2表达显著高于Hp阴性病例(P<0.01).结论 Hp感染及其诱导的COX-2表达可能是胃癌发生的早期事件之一.     

幽门螺杆菌感染与胃癌、慢性胃炎、溃疡病、异型增生的关系及PCNA表达

目的　探讨幽门螺杆菌 (Hp)感染的不同胃黏膜增殖性病变的演进中增殖细胞核抗原 (PCNA)的表达及其意义。方法　对 13 0例病理证实的不同胃黏膜病变应用免疫组化方法检测 PCNA标记指数 (L I) ,Warthin-starry法检测 Hp感染。结果　 PCNA -L I在浅表性胃炎为 2 2 .0 0± 16.95,萎缩肠化性胃炎为 46.45± 19.10 ,溃疡病为 45.75± 18.15,异型增生为 61.0 6± 2 0 .67。在萎缩肠化性胃炎、溃疡病、异型增长及胃癌组织中均高于浅表性胃炎 (P<0 .0 5)。萎缩肠化型胃炎、溃疡病、异型增生及胃癌中 Hp感染阳性组 PCNA阳性表达均高于 Hp阴性组 (P<0 .0 5)。结论　 PCNA表达和 Hp感染与胃黏膜增殖和恶化有关     

胃癌及癌前病变与幽门螺杆菌感染相关性的临床分析

目的:测定幽门螺杆菌在萎缩肠化生胃炎,异型增生及胃癌中感染情况,探讨Hp与它们的相关性。方法:萎缩肠化生胃炎(A组)患者342例,异型增生(B组)229例,胃癌患者(C组)298例,采用Hp抗体ELISA法检测血清抗Hp-IgG抗体。结果:肠化生患者较非肠化生胃黏膜中的Hp感染多见。异型增生和胃癌的Hp感染率均高于萎缩性胃炎组(P<0.05),异型增生和胃癌两者间的Hp感染率亦存在差异(P<0.05)。幽门螺杆菌感染的萎缩肠化生胃炎及异性增生较非幽门螺杆菌感染者发生癌变的差异性显著,P<0.05;幽门螺杆菌感染的胃癌5年生存期显著短于非感染者,P<0.05。结论:Hp感染与萎缩肠化生胃炎,异型增生及胃癌有密切相关性,并缩短萎缩肠化生胃炎,异型增生癌变时间,缩短胃癌5年生存时间。     

不同胃黏膜病变中iNOS表达与Hp的关系

目的:检测诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)在胃癌前病变及胃癌的表达,及其与幽门螺杆菌(Helicobacter pylori,Hp)感染的相关性,探讨Hp感染与胃癌发生的关系。方法:收集慢性浅表性胃炎(chronic superficial gastritis,CSG),慢性萎缩性胃炎伴肠上皮化生(Intestinal metaplasia,IM),慢性萎缩性胃炎伴上皮内瘤变(Intraepithelial neoplasia,IN)各30例,胃癌(gastric cancer,GC)40例。采用SP免疫组化法检测iNOS蛋白的表达,warthin-starry银染法检测胃黏膜Hp感染。结果:CSG、IM、IN、GC组织中iN-OS表达呈逐渐增强趋势,差异具有显著性(P<0.05)。结论:CSG、IM、IN、GC组织中Hp感染的胃黏膜组织中,iNOS的表达高于无Hp感染的患者。     

良性胃黏膜病变中Hp感染与Livin、Ki-67表达关系的研究

目的：观察Livin和Ki-67在Hp（＋/-）良性胃黏膜病变组织中的表达。方法：所有胃黏膜病变组织均来自内镜活检及手术切除标本,良性胃黏膜病变组织标本144例。采用免疫组化法测定上述胃黏膜病变组织及胃癌组织中Livin、Ki-67的表达,用甲苯胺蓝染色检测Hp。结果：Livin、Ki-67在Hp根治前后从慢性浅表性胃炎、慢性萎缩性胃炎、伴肠化、不典型增生组织中的表达率呈递增趋势,其中在慢性萎缩性胃炎和萎缩伴肠化的阳性表达率有统计学意义（ P〈0.05）。结论：在癌前病变阶段根除Hp可使部分萎缩和肠化减轻,能有效治疗Hp相关性胃炎,也可预防Hp相关性胃癌的发生。     

