不同类型胃息肉与幽门螺杆菌感染、粘膜炎症相关性的研究

目的 探讨不同类型胃息肉与幽门螺杆菌（Hp）感染以及与胃粘膜炎症、萎缩和肠上皮化生的相关性。方法 对2203例胃粘膜活检发现的278例胃息肉（检出率12.6%）进行组织学分类,并对胃窦粘膜活检组织同时行Hp检测及粘膜炎症、萎缩和肠上皮化生的观察,比较不同类型胃息肉的Hp感染率及其与癌相关病变的关系。结果 278例息肉中,组织学分类以小凹上皮增生型息肉为多见,有130例,占息肉总数的46.8%,胃体腺型增生性息肉67例,占24.1%,炎性息肉和腺瘤性息肉较少见,分别为55例（19.8%）和26例（9.4%）。约53.9%的胃息肉患者存在Hp感染,其中以小凹上皮增生型息肉感染率最高,达73.1%。这型息肉常伴有胃粘膜的活动性炎症,且粘膜萎缩和肠上皮化生的发生率均近腺瘤性病变。胃体腺型增生性息肉,Hp感染率、活动性炎症及萎缩、肠上皮化生等发生率均较低,提示这两种息肉在组织发生和病理生物学形态上存在差异。结论 小凹上皮增生型息肉的发生可能与Hp感染有关,且常伴有明显的活动性炎症以及粘膜萎缩的肠上皮化生,因此可能与胃癌的发生有潜在的关系。     

放大染色内镜临床应用进展

此文通过对放大内镜结合染色内镜在Barrett食管、食管癌、幽门螺杆菌(H.pylori)感染、胃粘膜肠上皮化生、胃癌、大肠粘膜病变等方面的应用介绍,阐述放大内镜对上述疾病早期诊断和治疗的价值,为临床诊断和治疗提供指导。     

根除幽门螺杆菌对胃黏膜组织学变化及胃癌患病率的3年随访研究

目的幽门螺杆菌(Helicobacter pylori,Hp)是导致胃黏膜病变的重要因子,研究Hp阳性患者根除Hp后对胃黏膜炎症、萎缩和肠上皮化生(IM)及胃癌患病率的关系。方法采用随机、对照研究方法,2006年1月-2009年6月间在我院胃镜检查同时行Hp及胃黏膜组织学检查者236例进行随访观察,3年后复查胃镜和组织病理学,评定组织学变化。分析治疗组(Hp阴性)和对照组(Hp阳性)在胃黏膜炎症、萎缩及IM的变化。结果对照组中胃黏膜的炎症、腺体的萎缩和肠化及发生胃癌的总人数明显高于治疗组的总人数,差异有显著性(P0.05)。结论根除Hp感染可减轻胃黏膜活动性炎症、萎缩和肠上皮化生以及胃癌的发病率。     

根除幽门螺杆菌对胃黏膜萎缩并肠上皮化生以及COX-2、C- met表达的影响

目的研究幽门螺杆菌(helicobacter pylori,Hp)根除前后胃黏膜萎缩和肠上皮化生的变化以及环氧合酶-2(cyclooxygenase-2,COX-2)和肝细胞生长因子受体(C-met)的表达。方法 13例患者均为胃镜加病理确诊有萎缩并肠化生合并HP感染,且成功根除HP感染者。用免疫组化方法半定量检测HP除前后萎缩性胃炎并肠上皮化生COX-2蛋白和C-met蛋白的表达。结果根除前和根除后1个月萎缩程度积分分别为1.3±0.3,1.2±0.7,根除后1个月与根除前比较无显著差异(P>0.05)。萎缩并肠化生胃黏膜C-met平均阳性细胞率从根除前53.2±12.4％下降至根除后48.8±7.7％,比较有显著差异(P=0.034)。胃黏膜COX-2平均阳性细胞率从根除前36.5±14.0％下降至根除后23.3±7.9％,有显著差异(P=0.023)。COX-2表达与C-met表达有一定的相关性(r=0.310,P<0.05)。结论 HP根除短期内不能逆转胃黏膜萎缩,但可使慢性萎缩性胃炎胃黏膜中COX-2和C-met癌基因表达下降。COX-2表达与C-met表达相关。     

