幽门螺杆菌感染与胃部疾病的相关性

[目的]探讨幽门螺杆菌（Hp）感染在胃癌发生发展中的作用。[方法]选择2009年1月至2012年12月经胃镜检查病理确诊胃部疾病439例患者,其中慢性浅表性胃炎163例、慢性萎缩性胃炎64例、胃食管反流病47例、胃溃疡79例、十二指肠溃疡54例、胃不典型增生12例和胃癌20例。采用C14呼气实验和快速尿素酶法,二项任意一项阳性均被诊断胃Hp阳性。[结果]胃部疾病439例患者中Hp阳性219例,阳性率为49．89％。胃癌患者的Hp阳性率比慢性胃炎患者Hp阳性率高（65．00％VS43．17％,χ^2=3．850,P=0．043）,也比胃食管反流病患者Hp阳性率高（65．00％vs34．04％,χ^2=5．477,19=0．019）,但与胃、十二指肠溃疡患者比较Hp阳性率无统计学差异（65．00％V863．91％,χ^2=0．009,／9=0．925）。60岁以下者,随年龄增长Hp感染率逐渐升高。[结论]胃幽门螺杆菌感染与胃溃疡、不典型增生和胃癌的发生有着密切的关系,幽门螺杆菌感染是胃癌的危险因素。根除Hp感染治疗可能有助于降低胃癌发生的风险。     

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。     

胃癌及癌前病变幽门螺杆菌感染与Ki67、iNO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iN-OS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。     

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。     

In vitro synthesis of SIgA and CEA and their relationship in gastric cancer tissue

The in vitro synthesis of secretory immunoglobulin A (SIgA) and carcinoembryonic antigen (CEA) was observed by tissue culture of biopsied gastric cancer tissue and gastric mucosa in other gastric diseases. The level of SIgA Synthesis in cultured gastric cancer tissue was lower than that in gastric mucosa in chronic atrophic gastritis, chronic superficial gastritis and normal stomach. The gastric mucosa of chronic gastritis can produce more SIgA than the normal gastric tissue, but the difference between chronic atrophic gastritis and chronic superficial gastritis was of no statistical significance. The CEA level was significantly higher in cancerous tissue than that in noncancerous ones, the amount of CEA synthesis by gastric mucosa in chronic atrophic gastritis was higher than that in chronic superficial gastritis and normal stomach. Well differentiated adenocarcinoma secreted much more SIgA and CEA than the poor-differentiated ones. The results suggest that the estimation of secretory function of SIgA and CEA be helpful for clinical diagnosis of gastric cancer.     

微小染色体维持蛋白4在胃癌中的表达及与幽门螺杆菌感染的关系

目的：探讨微小染色体维持蛋白4（minichromosome maintenance proteins4,MCMp4）在胃癌和癌前病变组织中的表达及与幽门螺杆菌（helicobacter pylori,Hp）感染的关系。方法：选取经病理证实的慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌4种不同胃黏膜病变的标本共140例,用免疫组织化学法检测标本中MCMp4的表达及幽门螺杆菌感染情况,分析MCMp4的表达与幽门螺杆菌感染的关系。结果：以慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌为序,4种病变中MCMp4的表达率和Hp的感染率呈逐渐增加的趋势。在胃癌中Hp感染组MCMp4的表达率高于非感染组（P〈0.05）,MCMp4的阳性表达率与Hp感染率之间呈正相关（r=0.457,P〈0.05）。结论：MCMp4表达和Hp的感染与胃癌的发生密切相关,检测这些指标可为胃癌诊断、预后判断和指导治疗提供参考。     

