Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P < 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P < 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.

Association of Helicobacter pylori babA2 with peptic ulcer disease and gastric cancer

AIM: To investigate the association between babA2 gene and peptic ulcer disease (PUD) and gastric cancer (GC) in Helicobacter pylori -infected populations. METHODS: We evaluated the relationship between babA2 and clinical outcomes (PUD and GC) using a meta-analysis. A literature search was performed using the PubMed and Web of Science databases for relevant case-control studies that met the defined inclusion criteria. The ORs and 95%CIs were calculated to estimate the association between babA2 genotype and clinical outcomes. A fixed-effect or random-effect model was performed depending on the absence or presence of significant heterogeneity. RESULTS: A total of 25 articles with 38 studies met the inclusion criteria and were finally included in this metaanalysis. The results showed that the babA2 genotype was significantly associated with an increased risk of PUD (OR = 2.069, 95%CI: 1.530-2.794, P < 0.001) and especially in the subgroup of duodenal ulcer (OR = 1.588, 95%CI: 1.141-2.209, P = 0.006). Moreover, a significant association between babA2 gene and PUD and duodenal ulcer (OR = 2.739, 95%CI: 1.860-4.032, P < 0.001; OR = 2.239, 95%CI: 1.468-3.415, P < 0.001, respectively) was observed in western countries but not in Asian countries. CONCLUSION: We demonstrated that the presence of babA2 may be associated with increased risks for PUD, especially duodenal ulcer, in western countries.

Use of lectin microarray to differentiate gastric cancer from gastric ulcer

AIM: To investigate the feasibility of lectin microarray for differentiating gastric cancer from gastric ulcer. METHODS: Twenty cases of human gastric cancer tissue and 20 cases of human gastric ulcer tissue were collected and processed. Protein was extracted from the frozen tissues and stored. The lectins were dissolved in buffer, and the sugar-binding specificities of lectins and the layout of the lectin microarray were summarized. The median of the effective data points for each lectin was globally normalized to the sum of medians of all effective data points for each lectin in one block. Formalin-fixed paraffin-embedded gastric cancer tissues and their corresponding gastric ulcer tissues were subjected to Ag retrieval. Biotinylated lectin was used as the primary antibody and HRP-streptavidin as the secondary antibody. The glycopatterns of glycoprotein in gastric cancer and gastric ulcer specimens were determined by lectin microarray, and then validated by lectin histochemistry. Data are presented as mean +/- SD for the indicated number of independent experiments. RESULTS: The glycosylation level of gastric cancer was significantly higher than that in ulcer. In gastric cancer, most of the lectin binders showed positive signals and the intensity of the signals was stronger, whereas the opposite was the case for ulcers. Significant differences in the pathological score of the two lectins were apparent between ulcer and gastric cancer tissues using the same lectin. For MPL and VVA, all types of gastric cancer detected showed stronger staining and a higher positive rate in comparison with ulcer, especially in the case of signet ring cell carcinoma and intra-mucosal carcinoma. GalNAc bound to MPL showed a significant increase. A statistically significant association between MPL and gastric cancer was observed. As with MPL, there were significant differences in VVA staining between gastric cancer and ulcer. CONCLUSION: Lectin microarray can differentiate the different glycopatterns in gastric cancer and gastric ulcer, and the lectins MPL and VVA can be used as biomarkers. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.

Gastric Cancer Revealed by a Perforated Ulcer: A Case Report and Review

Introduction: Gastric cancer is not typically a surgical emergency. However, it can evolve into urgent complications such as a perforation. We report a case of a perforated gastric ulcer that turned out to be a cancer. Observation: A 52-year-old man was admitted to the emergency department of Hubert-Koutoukou-Maga National University Medical Center in Cotonou for generalized abdominal pain. He was diagnosed with acute generalized peritonitis with perforated gastric ulcer, establishing a surgical indication. An antral perforation was found and a simple closure was performed. Anatomopathological examination of the surgical piece revealed a gastric adenocarcinoma within the granulation tissue. Following the impact assessment, he underwent a second surgery where a distal gastrectomy was performed with D2 lymphadenectomy followed by gastrojejunostomy. He developed an anastomotic gastrointestinal fistula during the postoperative period but was successfully medically treated. The patient received adjuvant chemotherapy with Epirubicin, Cisplatin and 5-Fluorouracil. The patient is still alive, 3 years after the gastrectomy. Conclusion: When faced with a perforated gastric ulcer, one must also consider a neoplastic cause. The emergency surgical treatment depends on the general condition of the patient and the pre-existing co-morbidities, the choice being made between a one-stage versus two-stage gastrectomy.