胃粘膜肠上皮化生CST—π的表达及其与H.pylori相关性研究

目的：探讨GST－π在胃癌发生过程中表达，及在肠化阶段在GST－π为代表的人体对致癌物解毒系统与H.pylori致毒作用间的相互作用。方法：利用S－P法对219例胃粘膜活检标本进行GST－π单克隆抗体的检测；利用HID－AbpH2.5-PAS粘蛋白组化学技术对171例肠化粘膜进行分型；利用HE及H.pylori-DNA PCR及ELISA方法对正常胃粘膜和肠化粘膜进行H.pylori的检测。对80例H.pylori阳性患进行H.pyrori根除治疗三个月后进行H.pylori、GST－π的检测。结果：正常胃粘膜未见GST－π的表达，肠化粘膜GST－π阳性率为69．5％，胃癌GST－π阳性率为44．4％，高于正常胃粘膜（P＜0．01），低于肠化粘膜（P＜0．05）。H.pylori阴性组SGT－π阳性率高于H.pylori阳性组（P＜0．05）。H.pylori根除治疗后，根除组GST－π表达高于未根除组（P＜0．05）。结论：正常胃粘膜→肠化粘膜→胃癌组织GST－π表达由无→高→低，GST－π弱阳性或阴性的Ⅲ型肠化与胃癌关系密切；肠化粘膜中GST－π弱阳性或阴性表达如合并H.pylori感染，胃癌发生的危险性增加，提示在肠化阶段H.pylori的致毒作用与机体对致癌物的解毒作用彼此相互拮抗。     

FICE放大内镜联合乙酸染色对诊断胃黏膜肠上皮化生的价值

目的探讨富士能智能分光染色内镜(FICE)放大内镜联合乙酸染色对胃黏膜肠上皮化生(GIM)的诊断价值。方法疑似GIM患者480例随机分为普通内镜组、乙酸染色组、美蓝染色组、FICE放大内镜联合乙酸染色组各120例,以病理诊断为金标准,比较不同方法诊断肠上皮化生的差异。结果普通内镜组与乙酸染色组诊断GIM的灵敏度、特异度、准确率差异无统计学意义(P>0.05),美蓝染色组与乙酸染色组的灵敏度、准确率差异有统计学意义(P<0.05)。FICE放大内镜联合乙酸染色组与美蓝染色组的特异度、准确率差异有统计学意义(P<0.05);FICE放大内镜联合乙酸染色组的阳性似然比、优势比、Kappa值均明显高于美蓝染色组,阴性似然比则明显低于后者(P<0.05)。结论 FICE放大内镜联合乙酸染色可提高GIM定向活检准确率,显著降低漏诊率及误诊率,且与病理诊断的一致性较好,具有更高的临床诊断应用价值。     

幽门螺杆菌相关性胃炎内镜随访研究

为了解Ｈｐ长期感染是否促进胃粘膜萎缩、肠上皮化生和异型增生的形成与发展，对首次胃镜检查诊断为慢性胃炎而不伴有肠化生和异型增生的１２０例Ｈｐ阳性患者和８７例Ｈｐ阴性患者进行内镜随访。随访时间３～８年，平均４．８年，随访次数２～１０次，活检组织进行Ｈｐ检查、病理学检查和ＡｇＮＯＲｓ，银染及ＰＣＮＡ免疫组化染色。结果Ｈｐ阳性患者其慢性萎缩性胃炎、肠化生、Ⅲ型肠化生和异型增生的发生率显著高于Ｈｐ阴性患者，Ｈｐ阳性胃粘膜ＰＣＮＡ标记指数和ＡｇＮＯＲｓ数也显著高于Ｈｐ阴性胃粘膜。表明Ｈｐ感染可能通过刺激胃粘膜细胞的过度增殖、更新加快，促进萎缩性胃炎和肠化生的形成与发展，从而增加患胃癌的危险性。     