幽门螺杆菌感染与不同胃粘膜病变中PCNA、bcl-2表达的关系

 目的　研究不同胃粘膜病变中幽门螺杆菌 (Hp)感染与细胞增生、凋亡的关系。 方法　采用SP免疫组化染色及图像分析方法 ,对 312例慢性萎缩性胃炎 (CAG)、肠上皮化生 (IM )、胃上皮不典型增生 (GED)及胃癌 (GC)中Hp感染与PCNA、bcl 2表达和DNA含量及倍体进行检测。 结果　在Hp感染组 ,从CAG→IM→GED→GC ,PCNA和bcl 2阳性表达率和高表达率均逐渐增高。尤其在IMIII、GEDII III和肠型GC中 ,PCNA高表达率分别明显或显著高于IMI II、GEDI和IMIII、GEDII III(P <0 .0 5 ,P <0 .0 1)。其DNA含量和倍体分析与PCNA的表达一致。Hp未感染组不同病变中各指标均不显示Hp感染组的变化特点。结论　Hp感染可引起胃上皮细胞增生水平显著增高 ,凋亡水平明显降低     

胃癌及癌前病变与幽门螺杆菌

目的　幽门螺杆菌 (Helicobacterpylori,Hpylori)感染与胃癌的关系一直倍受人们关注 ,检查胃癌及癌前病变 ,如萎缩性胃炎、肠腺化生、异型增生病人Hpylori感染情况 ,了解Hpylori感染与胃癌的关系。方法　通过胃镜钳取胃粘膜 ,用快速尿素酶试验法(RUT)、PCR法、HE银染法等三种方法同时检查 ,判定Hpylori感染 ,并作病理细胞学检查。共查萎缩性胃炎 89例、肠腺化生 64例、异型增生 47例、胃癌 3 0例 ,功能性消化不良 10 3例作为对照。结果　Hpylori阳性率在萎缩性胃炎、肠腺化生病人中较高 ,分别是79 3 %和 81 3 % ,与对照组功能性消化不良病人 (阳性率 61 2 % )相比有显著统计学差异 ,P值均小于 0 0 1。异型增生组Hp阳性率较低 72 % ,与对照组相比P >0 0 5 ,无显著统计学差异。胃癌病人与对照组相比P <0 0 5 ,Hp阳性率显著降低。结论　Hpylori感染与萎缩性胃炎、胃粘膜肠腺化生密切相关 ,与异型增生、胃癌无直接关系。Hpylori感染主要参与癌前病变的前期阶段 ,是胃癌的高危险因素     

胃癌及癌前病变幽门螺杆菌感染与Ki67、iNOS表达关系

[目的]探讨幽门螺杆菌(Hp)感染与Ki67、iNOS表达的关系,以及Hp感染导致胃癌形成的可能分子机制.[方法]应用尿素酶试验和组织切片革兰染色检测115例胃黏膜组织的Hp;用免疫组化SP法检测上述组织的Ki67、iNOS表达,分析Ki67和iNOS及Hp感染三者之间的关系.[结果]在正常黏膜、慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、不典型增生、腺癌组织中Hp检出率分别为0(0/8)、45.5%(5/11)、63.2%(12/19)、70.6%(12/17)、73.3%(11/15)、51.1%(23/45),病变各组中Ki67和iNOS表达阳性率与浅表性胃炎组比较均有显著性差异(P＜0.05).除胃癌组外,病变各组的Ki67和iNOS的表达阳性率与各组的Hp感染阳性率呈正相关;每一病变组中Hp( )组的Ki67和iNOS表达阳性率显著高于Hp(-)组,均有显著性差异(P＜0.05).[结论]幽门螺杆菌感染与Ki67和iNOS阳性表达有一定的相关性,Hp可能通过促使细胞增殖加速和凋亡异常而涉及胃癌的发生过程.     

幽门螺旋杆菌感染胃黏膜COX-2和P-gp表达与胃癌发生

背景与目的通过检测幽门螺旋杆菌(Helicobacter Pylori,H.pylori)感染胃粘膜组织环氧合酶-2(Cyclooxygenase-2,COX-2)和多药耐药-1(Multidrug resistance-1,MDR-1)基因表达产物P糖蛋白(P-glycoprotein,P-gp)表达,探讨幽门螺旋杆菌相关胃癌的发生机制,以及P-gp高表达的机制。材料与方法慢性胃炎155例(30例慢性浅表性、40例慢性萎缩性、45例肠化、40例非典型增生)及胃癌80例(肠型40例,弥漫型40例),COX-2和P-gp表达检测选择免疫组化S-P法,H.pylori感染检测采用快速脲素酶及改良Giemsa染色方法。结果H.pylori阳性感染率、COX-2和P-gp的阳性表达率,肠型胃癌均明显高于弥漫型胃癌(P<0.01)。慢性萎缩性胃炎、肠化、非典型增生及肠型胃癌中H.pylori感染与COX-2的表达呈正相关(P<0.01)。H.pylori感染的慢性浅表性胃炎、慢性萎缩性胃炎、肠化、非典型增生及肠型胃癌中COX-2的表达与P-gp的表达也均呈正相关(P<0.01)。结论H.pylori依赖的COX-2表达与P-gp表达有关,可能有助于胃癌形成以及胃癌对化疗抵制。     