Implantation of esophageal cancer onto post-dissection ulcer after gastric endoscopic submucosal dissection

A case in which implantation of esophageal squamous cell carcinoma onto a post-dissection gastric ulcer was strongly suspected is presented. A 72-yearold man with alcoholic liver cirrhosis underwent esophagogastroduodenoscopy(EGD). Esophageal cancer(EC)(Mt, 20 mm, 0-Is) and gastric cancer(GC)(antrum, 15 mm, 0-Ⅱc) were identified. Biopsy specimens revealed moderately differentiated squamous cell carcinoma(SCC) and differentiated adenocarcinoma, respectively. The GC was resected by endoscopic submucosal dissection(ESD) [14 mm × 9 mm, type 0-Ⅱc, tub1, p T1a(M), ly0, v0, HM(-), VM(-)]. Two months after ESD, radiation therapy was started for the EC, and an almost complete response was obtained. Nine months after the ESD, a follow-up EGD showed a submucosal tumor-like lesion with ulceration, located immediately under the post-ESD scar, and biopsy specimens showed moderately differentiated SCC. There were no similar lesions suggesting hematogenous or lymphatic metastasis in the stomach.

Rare case of Helicobacter pylori -related gastric ulcer: Malignancy or pseudomorphism?

Helicobacter pylori (H. pylori ) is a pathogen and the most frequent cause of gastric ulcers. There is also a close correlation between the prevalence of H. pylori infection and the incidence of gastric cancer. We present the case of a 38-year-old woman referred by her primary care physician for screening positron emission tomography-computed tomography (PET-CT), which showed a nodular strong accumulation point with standardized uptake value 5.6 in the gastric fundus. Gastroscopy was then performed, and a single arched ulcer, 12 mm in size, was found in the gastric fundus. Histopathological examination of the lesion revealed chronic mucosal inflammation with acute inflammation and H. pylori infection. There was an obvious mitotic phase with widespread lymphoma. Formal anti-H. pylori treatment was carried out. One month later, a gastroscopy showed a single arched ulcer, measuring 10 mm in size in the gastric fundus. Histopathological examination revealed chronic mucosal inflammation with acute inflammation and a very small amount of H. pylori infection. The mitotic phase was 4/10 high power field, with some heterotypes and an obvious nucleolus. Follow-up gastroscopy 2 mo later showed the gastric ulcer in stage S2. The mucosal swelling had markedly improved. The patient remained asymptomatic, and a follow-up PET-CT was performed 6 mo later. The nodular strong accumulation point had disappeared. Follow-up gastroscopy showed no evidence of malignant cancer. H. pylori-associated severe inflammation can lead to neoplastic changes in histiocytes. This underscores the importance of eradicating H. pylori , especially in those with mucosal lesions, and ensuring proper follow-up to prevent or even reverse early gastric cancer.

健胃方联合雷贝拉唑治疗胃溃疡临床效果观察

目的:探讨健胃方联合雷贝拉唑治疗胃溃疡的临床效果。方法:选取2022年8月—2023年8月收治的胃溃疡患者60例,随机分为对照组和观察组,每组30例。对照组给予雷贝拉唑治疗,观察组给予健胃方联合雷贝拉唑治疗,治疗2周后对比两组治疗总有效率、中医典型症状积分、溃疡愈合率及复发率。结果:治疗后,观察组总有效率高于对照组,差异有统计学意义(P<0.05);两组治疗后的中医典型症状积分均低于治疗前,且观察组低于对照组,差异有统计学意义(P<0.05);观察组内镜下溃疡治愈率高于对照组,差异有统计学意义(P<0.05);观察组复发率低于对照组,差异有统计学意义(P<0.05)。结论:健胃方联合雷贝拉唑治疗胃溃疡的临床疗效显著,可明显改善患者症状,溃疡愈合率高,复发率低,优于单纯西药治疗效果。