幽门螺杆菌相关性胃炎内镜随访研究

为了解Ｈｐ长期感染是否促进胃粘膜萎缩、肠上皮化生和异型增生的形成与发展，对首次胃镜检查诊断为慢性胃炎而不伴有肠化生和异型增生的１２０例Ｈｐ阳性患者和８７例Ｈｐ阴性患者进行内镜随访。随访时间３～８年，平均４．８年，随访次数２－１０次，活检组织进行Ｈｐ检查、病理学检查和ＡｇＮＯＲｓ，银染及ＰＣＮＡ免疫组化染色。结果Ｈｐ阳性患者其慢性萎缩性胃炎、肠化生、Ⅲ型肠化生和异型增生的发生率显著高于Ｈｐ阴性患者，Ｈｐ阳性胃粘膜ＰＣＨＡ标记指教和ＡｇＮＯＲｓ数也显著高于Ｈｐ阴性胃粘膜。表明Ｈｐ感染可能通过刺激胃粘膜细胞的过度增殖、更新加快，促进萎缩性胃炎和肠化生的形成与发展，从而增加患胃癌的危险性。     

胃粘膜肠上皮化生CST-Л的表达及其与H.pylori相关性研究

目的探讨GST-Л在胃癌发生过程中表达,及在肠化阶段以GST-Л为代表的人体对致癌物解毒系统与H.pylori致毒作用间的相互作用.方法利用S-P法对219例胃粘膜活检标本进行GST-Л单克隆抗体的检测:利用HID-AbpH2.5-PAS粘蛋白组化学技术对171例肠化粘膜进行分型;利用HE及H.pylori-DNA PCR及ELISA方法对正常胃粘膜和肠化粘膜进行H.pylori的检测.对80例H.pylori阳性患者进行H.pylori根除治疗三个月后进行H.pylori、GST-Л的检测.结果正常胃粘膜未见GST-Л的表达,肠化粘膜GST-Л阳性率为69.6%,胃癌GST-Л阳性率为44.4%,高于正常胃粘膜(P＜0.01),低于肠化粘膜(P＜0.05).H.pylori阴性组SGT-Л阳性率高于H.pylori阳性组(P＜0.05).H.pylori根除治疗后,根除组GST-Л表达高于未根除组(P＜0.05).结论正常胃粘膜→肠化粘膜→胃癌组织GST-Л表达由无→高→低,GST-Л弱阳性或阴性的Ⅲ型肠化与胃癌关系密切;肠化粘膜中GST-Л弱阳性或阴性表达如合并H.pylori感染者,胃癌发生的危险性增加,提示在肠化阶段H.pylori的致毒作用与机体对致癌物的解毒作用彼此相互拮抗.     

胃息肉与HP感染、粘膜炎症及粘膜萎缩相关性的研究

目的 探讨HP感染与胃息肉发生类型以及与粘膜炎症、萎缩和肠上皮化生的相关性。方法 对2203例胃粘膜活检发现的278例胃息肉(检出率12．6％)进行组织学分类．并对胃窦粘膜活检组织同时行HP检测和粘膜炎症、萎缩及肠上皮化生的观察,比较不同类型胃息肉的HP感染率及其与癌相关病变的关系。结果 278例息肉中．组织学分类以小凹上皮增生型息肉最为多见,有130例,占息肉总数的46.8％,胃体腺型增生性息肉67例、占24．1％。炎性息肉和腺瘤性息肉较少见．分别为55例(19．8％)和26例(9．4％)。约53．9%的胃息肉存在HP感染,其中以小凹上皮增生型息肉感染率最高．达73．1％。这型息肉常伴有胃粘膜的活动性炎症．且粘膜萎缩和肠上皮化生的发生率均接近腺瘤性病变。胃体腺型增生性息肉．无论是HP感染率,活动性炎症及萎缩、肠上皮化生等发生率均较低,提示这两种息肉在组织发生和病理生物学形态上存在差异。结论 小凹上皮增生型息肉的发生可能与HP感染有关．由于该型息肉常伴有明显的活动性炎症以及粘膜萎缩和肠上皮化生的变化．因此可能与胃癌的发生有潜在的相关性。     