IL-10在H.pylori相关性胃炎组织中的表达及与COX-2、iNOS的相关性

目的:观察IL-10在H.pylori相关性胃炎组织中的表达及与COX-2、iNOS的相关性。方法:选取74例H.pylori相关性胃炎患者,均行H.pylori检测确定H.pylori感染情况,行病理组织学检测明确病理分型、胃黏膜炎症程度,行免疫组化检测胃黏膜中IL-10、COX-2、iNOS表达。分析H.pylori感染情况、病理诊断与组织分型结果,明确慢性胃炎患者H.pylori感染与病理炎症程度、病理分型的关系、IL-10表达与H.pylori感染的关系、比较H.pylori阳性胃炎不同病理类型中COX-2、iNOS表达情况,分析H.pylori阳性胃炎患者IL-10与COX-2、iNOS表达的相关性。结果:74例慢性胃炎患者中,H.pylori阳性59例,阴性15例,H.pylori检出率79.73%。H.pylori阳性与阴性患者在炎症程度的分布方面有显著差异(P＜0.05),表现为H.pylori阳性患者中重度炎症患者居多,而阴性患者则以轻度为主。74例患者中31例为IL-10阳性、43例为IL-10阴性。IL-10阳性患者中的H.pylori阳性率(93.55%)显著高于IL-10阴性(69.77%)患者(P＜0.05);病理分型的差异无统计学意义(P＞0.05)。COX-2阳性表达率在H.pylori阳性患者中为59.32%,显著高于H.pylori阴性患者的20.00%(P＜0.01);iNOS阳性表达率为61.02%,显著高于阴性患者的20.00%(P＜0.01)。H.pylori阳性不同病理类型胃炎患者的IL-10阳性率差异无统计学意义(P＞0.05);H.pylori阳性胃炎(IM+Dy)患者的COX-2阳性率(84.62%)高于CSG(44.00%)患者(P＜0.05);CAG患者的iNOS阳性率(80.95%)显著高于CSG(44.00%)患者(P＜0.05)。H.pylori阳性胃炎患者的IL-10表达与COX-2(r=-0.566,P＜0.001)、iNOS(r=-0.465,P＜0.001)表达均呈现显著负相关。结论:IL-10为H.pylori相关性胃炎的保护因子,在H.pylori阳性患者中具有高阳性率。且IL-10与H.pylori阳性患者的COX-2、iNOS表达呈较强负相关,可通过对COX-2、iNOS表达的下调作用降低慢性胃炎患者的恶性病变风险。     

Ectopic expression of guanylyl cyclase C and endogenous ligand guanylin correlates significantly with Helicobacter pylori infection in gastric carcinogenesis

The molecular mechanisms leading to gastric carcinogenesis still remain unclear. Recently, several studies demonstrated that over-expression of guanylyl cyclase C (GCC) has been detected in intestinal-type gastric cancer (GC) and precursor lesions. Our objective was to explore the expression levels of GCC and endogenous ligands guanylin (GN) and uroguanylin (UGN) and the correlation between Helicobacter pylori (H. pylori) and GCC, GN, and UGN expressions in patients at different stages from normal mucosa to superficial gastritis, atrophic gastritis, intestinal metaplasia (IM), dysplasia, and finally adenocarcinoma. The expression of GCC and GN was absent in the distal normal gastric tissues and superficial gastritis in all cases, whereas they were measured in IM, dysplasia, and GC. The expression of GCC and GN was closely related to intestinal-type GC. From superficial gastritis to gastric carcinomas, the H. pylori positive rate was 19.7, 33.3, 69.6, 80.0, and 82.1%, respectively. The positive correlation was found between GCC and GN in IM, dysplasia, and GC. Also, the positive correlation was found between GCC, GN, and H. pylori infection in them. These results demonstrate that the detection of GCC and GN will be beneficial to diagnosis human gastric carcinoma and precancerous lesions. Ectopic expression of GCC and GN in human gastric mucosa and H. pylori infection may play an important role in the carcinogenesis of the intestinal-type GC.     