Gastric juice acidity in upper gastrointestinal diseases

AIM: To search the independent factors determining gastric juice acidity and to investigate the acidity of gastric juices in various benign and malignant upper gastrointestinal diseases. METHODS: Fasting gastric juice acidity of 165 healthysubjects and 346 patients with esophageal ulcer (n = 21), gastric ulcer (n = 136), duodenal ulcer (n = 100) or gastric cancer (n = 89) were measured and compared. Additionally, gastric specimens were taken from the antrum and body for rapid urease test and histological examination. RESULTS: Multivariate analysis revealed that bile stain of gastric juice, high acute inflammatory score of the corpus, and atrophy of the corpus were independent risk factors for the development of gastric hypoacidity with odds ratios of 3.1 (95% CI: 1.3-7.3), 3.1 (95% CI: 1.2-7.9) and 3.5 (95% CI: 1.3-9.2). Esophageal ulcer and duodenal ulcer patients had a lower pH level (1.9 and 2.1 vs 2.9, both P < 0.05) of gastric juices than healthy subjects. In contrast, gastric ulcer and gastric cancer patients had a higher pH level (3.4 and 6.6 vs 2.9, both P < 0.001) than healthy controls. Hypoacidity existed in 22%, 5%, 29%, 5% and 88% of healthy subjects, esophageal ulcer, gastric ulcer, duodenal ulcer and gastric cancer patients, respectively. CONCLUSION: Bile reflux, atrophy and dense neutrophil infiltrate of the corpus are three independent factors determining the acidity of gastric juice.

Efficacy of treatment with rebamipide for endoscopic submucosal dissection-induced ulcers

AIM:To prospectively compare the healing rates of endoscopic submucosal dissection(ESD)-induced ulcers treated with either a proton-pump inhibitor(PPI)or rebamipide.METHODS:We examined 90 patients with early gastric cancer who had undergone ESD.All patients were administered an intravenous infusion of the PPI lansoprazole(20 mg)every 12 h for 2 d,followed by oral administration of lansoprazole(30 mg/d,5 d).After7-d treatment,the patients were randomly assigned to 2 groups and received either lansoprazole(30 mg/d orally,n=45;PPI group)or rebamipide(300 mg orally,three times a day;n=45;rebamipide group).At 4and 8 wk after ESD,the ulcer outcomes in the 2 groups were compared.RESULTS:No significant differences were noted in patient age,underlying disease,tumor location,Helicobacter pylori infection rate,or ESD-induced ulcersize between the 2 groups.At both 4 and 8 wk,the healing rates of ESD-induced ulcers were similar in the PPI-treated and the rebamipide-treated patients(4 wk:PPI,27.2%;rebamipide,33.3%;P=0.5341;8 wk:PPI,90.9%;rebamipide,93.3%;P=0.6710).At 8 wk,the rates of granulation lesions following ulcer healing were significantly higher in the PPI-treated group(13.6%)than in the rebamipide-treated group(0.0%;P=0.0103).Ulcer-related symptoms were similar in the2 treatment groups at 8 wk.The medication cost of 8-wk treatment with the PPI was 10945 yen vs 4889 yen for rebamipide.No ulcer bleeding or complications due to the drugs were observed in either treatment group.CONCLUSION:The healing rate of ESD-induced ulcers was similar with rebamipide or PPI treatment;however,rebamipide treatment is more cost-effective and prevents granulation lesions following ulcer healing.

Update of Aetiological Patterns of Adult Gastric Outlet Obstruction in Accra, Ghana

Background: The aetiology of gastric outlet obstruction globally has evolved from benign to malignant causes, but there seem to be no recent data on the trends in Ghana. The aim was, therefore, to identify the current patterns in the aetiology of gastric outlet obstruction in the adult population in Ghana. Methodology: This was a retrospective review of all confirmed cases of gastric outlet obstruction in the last decade, spanning from June 2004 to May 2014, that were managed at the Korle Bu Teaching Hospital. Results: A total of 107 patients were managed for gastric outlet obstruction with a male to female ratio of 2.15:1 and most of the patients making 71.3% of cases belonged to the age range of 40 to 60 years. The predominant aetiology for gastric outlet obstruction was found to be gastric cancer (55.140%), followed by peptic ulcer disease (27.103%). Conclusion: The aetiology of gastric outlet obstruction in Ghana has evolved from benign to malignant causes, following current global trends. Gastric cancer is now the most important cause of gastric outlet obstruction in Ghana, followed by peptic ulcer disease which predominates as the commonest benign cause.