根除幽门螺杆菌对胃癌患病率及胃黏膜组织学变化的八年随访研究

目的观察胃癌高发区中幽门螺杆菌(Hp)阳性患者根除Hp后8年的胃癌患病率及胃黏膜组织学变化,探讨Hp感染与胃黏膜组织学变化的关系。方法1996年在胃癌高发区山东烟台市自然人群中整群抽样选择1006例成年人(年龄35～75岁,入组时无胃癌患者)。将Hp阳性患者552例随机分为治疗组(T组,276例)和安慰剂组(P组,276例),采用随机、双盲、安慰剂对照平行试验方法,T组给予奥美拉唑、羟氨苄青霉素和克拉霉素口服治疗1周,P组给予安慰剂对照。停药1个月后行13C尿素呼气试验(13CUBT),T组Hp根除率为89%。再按Hp状况重新分为Hp根除组(246例)和Hp阳性组(306例),分别于1、5、8年后进行内镜复查。将8年后复查胃镜及相同部位胃黏膜组织病理检查与8年前结果进行比较。结果①8年随访共发现7例胃癌患者,Hp根除组1例,Hp阳性组6例,两组胃癌患病率按人年计算:Hp根除组为1/1968人年、Hp阳性组为6/2448人年。用泊松分布比较,两组胃癌患病率差异有统计学意义(P<0.05)。②5年随访时两组胃癌患病率及死亡共6例,Hp根除组1例,Hp阳性组5例,两组胃癌患病率按人年计算:Hp根除组为1/1230人年,Hp阳性组为5/1530人年。用泊松分布比较,两组胃癌患病率差异无统计学意义(P>0.05)。③Hp根除8年后,患者胃体部萎缩进展缓慢,而Hp阳性组患者胃体部萎缩发生率明显增加,两组相比差异有统计学意义(P<0.01)。根除Hp8年后胃窦部萎缩肠化改变两组间差异无统计学意义(P>0.05)。结论Hp感染可增加胃癌发病率,根除Hp有利于减少胃癌发生,并可使胃体部萎缩进展缓慢。持续Hp感染可使萎缩及肠化呈进行性加重。     

Helicobacterpylori infection and gastropathy： A comparison between Indonesian and Japanese patients

AIM: To compare the effects of Helicobacter pylori ( H pylori) infection on gastropathy between Indonesian and Japanese patients.METHODS: Biopsy specimens were obtained during upper gastrointestinal endoscopy from 167 subjects (125 Indonesians and 42 Japanese) with uninvestigated symptoms of dyspepsia. The specimens were analyzed for the presence of H pylori using urease analysis, histopathology, and cell culture. The grade and activity of gastritis was assessed using the updated Sydney system.RESULTS: The percentages of Indonesian and Japanese patients who were H pylori-positive at the antrum or body of the stomach were similar (68% and 59.5%, respectively; P = 0.316). Of those who were H pylori-positive, more Japanese patients than Indonesian patients had high levels of polymorphonuclear cells ( P = 0.001), mononuclear cells ( P = 0.013), glandular atrophy ( P = 0.000), and intestinal metaplasia ( P = 0.011) in both the antrum and body of the stomach.CONCLUSION: The grade of gastritis and prevalence of mucosal atrophy and intestinal metaplasia were higher in Japanese patients. The difference between Indonesian and Japanese patients was significant.     

Latest insights into the effects of Helicobacter pylori infection on gastric carcinogenesis

There appears to be the strong association between Helicobacter pylori (H pylori) and gastric cancer. We reviewed the latest evidences about the effects of H pylori infection on gastric carcinogenesis, classified into epidemiology, dynamics of gastric mucosal changes, DNA damages, virulence factors, host factors, and source of gastric malignancy. Through the considerable progress made in research into virulence factors resulting from differences between H pylori strains, such as cagA positivity, as well as into host factors, such as gene polymorphisms, a diverse spectrum of H pylori-associated diseases, including gastric cancer, is beginning to lend itself to elucidation. The impact of the novel hypothesis advanced by Houghton et al proposing bone-marrow derived stem cells (BMDC) as a potential source of gastric malignancy on evolving research remains to be seen with interest. Further progress in research into H pylori eradication as a viable prophylaxis of gastric cancer, as well as into the mechanisms of gastric carcinogenesis, is to be eagerly awaited for the current year and beyond.     

Surveillance strategies for precancerous gastric conditions after Helicobacter pylori eradication: There is still need for a tailored approach

Prevailing evidence declares that Helicobacter pylori (H. pylori) eradication therapy could shift precancerous gastric conditions (PGC) and positively confines gastric cancer (GC) risk during long-term endoscopic follow-up. Nonetheless, there is a yet unsolved controversy regarding the best-individualized surveillance strategies following H. pylori eradication, based on malignant risk stratification. This last dispute is due to the uncertainty of contemporary evidence and the role of H. pylori inflammatory changes in underestimating PGC at the index endoscopy. However, the current state of the art suggests that it is reasonable that high-quality endoscopy with histological assessment for the most accurate diagnosis of PGC may be delayed in selected high-risk patients without alarm signs for malignancy, following the eradication of H. pylori. Notwithstanding, these aspects need to be further examined in the next future to establish and optimize the most beneficial and cost-effective strategies for recognizing and managing H. pylori-positive patients with PGC in the short- and long-term follow-up. Accordingly, additional studies are yet required to sharpen the hazard stratification of patients with the greatest chance of GC evolution, also recognizing the evolving racial, ethnic, immigration factors and the necessity of novel biomarkers to limit GC development or accomplish a diagnosis of malignancy at an early stage.     

