含左氧氟沙星的四联药物10日序贯疗法根除幽门螺杆菌疗效观察

目的 观察雷贝拉唑、克拉霉素、左氧氟沙星、阿莫西林(四联药物)10日序贯疗法根除幽门螺旋杆菌(HP)的疗效及安全性.方法 将经胃镜确诊的消化性溃疡和慢性胃炎伴胃黏膜萎缩或糜烂且幽门螺杆菌阳性的80例成人患者随机分成治疗组和对照组各40例.治疗组前5d口服雷贝拉唑10 mg、阿莫西林1 000 mg,2次/d;后5d口服雷贝拉唑10 mg、克拉霉素500 mg,2次/d;左氧氟沙星500 mg,1次/d.对照组采用传统的三联疗法(雷贝拉唑10 mg、阿莫西林1 000mg、克拉霉素500 mg,2次/d,共10 d).结果 治疗组及对照组HP根除率分别为92.5％(37/40)、75％(30/40),P＜O.05;不良反应发生率分别为7.5％、10％,两组相比差异无统计学意义.结论 四联药物10日序贯疗法对成人HP的根除率明显优于传统三联疗法,且较为安全.     

序贯疗法根除幽门螺杆菌的研究

目的 探讨阿莫西林、克拉霉素、奥硝唑10 d序贯疗法在幽门螺杆菌根除治疗中的价值.方法 86例慢性糜烂性胃炎、萎缩性胃炎、消化性溃疡、胃镜胃窦部快速尿素酶试验(RUT),14C-尿素呼气试验(14C-UBT)均阳性的患者随机分为两组:试验组46例,行10d序贯疗法,前5 d应用雷贝拉唑20 mg,Bid,阿莫西林1.0 g,Bid.后5 d雷贝拉唑20mg,Bid,克拉霉素0.5 g,Bid,奥硝唑0.5 g,Bid.对照组40例,应用雷贝拉唑20 mg,Bid,克拉霉素0.5 g,Bid,阿莫西林1.0 g,Bid,10 d.结果 停药4周后复查胃镜RUT及14CUBT,两者均阴性,试验组41例,89.1%,明显高于对照组27例67.5%.两组比较差异显著(P＜0.05).副作用发生率,试验组3例,6.5%,对照组12例,30.0%,后者明显高于前者(P＜0.01).结论 阿莫西林、克拉霉素、奥硝唑联合质子泵抑制药10日序贯疗法可以明显提高Hp根除率.     

8d与10d序贯疗法根除幽门螺杆菌的疗效比较

目的:比较雷贝拉唑、阿莫西林、克拉霉素、奥硝唑组成的8d与10d序贯疗法根除幽门螺杆菌(H.pylori)的疗效.方法:将经胃镜检查确诊为慢性胃炎和消化性溃疡,且H.pylori阳性的217例患者随机分为2组,8d组(n=104)方案:前4d,雷贝拉唑+阿莫西林;后4d,雷贝拉唑+克拉霉素+奥硝唑.10d组(n=113)方案:前5d,雷贝拉唑+阿莫西林;后5d,雷贝拉唑+克拉霉素+奥硝唑.根除治疗后复查14C-尿素呼气试验,比较两组H.pylori根除率.结果:8d组和10d组H.pyloriITT根除率分别为89.3%和91.2%,PP根除率分别为92.0%和93.7%.两种分析方法比较两组的根除率差异均无统计学意义(P>0.05),但8d序贯疗法降低了成本-效果比,减轻了患者的经济负担.两种方案症状缓解率及不良反应发生率的差异无统计学意义(P>0.05).结论:8d序贯疗法可以获得较高的H.pylori根除率和症状缓解率,且经济、安全,是一种可供选择的一线治疗方案.     

含替硝唑序贯疗法根除幽门螺杆菌62例

目的: 观察由泮托拉唑、替硝唑、阿莫西林、克拉霉素组成的10日序贯疗法根除幽门螺杆菌( H pylori)的疗效.方法: 将经胃镜检查确诊为慢性胃炎和消化性溃疡且H pylori阳性的患者120例随机分为两组, 治疗组(62例)方案为前5 d给予泮托拉唑+阿莫西林, 后5 d给予泮托拉唑+克拉霉素+替硝唑;对照组(58例)三联疗法为泮托拉唑+阿莫西林+克拉霉素, 疗程7 d. 比较治疗后两组患者H pylori根除率.结果: 治疗组和对照组H pylori ITT根除率分别为83.87%和67.24%, PP根除率分别为89.66%和72.22%, 两组分别有统计学意义( P<0.05).结论: 含替硝唑的10日序贯疗法治疗H pylori感染具有较高的根除率.     