EPIYA基序与幽门螺杆菌感染相关胃病关系的研究进展

幽门螺杆菌(Hp)是一种人类主要致病菌,人体在感染Hp后会引发慢性胃炎、消化性溃疡、胃癌等一系列胃肠道疾病。近年来,随着这些疾病的发病率升高,它们的病因及发病机制日益在世界范围内受到许多学者的关注。而Hp的毒力基因之一即细胞毒素相关基因A(CagA)的致病机制也因此受到重视,谷氨酸-脯氨酸-异亮氨酸-酪氨酸-丙氨酸组成的重复序列(EPIYA基序)与Hp感染相关胃病也成为目前研究的热点。该文就EPIYA基序与Hp感染相关胃病的关系作一简要综述。

血清胃蛋白酶原PGI/PGII联合胃泌素-17预测胃溃疡继发癌变

背景筛选胃溃疡继发癌变的敏感性标志物对胃癌的预防和治疗具有重要意义.先前的研究提示胃蛋白酶原和胃泌素-17(gastrin-17,G-17)可能在早期胃癌的预测方面有一定的参考价值,但尚无确切统一的观点.目的探讨血清胃蛋白酶原Ⅰ(pepsinogenⅠ,PGⅠ)/胃蛋白酶原Ⅱ(pepsinogenⅡ,PGⅡ)联合G-17预测胃溃疡继发癌变的临床价值,为胃癌的早期诊断提供敏感性生化标志物.方法回顾性总结2020-07/2023-04我院初诊为胃溃疡患者215例,根据胃镜下组织病理学诊断分为单纯溃疡组184例和胃癌组31例.入院检测血清PGⅠ、PGⅡ、G-17和肿瘤标志物[包括癌抗原(cancer antigen,CA)724、CA199、癌胚抗原(carcinoembryonic antigen,CEA)和铁蛋白],13C呼气试验测定幽门螺旋杆菌(Helicobacter pylori,H.pylori)感染超基准(delta over baseline,DOB)值.结果两组性别、年龄、DOB值和病程比较无明显差异(P>0.05).与单纯溃疡组相比,胃癌组血清PGⅡ、G-17、CA724、CA199和CEA水平升高,而PGⅠ、铁蛋白和PGI/PGII下降(P<0.05).Spearman检验显示,PGⅠ/PGⅡ与G-17、CA724、CA199和CEA呈负相关,与铁蛋白呈正相关(P<0.05).G-17与CA724、CA199和CEA呈正相关,与铁蛋白呈负相关(P<0.05).受试者工作曲线(receiver operating curve,ROC)显示,PGⅠ/PGⅡ和G-17诊断胃溃疡继发癌变的曲线下面积(area under curve,AUC)分别为0.804和0.742,PGⅠ/PGⅡ和G-17联合诊断的AUC为0.899,显著高于单一指标(P<0.05).结论血清PGⅠ/PGⅡ下降和G-17升高与胃溃疡继发癌变紧密相关,PGⅠ/PGⅡ联合G-17对胃溃疡继发癌变的预测性能较好,PGⅠ/PGⅡ和G-17可作为早期诊断胃癌的敏感性标志物.

瑞巴派特联合兰索拉唑治疗早期胃癌内镜下黏膜剥离术后溃疡的效果

目的观察瑞巴派特联合兰索拉唑治疗早期胃癌内镜下黏膜剥离(ESD)术后溃疡的效果。方法选取2021年2月—2023年2月烟台海港医院收治的70例早期胃癌ESD术后溃疡患者,按双色球法分为对照组与观察组,每组35例。对照组采用兰索拉唑治疗,观察组在对照组基础上加用瑞巴派特治疗,2组均持续治疗1个月。比较2组临床疗效,治疗前后黏膜厚度评分、腺体密度评分、血清炎性因子[白介素-6(IL-6)、C反应蛋白(CRP)]及治疗过程中不良反应发生情况。结果观察组治疗总有效率高于对照组(97.14%vs.77.14%,χ^(2)=4.590,P=0.032)。治疗1个月后,2组黏膜厚度评分与腺体密度评分均较治疗前明显下降,且观察组低于对照组(P<0.01);2组血清IL-6、CRP水平均较治疗前明显下降,且观察组低于对照组(P<0.01)。2组不良反应总发生率比较,差异无统计学意义(P>0.05)。结论早期胃癌ESD术后溃疡患者采用瑞巴派特联合兰索拉唑可更好地减缓胃黏膜及腺体病变程度,减轻炎性反应,增强疗效,且不会增加不良反应,安全性较高。