Prevalence and risk factors for upper gastrointestinal diseases in health check-up subjects: a nationwide multicenter study in Korea

Objectives: The prevalence of upper gastrointestinal disease is expected to change following advances in socioeconomic status and improved hygiene in Korea. The aim of this study was to investigate the recent trends in upper gastrointestinal diseases based on endoscopic findings and Helicobacter pylori (H. pylori) seroprevalence in subjects undergoing health check-up at tertiary centers in Korea.

Methods: A multicenter cross-sectional study was conducted at nine healthcare centers between September 2016 and June 2017. The subjects were evaluated using questionnaires, upper endoscopy and H. pylori serology tests. The results were compared with previous data in our study group obtained from eight tertiary healthcare centers in 2011 (n?=?4023).

Results: In total, we prospectively enrolled 2504 subjects undergoing health check-up. The prevalence of reflux esophagitis (RE) was 9.7%, which showed an increasing but insignificant trend since 2011 (8.8%). The prevalence of active and healing-stage benign gastric ulcer and duodenal ulcer (DU) was 1.6% and 1.2%, respectively, which confirmed a significant decrease since 2011 (4.1%; p?p?=?.005, respectively). The prevalence of gastric cancer was 0.5%, representing an increasing trend since 2011 (0.12%; p?=?.003). H. pylori seroprevalence was 51.3%, which significantly decreased from 2011 (59.8%; p?H. pylori seropositivity was a significant risk factor for DU (p?p?Conclusions: The significant decrease of H. pylori seroprevalence in the past five years altered the incidence of upper gastrointestinal disease.     

A combination of the Helicobacter pylori stool antigen test and urea breath test is useful for clinical evaluation of eradication therapy: a multicenter study

BACKGROUND: Helicobacter pylori stool antigen (HpSA) test is a new tool for evaluating the H. pylori infection. The present study was carried out to investigate the clinical usefulness of the HpSA test in the evaluation of eradication therapy by comparing it with the (13)C-urea breath test (UBT). METHODS: One hundred and five patients received eradication therapy for H. pylori. After more than 8 weeks, the success of the therapy was evaluated by the HpSA test and the UBT. Concordant results were regarded as a final diagnosis, but when the results were discordant, histological examination was carried out. RESULTS: Of the 105 patients receiving eradication therapy for H. pylori, 25 patients were regarded as H. pylori positive by the UBT and and 20 patients were regarded as H. pylori positive by the the HpSA test. Nine patients (8.6%) showed discordant results (seven cases with UBT(+) and HpSA(-), and two with UBT(-) and HpSA(+)). Five cases out of nine were ultimately judged as having a false-positive result of the UBT, and in these cases the UBT values were relatively low (below 10 per thousand). The final diagnostic accuracies of the UBT and the HpSA test were 94.3% (88.0-97.9%; 95% CI) and 97.1% (91.9-99.4%), respectively. When we used the HpSA test in cases with weakly positive UBT values, we were able to diagnose the correct status of H. pylori infection after eradication in 99% of all patients (94.8-100.0%). CONCLUSION: The HpSA test is a useful tool for the evaluation of eradication therapy and a combination of the HpSA test and UBT is clinically recommended.     