序贯疗法与三联疗法根除幽门螺杆菌的疗效及对反流性食管炎愈合率的影响

目的比较10天序贯疗法与10天标准三联疗法根除幽门螺杆菌（HP）的疗效,并观察根除HP对反流性食管炎愈合率的影响。方法将76例反流性食管炎合并HP感染的患者随机分为3组：序贯疗法治疗组32例,埃索美拉唑＋阿莫西林,每日2次,共用5天,随后5天用埃索美拉唑＋克拉霉素＋替硝唑,每日2次;三联疗法治疗组24例,埃索美拉唑＋克拉霉素＋阿莫西林,每日2次,疗程10天,两组抗HP疗程结束后继续给予埃索美拉唑,每日2次,总疗程8周;对照组20例：单用埃索美拉唑,每Et2次,疗程8周。疗程结束后复查胃镜,并行HP检测。结果序贯疗法与三联疗法对幽门螺杆菌的根除率分别为87．50％和58．33％,两组比较差异有统计学意义（P〈0．05）。HP根除患者和未根除患者食管炎治愈率分别为83．33％和91．18％,两者比较差异无统计学意义;3组食管炎的治愈率分别为87．50％、83．33％和90％,三者之间比较差异无统计学意义。结论在食管炎患者中,序贯疗法HP根除率明显优于三联疗法;根除幽门螺杆菌对反流性食管炎8周愈合率无明显影响。     

改良序贯疗法根除幽门螺杆菌的疗效观察

目的探讨雷贝拉唑、阿莫西林、左氧氟沙星、克拉霉素组成的10d序贯疗法根除幽门螺杆菌(Hp)的疗效及安全性。方法将110例Hp阳性患者分成两组,治疗组采用改良序贯疗法;对照组采用标准三联疗法。疗程结束4周后复查碳14呼气试验,观察Hp根除率和不良反应。结果治疗组按意图治疗和按试验方案分析Hp根除率分别为91.7%和94.8%,对照组分别为76.0%和79.1%,两组根除率比较差异有统计学意义(P0.05);治疗组和对照组不良反应分别为2例和3例。结论雷贝拉唑、阿莫西林、左氧氟沙星组成的10d序贯疗法是一种疗效高、不良反应少的Hp根除方案,可以作为治疗Hp感染的一种选择方案。     

改良序贯疗法补救治疗幽门螺旋杆菌感染的临床疗效

目的:比较铋剂四联组、10 d改良序贯组、14 d改良序贯组补救根除幽门螺旋杆菌(Helicobacter pylori,H.pylori)感染的效果差异.方法:将首次铋剂四联疗法根除H.pylori失败的195例慢性胃炎、消化性溃疡患者,随机分为铋剂四联组、10 d改良序贯组、14 d改良序贯组,每组65例.A组(铋剂四联组)给予雷贝拉唑、阿莫西林、左氧氟沙星、胶体果胶铋;B组(10 d改良序贯组)前5 d予雷贝拉唑、阿莫西林,后5 d予雷贝拉唑、左氧氟沙星、呋喃唑酮;C组(14 d改良序贯组)前7 d予雷贝拉唑、阿莫西林,后7 d予雷贝拉唑、左氧氟沙星、呋喃唑酮.所有患者在疗程结束停药4 wk后行~(14)C尿素呼气试验.记录3组患者药物不良反应.结果:A、B、C组根除率分别为75.4%、89.2%、95.4%,同A组相比,B组根除率(χ~2=0.039,P0.05)和C组根除率(χ~2=0.001,P0.05)明显提高,差异有统计学意义.B组高于C组,差异无统计学意义(χ~2=0.188,P0.05).A组不良反应率为27.7%、B组不良反应率26.2%、C组不良反应率29.2%,差异无统计学意义(P0.05).结论:对于H.pylori补救治疗,改良序贯疗法疗效更好,且不良反应低,推荐14 d改良序贯疗法作为首选方案之一.     