慢性胃病伴肠上皮化生、胃癌与幽门螺旋杆菌感染的关系

目的探讨慢性胃病伴肠上皮化生、胃癌与幽门螺旋杆菌（helicobacter pylore,HP）感染的关系。方法采用warthin—strarry银染色方法,对380例慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织进行HP检测．应用（alcianblue—PH2．5-periodic—schiff,AB—PAS）、（high-iron—diamine-alcianblue—PH2．5,HID-AB）黏液组织化学方法,区别慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织伴有肠上皮化生的类型。结果总例数380例。HP阳性率为69．74％。慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织伴肠上皮化生的HP感染率分别为77．78％、85．71％、100．00％、80．95％。慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡及胃癌的癌旁组织伴肠上皮化生AB—PAS染色阳性率分别为86．84％、91．43％、93．33％、100．00％;HID—AB染色阳性率分别为34．21％、42．86％、53．33％、85．71％。癌旁组织的肠上皮化生中,78．57％为不完全大肠型,慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡伴肠上皮化生中,不完全小肠型比例分别为52．63％、54．28％、53．33％;不完全大肠型比例分别为28．95％、31．43％、20．00％。结论HP感染与慢性胃病伴肠上皮化生及胃癌的发生密切相关。癌旁组织的不完全大肠型肠上皮化生与胃癌的发生密切相关;慢性胃病组织当中的小灶状不完全大肠型上皮化生具有潜在发生癌变的可能性。     

Severity of gastritis determines glandular stomach carcinogenesis in Helicobacter pylori-infected Mongolian gerbils

Helicobacter pylori (H. pylori) infection causes chronic gastritis and is also related to gastric carcinoma. The present study focused on severity of H. pylori-induced gastritis as a determinant of carcinogenesis. Seven-week-old male Mongolian gerbils were inoculated with H. pylori at experimental weeks 0, 12, or 18, then given N-methyl-N-nitorosourea (MNU) from weeks 20-40. At week 70, stomachs were then excised for histological examination 70, 58, or 52 weeks after H. pylori inoculation, respectively (Groups A, B, and C for long-, middle-, and short-term). The respective incidences of glandular stomach adenocarcinomas were 65.0% (13/20), 20.0% (2/10), and 23.0% (3/13) (P<0.05). Higher scores of infiltration of inflammatory cells, hyperplasia, intestinal metaplasia and mucosal bromodeoxyuridine (BrdU) labeling index in antrum and corpus mucosa, were seen in group A than B or C (P<0.05) and serum anti-H. pylori IgG titer and gastrin levels were also significantly higher, along with mRNA levels for mucosal interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). The results demonstrated the term and severity of H. pylori infection to play important roles in gastric carcinogenesis, with essential involvement of chronic inflammation, especially increased rates of cell proliferation, in H. pylori-associated carcinogenesis.     

Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer

We conducted a longitudinal cohort study to determine the association of Helicobacter pylori infection and the progression of chronic atrophic gastritis (CAG) with gastric cancer. A cohort of 4655 healthy asymptomatic subjects was followed for a mean period of 7.7 years. H. pylori infection was established by serum specific antibodies and the presence of CAG was confirmed by serum pepsinogen. During the follow-up period, 45 gastric cancer cases were detected (incidence rate, 126/100000 person-years). A univariate analysis after adjustment for age showed that both H. pylori and CAG were significantly associated with gastric cancer. To clarify the interaction between H. pylori and CAG, an analysis stratified by H. pylori- and CAG-status was performed. No cancer developed in the H. pylori(-)/CAG(-) group during the study period. This supports the theory that it is quite rare for any type of gastric cancer to develop in an H. pylori-free healthy stomach. With the progression of H. pylori-induced gastritis, the risk of gastric cancer increased in a stepwise fashion from CAG-free gastritis [H. pylori(+)/CAG(-) group] (HR=7.13, 95%CI=0.95-53.33) to CAG [H. pylori(+)/CAG(+) group] (HR=14.85, 95%CI=1.96-107.7) and finally to severe CAG with extensive intestinal metaplasia [H. pylori(-)/CAG(+) group] (HR=61.85, 95%CI=5.6-682.64) in which loss of H. pylori from the stomach is observed. Therefore, it is probable that H. pylori alone is not directly associated with stomach carcinogenesis. Instead, H. pylori appears to influence stomach carcinogenesis through the development of CAG. The observed positive correlation between the extent of H. pylori-induced gastritis and the development of cancer was strong, especially for the intestinal type. These results are compelling evidence that severe gastritis with extensive intestinal metaplasia is a major risk factor for gastric cancer, and they confirm the previously described model of stomach carcinogenesis: the gastritis-metaplasia-carcinoma sequence.     