热休克蛋白27和三叶因子Ⅱ在胃癌中的表达及与幽门螺杆菌感染关系的研究

背景与目的： 探讨热休克蛋白27(heat shock protein27, HSP27)、三叶因子Ⅱ(trefoil factors2, TFF2)在胃癌和癌前病变组织中的表达及其与幽门螺杆菌(helicobacter pylori, Hp)感染的关系。 材料与方法： 选取经病理证实的慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌4种不同胃黏膜病变的标本共140例,用免疫组化法检测标本中HSP27和TFF2的表达及幽门螺杆菌的感染情况,分析HSP27和TFF2的表达与幽门螺杆菌感染的关系。 结果： 除TFF2在胃癌组织中表达降低外,在慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌中,HSP27、TFF2的表达率和Hp的感染率依次呈逐渐增加的趋势。Hp感染组HSP27的表达率高于阴性组,HSP27的阳性表达率与Hp感染率之间呈正相关(r=0.235, P<0.05),Hp感染组TFF2的表达率低于阴性组,TFF2的阳性表达率与Hp感染率之间呈负相关(r=－0.259, P<0.05)。 结论： HSP27、TFF2表达和Hp感染与胃癌的发生密切相关,检测这些指标可为胃癌诊断、预后判断和指导治疗提供依据。     

幽门螺杆菌与胃癌相关性研究

［目的］研究幽门螺杆菌（Ｈｐ）与胃癌发生之间的关系。［方法］用美蓝染色对７４１例胃炎性病变和１３１例胃癌病人之胃粘膜活检组织的Ｈｐ感染情况进行检测。［结果］胃癌组和慢性萎缩性胃炎组（ＣＡＧ）Ｈｐ检出率分别为６２．５９％和６１．６０％,明显高于慢性浅表性胃炎组（ＣＳＧ）的３８．６１％（Ｐ＜０．０１）;胃癌组中,伴有癌周粘膜肠化生者Ｈｐ检出率明显高于不伴肠化生者（Ｐ＜０．０５）;在活动性ＣＳＧ和ＣＡＧ中,Ｈｐ检出率分别为８９．４１％和９０．５３％,而在非活动性ＣＳＧ和ＣＡＧ中仅分别为１．７１％和１．２３％,两者差异非常显著（Ｐ＜０．０１）。［结论］提示Ｈｐ感染与胃癌的发生有显著的相关性;Ｈｐ有可能通过引发活动性胃炎、腺体萎缩、上皮肠化生等方式参与胃癌的发生。     

pERK在胃癌中的表达及临床意义

[目的]研究磷酸化细胞外信号调节激酶（pERK）在胃腺癌、慢性萎缩性胃炎及浅表性胃炎组织中的表达及意义。[方法]RT-PCR法检测胃腺癌、慢性萎缩性胃炎和浅表性胃炎新鲜组织中pERK mRNA表达;免疫组化法分别检测胃腺癌、慢性萎缩性胃炎和浅表性胃炎组织中pERK蛋白表达,并分析其蛋白表达与胃癌临床病理参数间的相关性。[结果]RT-PCR半定量结果显示,胃癌组织中pERK mRNA的相对表达水平（2.35±0.36）明显高于慢性萎缩性胃炎组织（1.18±0.25）及浅表性胃炎组织（0.68±0.10）（P均〈0.01）。免疫组织化学结果显示,pERK蛋白在胃癌组织中的阳性表达率（88.3%）高于慢性萎缩性胃炎（43.3%）及浅表性胃炎组织（5.0%）（P均〈0.01）。胃癌组织中pERK蛋白表达与胃癌分化程度、分期、淋巴结转移等明显相关。[结论]pERK在胃癌中高表达,pERK在正常细胞向恶性细胞转化的过程中可能扮演了重要角色,检测pERK表达可能有助于胃腺癌的预防及早期诊断。     

Helicobacter pylori antibody responses and evolution of precancerous gastric lesions in a Chinese population