序贯疗法与标准四联疗法对幽门螺杆菌根除失败后补救治疗的疗效分析

近年经典三联疗法的幽门螺杆菌（11．pylori）根除疗效明显降低,选择有效补救疗法对Hpylori根除失败者有重要意义。目的：比较序贯疗法与标准四联疗法对且pylori根除失败者的疗效。方法：将98例Hpylori根除失败者随机分为序贯疗法组（前5d予奥美拉唑20mg＋阿莫西林1000mgbid,后5d予奥美拉唑20mg＋左氧氟沙星200mg＋克拉霉素500mgbid）和标准四联疗法组（予奥美拉唑20mg＋胶体次枸橼酸铋钾220mg＋阿莫西林1000mg＋克拉霉素500mgbid,疗程7d）。停药4周后复查”C一尿素呼气试验,评估Hpylori根除疗效。结果：共95例患者完成方案,序贯疗法组11Tr和PP分析的Hpylori根除率均显著高于标准四联疗法组（ITF：89．8％对71,4％,PP：91．7％对74。5％,P〈0．05）,序贯疗法组临床症状改善的总有效率亦显著高于标准四联疗法组（95．8％对80．9％,P〈0．05）,两组不良反应发生率无明显差异（P〉0．05）。结论：对Hpylori根除治疗失败的患者,序贯疗法和标准四联疗法均可作为有效的补救治疗方案,但10d序贯疗法的疗效优于7d标准四联疗法。     

标准三联疗法与序贯疗法治疗幽门螺杆菌阳性胃溃疡的疗效对比

目的对比分析标准三联疗法与序贯疗法对幽门螺杆菌(H.pylori)阳性胃溃疡患者的疗效。方法选择2013年2月至2015年12月在我院进行诊治的胃溃疡患者165例,随机分为两组。对照组予以三联疗法(阿莫西林1 000 mg+雷贝拉唑肠溶片20 mg+克拉霉素500 mg,2次/d)进行治疗10 d。观察组予以序贯疗法(前5 d予阿莫西林1 000 mg+雷贝拉唑肠溶片20 mg,2次/d;后5 d予左氧氟沙星200mg+雷贝拉唑肠溶片20 mg+克拉霉素500 mg,2次/d)。比较两组的Glasgow评分、症状评分、H.pylori根除及不良反应情况。结果观察组的H.pylori根除率明显高于对照组(P0.05);两组治疗后的Glasgow评分均明显降低(P0.05),且观察组明显低于对照组(P0.05);两组治疗后的腹胀、腹痛和反酸嗳气评分均明显降低(P0.05),且观察组明显低于对照组(P0.05);观察组便秘、腹泻、乏力、口苦等不良反应发生率明显低于对照组(P0.05)。结论序贯疗法在治疗胃溃疡中改善患者症状,根除H.pylori及良良反应等均优于标准三联疗法,可以作为H.pylori阳性胃溃疡患者的初治首选方案。     

10d序贯疗法对根除幽门螺杆菌疗效的随访研究

背景:幽门螺杆菌(H.pylori)与慢性胃炎、消化性溃疡、胃癌和胃黏膜相关淋巴组织(MALT)淋巴瘤密切相关,但标准三联疗法的根除率逐年下降。目的:比较10 d序贯疗法和三联疗法根除H.pylori的疗效。方法:将经快速尿素酶试验(RUT)和~(14)C-尿素呼气试验(UBT)证实为H.pylori阳性的106例消化性溃疡、慢性糜烂性胃炎和萎缩性胃炎患者随机分为以雷贝拉唑为基础的10 d序贯疗法组(n=56)和三联疗法组(n=50)。治疗结束4周后复查RUT和,~(14)C-UBT,评估H.pylori根除情况;随访1年后再复查~(14)C-UBT评估H.pylori复发情况。结果:共93例患者按方案完成治疗。10 d序贯疗法组H.pylori根除率按意向治疗(ITT)和按方案(PP)分析均显著高于三联疗法组(ITF:89.3%对62.0%,P0.01;PP:94.3%对77.5%,P0.05);10 d序贯疗法组不良反应发生率(7.1%对30.0%,P0.01)和随访1年后的H.pylori复发率(6.0%对25.8%,P0.01)均显著低于三联疗法组。结论:以雷贝拉唑为基础的10 d序贯疗法可明显提高H.pylori根除率,提高患者的依从性,减少不良反应的发生。     