窄带成像内镜对胃良恶性溃疡的诊断价值研究

目的观察研究窄带成像技术(NBI)对内镜下胃良、恶性溃疡的鉴别诊断价值。方法对58例常规胃镜检查发现胃溃疡的患者依次采用常规模式、NBI模式及靛胭脂染色放大方法进行观察,重点观察溃疡周边黏膜的胃小凹及微血管,评价各检查方法图像的清晰度,于改变最显著部位活检行病理学检查。结果58例胃溃疡患者中,良性溃疡37例,恶性溃疡21例。在观察溃疡轮廓方面,NBI与染色内镜或普通内镜之间差异有显著性,NBI最清晰;对于溃疡周边黏膜胃小凹的形态观察,NBI或染色内镜均优于普通内镜;在对溃疡周边黏膜微血管的观察中,NBI具有绝对优势。NBI模式下,胃小凹形态分为6种类型,恶性溃疡周边黏膜胃小凹多为Ⅵ型,此型与胃癌病理学诊断符合率达94.8%,敏感性90.5%、特异性97.3%。NBI放大内镜下86.5%(32/37)的良性溃疡周边黏膜微血管走形规则,85.7%(18/21)的恶性胃溃疡周边黏膜可观察到不规则走形的微血管。结论NBI,电子染色,操作简便,对胃溃疡轮廓显示清晰,放大后更可清晰观察到溃疡周边黏膜的胃小凹及微血管形态,有助于提高胃癌的靶向活检准确率,对提高早期胃癌的检出率具有潜在的重要意义。

霉菌、幽门螺杆菌及双菌种感染在胃溃疡、胃癌中检出的意义(英文)

探讨霉菌、幽门螺杆菌(Hp)单菌种感染和霉菌、Hp(双菌种)同时感染在胃癌及胃溃疡中的组织病理学变化、发病情况及意义。采用常规石蜡切片,HE染色和PAS、Giemsa特殊染色、免疫组织化学染色及PCR方法,对223例慢性浅表性胃炎、111例慢性萎缩性胃炎、116例胃溃疡、121例胃癌纤维胃镜活检标本进行回顾性研究。结果显示,慢性浅表性胃炎、慢性萎缩性胃炎未检出双菌种感染。胃溃疡双菌种感染11例,检出率9.5%;胃癌双菌种感染21例,检出率17.4%。双菌种感染在胃癌及胃溃疡中的发现,表明双菌种感染可能是导致胃溃疡、胃癌发生的又一致病因素。

幽门螺杆菌毒力基因分型和宿主遗传多态性与胃病关系研究进展

幽门螺杆菌(Helicobacter pylori)感染能导致慢性胃炎、消化性溃疡、胃粘膜相关的淋巴样组织(Mu-cosa-associated lymphoid tissue,MALT)淋巴瘤和胃腺癌等疾病的发生。1994年世界卫生组织国际癌症研究中心(IARC)将H.pylori列为胃癌第一级因子。H.pylori感染引起的不同临床结局主要与H.pylori致病因子和宿主遗传易感性有关,大部分重大疾病发生在特定的细菌毒力因子(如cagA,vacA)与易感宿主遗传背景共同存在时。文章综述了H.pylori菌株的毒力基因的分型和宿主的遗传多态性对胃病发生的影响。