Helicobacter pylori‐specific proteins are involved in gastric carcinogenesis. To investigate the seroprevalence of six H. pylori‐specific antibodies in patients with different gastric histology, and the impact of seropositivities on the evolution of precancerous gastric lesions, a follow‐up study was conducted in Linqu County, China. The seropositivities for CagA, VacA, GroEL, UreA, HcpC and gGT were assessed by recomLine analysis in 573 H. pylori‐positive subjects and correlated with evolution of precancerous gastric lesions. We found that the score of H. pylori recomLine test was significantly increased in subjects with chronic atrophic gastritis (CAG, p < 0.0001) or intestinal metaplasia (IM, p = 0.0125), and CagA was an independent predictor of advanced gastric lesions, adjusted odds ratios (ORs) were 2.54 (95% CI = 1.42–4.55) for IM and 2.38 (95% CI = 1.05–5.37) for dysplasia (DYS). Moreover, seropositivities for CagA and GroEL were identified as independent predictors for progression of gastric lesions in a longitudinal study, and ORs were 2.89 (95% CI = 1.27–6.59) and 2.20 (95% CI = 1.33–3.64), respectively. Furthermore, the risk of progression was more pronounced in subjects with more than three positive antigens (p_{for trend} = 0.0003). This population‐based study revealed that seropositivities for CagA and GroEL might be potential markers to identify patients infected with high‐risk H. pylori strains, which are related to the development of GC in a Chinese high‐risk population, and recomLine test might serve as a tool for risk stratification.     

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.     

血清PGⅠ、PGⅡ及G-17检测在胃癌及萎缩性胃炎中的诊断价值分析

目的 分析检测血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)及胃泌素17(G-17)在胃癌及萎缩性胃炎中的诊断价值.方法 选取接受胃镜检查的患者865例,其中浅表性胃炎患者339例作为浅表性胃炎组,萎缩性胃炎患者318例作为萎缩性胃炎组,胃癌患者208例作为胃癌组.采用酶联免疫吸附试验(ELISA)检测3组患者的血清G-17水平;采用胶乳免疫比浊法检测3组患者的血清PGⅠ、PGⅡ水平,并计算胃蛋白酶原比值(PGR);采用单纯取胃体组织做快速尿素酶测定(RUT)法和幽门螺旋杆菌(HP)尿素酶抗体检测试剂盒检测HP值.对3组患者的各指标进行比较,评价其诊断胃癌和萎缩性胃炎的价值.结果 胃癌组患者的PGⅠ水平低于萎缩性胃炎组和浅表性胃炎组(P﹤0.05);萎缩性胃炎组和胃癌组患者的PGⅡ水平低于浅表性胃炎组(P﹤0.05);胃癌组患者的G-17水平高于浅表性胃炎组和萎缩性胃炎组(P﹤0.05);胃癌组患者的PGR值小于浅表性胃炎组和萎缩性胃炎组,萎缩性胃炎组患者的PGR值小于浅表性胃炎组(P﹤0.05).PGⅠ和PGR检测胃癌的灵敏度分别为88.9%、86.9%,特异度分别为73.6%、59.4%;PGⅠ、PGR和G-17检测萎缩性胃炎的灵敏度分别为69.9%、70.8%、66.1%,特异度分别为49.8%、51.4%、64.2%.HP阳性患者的PGⅠ和PGⅡ水平均高于HP阴性患者,PGR值小于HP阴性患者(P﹤0.05).结论 血清检测PG水平的方法在诊断胃癌时的特异度和灵敏度均较高,是胃癌患者诊断的一个重要血清学指标,可用于胃癌的早期诊断.     