Endoscopic Kyoto classification of Helicobacter pylori infection and gastric cancer risk diagnosis

Recent advances in endoscopic technology allow detailed observation of the gastric mucosa.Today,endoscopy is used in the diagnosis of gastritis to determine the presence/absence of Helicobacter pylori(H.pylori)infection and evaluate gastric cancer risk.In 2013,the Japan Gastroenterological Endoscopy Society advocated the Kyoto classification,a new grading system for endoscopic gastritis.The Kyoto classification organized endoscopic findings related to H.pylori infection.The Kyoto classification score is the sum of scores for five endoscopic findings(atrophy,intestinal metaplasia,enlarged folds,nodularity,and diffuse redness with or without regular arrangement of collecting venules)and ranges from 0 to 8.Atrophy,intestinal metaplasia,enlarged folds,and nodularity contribute to gastric cancer risk.Diffuse redness and regular arrangement of collecting venules are related to H.pylori infection status.In subjects without a history of H.pylori eradication,the infection rates in those with Kyoto scores of 0,1,and≥2 were 1.5%,45%,and 82%,respectively.A Kyoto classification score of 0 indicates no H.pylori infection.A Kyoto classification score of 2 or more indicates H.pylori infection.Kyoto classification scores of patients with and without gastric cancer were 4.8 and 3.8,respectively.A Kyoto classification score of 4 or more might indicate gastric cancer risk.     

Gastric adenocarcinoma of fundic gland type with signet-ring cell carcinoma component: A case report and review of the literature

A depressed lesion was found at a gastric angle of 76-yearold Japanese woman by esophagogastroduodenoscopy. Four years prior, she was diagnosed with a Helicobacter pylori infection but no eradication was performed. The pathological diagnosis of biopsy specimens was signet-ring cell carcinoma. Endoscopic submucosal dissection(ESD) was performed. Histopathological examination of the ESD specimen revealed proliferation of well-differentiated tubular adenocarcinoma mimicking fundic gland cells at the deep layer of the lamina propria mucosae. These tumor cells expressed focally pepsinogen-Ⅰ, diffusely MUC6, and scattered H~+/K~+ ATPase according to immunohistochemistry. Therefore, we diagnosed this tumor as gastric adenocarcinoma of fundic gland type(GA-FG). Adjacent to the GA-FG, proliferation of signet-ring cell carcinoma which diffusely expressed MUC 2 and MUC 5AC was observed. Intestinal metaplasia was focally observed in the surrounding mucosa of the signet-ring cell carcinoma. To the best of our knowledge, this is the first case report of GA-FG with a signet-ring cell carcinoma component. The origin of signet-ring cell carcinoma, i.e., whether it accidentally arose from a non-neoplastic mucosa and coexisted with the GA-FG or dedifferentiated from the GA-FG is unclear at present. We expect the accumulation of similar cases and further analysis to clarify this issue.     

以复方铋剂为主的四联疗法根除幽门螺杆菌全国多中心临床研究

目的　观察以复方铋剂 (丽珠胃三联 ,含胶体枸橼酸铋 2 2 0mg、克拉霉素 2 5 0mg和替硝唑5 0 0mg)为中心的三联和四联疗法治疗幽门螺杆菌 (Hp)相关性胃炎及消化性溃疡的疗效 ,并比较丽珠胃三联、丽珠胃三联与H2 受体拮抗剂 (H2 RA)或质子泵抑制剂 (PPI)组成的四联疗法 1周与 2周方案的治疗效果。方法　胃镜和组织学证实Hp阳性的 734例患者中 ,除胃溃疡 12 6例随机入选A2、B2和C2组外 ,十二指肠溃疡 2 0 4例和慢性活动性胃炎 4 0 4例随机分成A1、A2、B1、B2及C1、C2组。A1组 :奥美拉唑 2 0mg +丽珠胃三联 4片 ,均每日 2次× 1周 ;A2组 :组方同前× 2周。B1组 :泰胃美 4 0 0mg +丽珠胃三联 4片 ,均每日 2次× 1周 ;B2组 :组方同前× 2周。C1组 :丽珠胃三联 4片 ,每日 2次× 1周 ;C2组 :组方同前× 2周。治疗结束 4周后 ,溃疡病患者复查胃镜 ,观察溃疡愈合和Hp感染状态 ,胃炎患者作13 C UBT ,观察Hp根除率 ,并采用PP和ITT分析。 结果　按PP分析 ,A2组 (95 .74 % )的Hp根除率显著高于A1(86 .2 7% )、B1(90 .10 % )、C1(84 .0 0 % )和C2组 (88.4 9% ) ;按ITT分析 ,C1组 (5 2 .17% )的溃疡愈合率显著低于A2 (76 .92 % )和B2组 (81.5 8% )。结论　丽珠胃三联是目前根除Hp和愈合消化性溃疡的一种有效且价廉的方