胃溃疡内镜随访价值分析

目的重新讨探胃溃疡内镜随访的价值。方法病例来源为我科2002年10月至2005年11月胃镜检查病人,其中胃溃疡1699例,459例有胃镜随访记录。459例中良性溃疡363例,性质待定溃疡96例。我们对其资料进行了分析。结果459例溃疡共随访593次,平均1.3次/人。经平均9个多月的随访,共发现14例(3.05%)胃癌,其中9例来源于良性溃疡,5例来源于性质待定溃疡,二者无统计学差异。在随访中也发现38例(8.27%)在经2月以上的正规治疗后溃疡未愈或复发,其中8例判为性质待定溃疡,而8例中6例第1次胃镜诊为良性溃疡。溃疡未愈或复发与胃黏膜不典型增生及幽门螺杆菌(H.pylori)未根除有关。结论我国为胃癌高发区,良性溃疡及性质待定溃疡均有必要进行内镜随访。

慢性胃炎、胃溃疡及胃癌患者血清胃蛋白酶原水平的研究

目的研究胃疾病患者血清胃蛋白酶原水平变化规律并确定适合我区胃癌筛查的血清胃蛋白酶原标准。方法采用酶联免疫吸附实验(ELISA)对351例患者血清胃蛋酶原亚群(PGⅠ、PGⅡ)含量测定,并行胃镜及病理学检查。结果 351例慢性胃疾病及胃癌患者血清胃蛋白酶原水平与胃黏膜病变的程度密切相关,与浅表性胃炎相比萎缩性胃炎、胃癌血清PGⅠ、PGⅠ/PGⅡ水平明显降低(P<0.01);与浅表性胃炎相比消化性溃疡的血清PGⅠ、PGⅡ水平明显升高(P<0.05)。我区胃癌筛查的最佳临界值为PGⅠ≤43.37μg.L-1或PGⅠ/PGⅡ≤2.47,并且灵敏度是94.0%,特异度是55.3%。结论血清胃蛋白酶原水平与胃黏膜病变的程度密切相关,从灵敏度、特异度分析PGⅠ≤43.37μg.L-1、PGⅠ/PGⅡ≤2.47,是我区胃癌和慢性萎缩性胃炎筛查较为合适的异常界定值。

幽门螺杆菌相关性胃溃疡与胃癌中NF-κB、TFF3的表达及意义

目的探讨核转录因子-κB(NF-κB)和三叶因子3(TFF3)在胃溃疡和胃癌中表达的意义,以及与幽门螺杆菌(H.pylori)感染的关系。方法胃溃疡组(GU)60例,胃癌组(GC)70例,应用免疫组化方法测定TFF3和NF-κBp65的表达,同时检测H.pylori感染情况。结果 GC中NF-κBp65和TFF3表达水平均高于GU(P<0.01)。GC中NF-κBp65表达与TFF3表达呈显著正相关(r=0.350,P=0.003)。GU中H.pylori阳性病例中NF-κBp65、TFF3表达显著高于H.pylori阴性病例(P均<0.05)。H.pylori感染病例中,GC组的NF-κBp65、TFF3表达水平均比GU组高(P均<0.05);H.pylori阴性病例中,GC组的NF-κBp65、TFF3表达水平亦均比GU组高(P均<0.01)。结论 NF-κBp65和TFF3的高表达与胃癌的发生发展有着密切的关系,二者可能存在协同作用。H.pylori感染可以上调宿主胃黏膜NF-κBp65和TFF3的表达,表达的差异与胃溃疡和胃癌两种不同疾病转归相关。

免疫印迹法检测幽门螺旋杆菌及其分型的临床应用

本文通过检测患者血清中幽门螺旋杆菌抗体及分型 ,借以评价幽门螺旋杆菌的感染情况 ,并分析与临床各种胃部疾病的关系 ,为临床诊断与治疗提供依据。采用免疫印迹法检测 5 6例有明确病理诊断的胃部疾病患者的幽门螺旋杆菌的感染情况 ,并作 74例正常对照。结果显示 ,胃部良性疾病患者的CagA阳性率为 6 2 5 %,VacA阳性率为 6 0 0 %,分别高于正常对照的 4 4 5 %和 4 7 3%,尤其胃癌CagA和VacA阳性率都为 1 0 0 %,明显高于其他良性胃部疾病 ;试验还发现幽门螺旋杆菌阳性率随年龄的增长而升高这一趋势。胃部疾病与幽门螺旋杆菌的感染 ,尤其是产毒菌株的感染密切相关 ,免疫印迹法可以应用在临床检测幽门螺旋杆菌抗体 ,并能够判断是否为产毒菌株感染 ,为临床早期制定治疗方案提供有效依据。