Role of Helicobacter pylori infection among offspring or siblings of gastric cancer patients

A positive family history is an increased risk factor for gastric cancer within family members, and one of the possible causes of this is the intrafamilial clustering of Helicobacter pylori infection. Our study examined the prevalence of H. pylori infection, serum antibodies to CagA and VacA and atrophic gastritis and/or intestinal metaplasia in the offspring or siblings of gastric cancer patients. A total of 726 subjects included 300 relatives of 300 separate gastric cancer patients and 426 controls. All subjects underwent upper gastrointestinal endoscopic examination with a rapid urease test. Blood samples were obtained to test for the presence of serum antibodies to the CagA and VacA proteins of H. pylori. The prevalence of H. pylori infection was higher in relatives of cancer patients (75.3%) than in controls (60.1%), and the adjusted odds ratio was 2.1 (95% CI 1.5-2.9). When either siblings or 2 or more family members were gastric cancer patients, the prevalence of H. pylori infection was much higher compared to the prevalence in controls. There was no specific relationship between CagA and VacA, and H. pylori infection. Atrophic gastritis and/or intestinal metaplasia were more frequently found in H. pylori-infected relatives of cancer patients (26.1%) than in H. pylori-infected controls (12.9%). These results strongly support a role for H. pylori infection in familial aggregation of gastric cancer. The prophylactic eradication of H. pylori infection in the offspring or siblings of gastric cancer patients may be clinically beneficial.     

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1–1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.     

胃癌组织中HSP70与Cyclin D1的表达及意义

目的:探讨热休克蛋白70 (heatshock protein 70,HSP70)与细胞周期蛋白D1(Cyclin D1)在胃癌组织中的表达。方法:应用免疫组化SABC 与SP 法检测胃癌、不典型增生、萎缩性胃炎及浅表性胃炎组织中HSP70 与Cyclin D1 的表达。结果:HSP70与Cyclin D1 在浅表性胃炎、萎缩性胃炎、不典型增生和胃癌中的表达阳性率,随病变的进展而升高。HSP70 的表达阳性率分别为42. 9% (12/28)、57. 1%(24/42)、64. 3%(9/19)和77 .1%(37/48),其中萎缩性胃炎、不典型增生及胃癌与浅表性胃炎相比,差异有统计学意义,P<0 .05。Cyclin D1 的表达阳性率分别为7 .1% ( 2/28 )、19 .0% ( 8/48 )、35 .7%(5/14)和52. 1% (25/48),其中不典型增生、胃癌与萎缩性胃炎相比,差异有统计学意义,P<0. 05。大多数受检胃癌组织中,HSP70与Cyclin D1的表达有相关性。结论:HSP70与Cyclin D1 过度表达,在胃癌的产生过程中可能起重要作用。     

幽门螺杆菌相关性胃病的细胞增殖与凋亡的研究

目的 观察幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒ ｐｙｌｏｒｉ,Ｈｐ）感染对其相关性胃病的细胞增殖与凋亡的影响,进行探讨胃癌的发生机理。方法 研究对象为正常人（ｎｏｒｍａｌ ｓｕｂｊｅｃｔｓ,ＮＳ）及慢性浅表性胃炎（ｃｈｒｏｎｉｃ ｓｕｐｅｒｆｉｃｉａｌ ｇａｓｔｒｉｔｉｓ,ＣＳＧ）、慢性萎缩性胃炎（ｃｈｒｏｎｉｃ ａｔｒｏｐｈｉｃ ｇａｓｔｒｉｔｉｓ,ＣＡＧ）、慢性萎缩性胃炎伴肠上皮化生（ｃｈｒｏ     