p16,Cyclin D1在胃癌发生过程中的表达

研究ｐ１６，ＣｙｃｌｉｎＤ１在胃癌发生过程中的表达。方法：采用免疫组化ＡＢＣ法，检测胃癌、不典型增生、萎缩性胃炎及正常胃粘膜组织Ｐ１６和ＣｙｃｌｉｎＤ１的表达。结论：Ｐ１６和ＣｈｃｌｉｎＤ１在胃上皮癌变过程中起着重要作用，其在胃癌中的反向表达趋势提人才是可能存在相互抑制机制。     

CONTRASTIVE STUDY OF THE TISSUE EXPRESSION AND SERUM CONCENTRATION OF PEPSINOGEN C IN GASTRIC MUCOSA DISEASES

Objective： To estimate the practical values of pepsinogen C （PGC） dynamic expression and the levels of serum pepsinogens in gastric cancer screening and diagnosis. Methods： 129 cases gastric mucosa biopsies and serum specimens were examined. The expression of PGC in stomach mucosa was detected by immunohistochemistry. The serum concentration of pepsinogen A （sPGA） and pepsinogen C （sPGC） were determined by ELISA. Results： The positive rate of PGC antigen expression decreased in superficial gastritis （100%）, gastric ulcer or erosion （80.00%）, atrophic gastritis （34.48%） and gastric cancer （11.43%） in sequence （P〈0.05）. There was no statistics difference in concentration of sPGA and sPGC among the above 4 groups. The ratio of sPGA/sPGC decreased in superficial gastritis, gastric ulcer or erosion, atrophic gastritis and gastric cancer in sequence （P〈0.05）. There was specific correlation between the expression of PGC in stomach mucosa and the levels of sPGA/sPGC ratio in serum （rs =0.297, P=0.001）. Conclusion： Tissue expression of PGC has close relationship with different gastric diseases. The ratio of sPGA/sPGC is relative with the tissue expression of PGC antigen and may be a convenient and economic maker in screening and diagnosis of gastric cancer.     

Compartment theory in Helicobacter pylori-associated gastric carcinogenesis

BACKGROUND: The compartment theory has not been well investigated in gastric carcinogenesis. This study was aimed at examining the compartment alterations through the Helicobacter pylori (H. pylori)-related chronic gastritis-intestinal metaplasia-carcinoma sequence, and investigating the long-term effect of bacterial eradication on the compartment changes. PATIENTS AND METHODS: Gastric biopsy specimens were obtained from subjects with H. pylori-negative normal mucosa (N = 12), H. pylori-positive non-metaplastic gastritis (N = 42), H. pylori-positive intestinal metaplasia (N = 21) and intestinal-type adenocarcinoma (N = 20). The specimens were immnostained for monocloncal antibodies against the proliferating cell nuclear antigen (PCNA) for proliferating analysis. Additionally, 50 patients with H. pylori-positive gastritis were enrolled to investigate the long-term effect of bacterial eradication on the compartment changes of gastric epithelium. RESULTS: The mean PCNA labeling indices (L.I.) of non-metaplastic gastritis, intestinal metaplasia and adenocarcinoma were significantly higher than that of normal mucosa (31.1, 49.2 and 40.7 vs. 21.4; p < 0.01, 0.001 and 0.001, respectively). The proliferating zone was principally located in the lower compartment of normal mucosa. In patients with intestinal metaplasia, there was a full expansion (phase 1 change) of proliferating zone to the middle compartment of gastric pits (ratio of L.I. between middle and lower compartment = 1.00). The proliferating cells were evenly distributed in adenocarcinoma (complete loss of compartmentalization). Eradiation of H. pylori led to a reversion of compartment changes of gastric epithelium in patients with chronic gastritis. CONCLUSION: H. pylori-related gastric carcinogenesis is a multistep process involving progressive alterations of proliferating activity as well as loss of compartmentalization. Eradication of H. pylori reverses the changes in growth kinetics of gastric epithelium.