CYP1A1和GSTM1与胃癌、萎缩性胃炎和胃溃疡等易感性的研究

目的：探讨细胞色素氧化酶基因（CYP1A1）和谷胱甘肽转硫酶基因（GSTM1）多态性与胃癌和萎缩性胃炎等胃部疾病易感性的关系。方法：对病理诊断的胃癌（GC）102例，慢性萎缩性胃炎（CAG）110例，胃溃疡（GU）62例，慢性浅表性胃炎（CSG）103例，十二指肠溃疡（DU）62例，正常人62例的CYP1A1和GSTM1基因型采用序列特异性引物的聚合酶链反应（PCR－SSP）方法进行测定，关联度分析采用病例对照研究方法，结果：非条件Logistic回归在调整年龄，性别，文化程度和职业4个因素后，GG，CAG和GU与CYP1A1 G／G，GSTM10／0基因型，幽门螺杆菌（Hp)感染及吸烟有关联，同时基因型间存在明显的交互作用，没有发现DU和CSG与CYP1A1和GSTM1基因型有关联，但DU与幽门螺杆菌（Hp)感染有关联，而且Hp感染，吸烟与CYP1A1 G／G型之间存在交作用。结论：CYP1A1 G／G，GSTM10／0基因型与GC，CAG，GU的易感性有磁联，两个基因型之间及它们各自与Hp感染与吸烟之间有交互作用。     

胃黏膜良恶性病变幽门螺杆菌感染与p53、bcl-2、PCNA表达

［目的］探讨胃黏膜良恶性病变幽门螺杆菌(Hp)感染与突变型p５３、bcl-２、增殖细胞核抗原（PCNA）表达之间的关系。［方法］用免疫组织化学SP法对１１５例胃黏膜良、恶性病变［慢性浅表性胃炎(CSG)２５例，慢性萎缩性胃炎(CAG)２５例，异型增生(GED)２５例，胃癌(GCA)４０例］的胃镜活检标本进行幽门螺杆菌感染的检测和突变型p５３、bcl-２、PCNA表达的研究。［结果］在CSG、CAG、GED、GCA的各病变中幽门螺杆菌感染检出率分别为３６％(９／２５)、４８％(１２／２５)、７２％(１８／２５)、５８％(２３／４０)；与２０例正常胃黏膜Hp检测阳性率（２０％）作比较，除了CSG无统计学意义外，其余几组均有显著性差异(P＜０．０５)；突变型p５３检出率分别为０、０、２４％(６／２５)、５５％(２２／４０)；胃炎、异型增生、胃癌三者之比有显著性差异(P＜０．０５)；bcl-２检出率４４％（１１／２５）、５２％（１３／２５）、７６％（１９／２５）、５７．５％（２３／４０）；PCNA在CSG、CAG、GED、GCA中的表达呈现递增性，经Ridit检验P＜０．０５；Hp感染与PCNA表达强级(阳性细胞＞５０％)、p５３阳性病例均有显著相关性(P＜０．０１)。［结论］Hp的感染与突变型p５３、bcl-２、PCNA在胃黏膜异型增生，胃     

胃粘膜灶性异型增生的形态研究

３９６例活检胃粘膜炎症性病变中１９．９％找见异型增生灶，其由单个至１０多个细胞构成，可向管腔内或外突起。其检出率为糜烂性胃炎的８．０％，浅表性胃炎的１０．９％，萎缩性胃炎的３８．４％，慢性溃疡的１８．９％。灶性异型增生细胞ＰＣＮＡ阳性表达６１．３％；ＡｇＮＯＲ计数３．８１～８．７２个，提示ＰＣＮＡ和ＡｇＮＯＲ检测可帮助判断胃粘膜灶性异型增生。     

胃液中一组新肿瘤相关抗原MG—Ags的测定及其在胃癌诊断中的价值

本文应用6种胃癌单克隆抗体混合物,以酶联结合抑制法分别测定了47例胃癌、28例慢性浅表性胃炎,15例慢性萎缩性胃炎,27例消化性溃疡,14例食管癌者患者胃液中上述单抗的相应抗原MG-Ags的含量。以抑制率≥60％计算各组阳性率,分别为78.7％、14.3％、33.0％、14.8％、和7.1％。并在胃癌组中观察到,随着癌灶增大,MG-Ags含量增加。酶联结合抑制法操作简便,重复性、敏感性、特异性较好。用此法测定胃液中肿瘤相应抗原的MGs含量,有助于临床诊断,有助于判定病情进展,治疗效果和预后,也有助于在高危人群中检出胃癌。