不同幽门螺杆菌根除方案对功能性消化不良影响的临床研究

背景:功能性消化不良(FD)是常见的功能性胃肠病,幽门螺杆菌(H.pylori)是FD的重要致病因素之一。目的:探讨不同H.pylori根除方案对FD患者临床症状的疗效。方法:160例H.pylori(+)FD患者随机分为10d序贯治疗组(60例)、7d三联治疗组(60例)和对照组(40例)。所有患者于停药4周后复查~(14)C-尿素呼气试验以评估H.pylori根除率。患者于治疗前、治疗后第3、6、12个月评估FD症状。结果:10d序贯治疗组、7d三联治疗组和对照组的H.pylori根除率分别为93.2%、74.1%和48.6%(符合方案分析)以及91.7%、71.7%和42.5%(意向治疗分析),各组相比差异有统计学意义(P0.05)。治疗后第6、12个月,10d序贯治疗组和7d三联治疗组中H.pylori根除者的FD症状改善率显著高于对照组(P0.05),但两治疗组之间无明显差异。结论:10d序贯治疗和7d三联治疗的FD症状改善率无明显差异,但前者H.pylori根除率高于后者,临床可推荐10d序贯疗法治疗H.pylori(+)FD患者。     

乙、丙型肝炎病毒及幽门螺杆菌在慢性肝炎、肝硬化患者胃黏膜的表达

目的 探讨乙、丙型肝炎病毒(HBV、HCV)的泛嗜性及幽门螺杆菌(Helicobacter pylori)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)、丙型肝炎病毒抗原(HCVAg)检测及快速尿素酶、品红染色和免疫组化法检测H.pylori抗原(HPAg)。结果 慢肝组有不同程度的胃黏膜慢性炎症者达92.9％(26/28)、肝硬化组为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多。72例慢性肝病者中有51例胃黏膜HBVAg阳性,其中HBsAg、HBcAg双阳性31例。肝硬化组HBsAg或HBcAg表达及HBsAg、HBcAg双阳性者均高于慢肝组(P均<0.05)。51例慢性肝病胃黏膜中有33例占64.7％有HCVAg表达;其中22例占52.4％与HBsAg或(和)HBcAg同时表达。在慢肝和肝硬化组有炎症的胃黏膜中H.pylori阳性率分别为67.9％(20/26)、69.0％(29/42),与对照组相比无显著差别。慢性肝病H.Pylori阳性、阴性者胃黏膜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、H     

Expression of mutant type-p53 products in H pylori-associated chronic gastritis

AIM:To investigate the mutation of p 53 immuno-histochemically in non-tumorous gastric mucosa with H pylori infection before and after H pylori eradication therapy.METHODS:53 subjects(36 male,17 female,mean age ± SEM,57.1 ± 12.1)undergoing endoscopic examination were included in this study.42 of 53 patients were H pylori-positive,and 11 were H pylori-negative.All H pylori-positive patients had successful eradication therapy.Biopsy specimens were taken from five points of the stomach,as recommended by the updated Sydney system.Immunohistochemical studies were performed by using primary antibodies against p53(DO-7 and PAb240).RESULTS:p53(DO-7 and PAb240)immunoreactivity was shown in the neck region of the gastric pits,however,quite a few cells were found to be immunopositive for p 53(PAb240)in the H pylori-infected gastric mucosa.The proportion of patients immunopositive for p 53(PAb240)was significantly reduced 6 mo after eradication [28/42(66.7%)to 6/42(14.3%)](P < 0.05),while the biopsies taken from H pylori-negative patients showed no immunoreactivity for p53(PAb240).p53(PAb240)-positive patients were divided into two groups by the number of positive cells detected:one with more than six positive cells per 10 gastric pits(group A,n = 12),and the other with less than five positive cells per 10 gastric pits(group B,n = 30).Atrophy scores in group A were significant higher than those in group B at the greater curvature of the antrum(group A:2.00 ± 0.14 vs group B:1.40 ± 0.15,P = 0.012),the lesser curvature of the corpus(group A:2.00 ± 0.21 vs group B:1.07 ± 0.23,P = 0.017),and the greater curvature of the corpus(group A:1.20 ± 0.30vs group B:0.47 ± 0.21,P = 0.031).Group A showed significant higher intestinal metaplasia scores than group B only at the lesser curvature of the antrum(group A:2.10 ± 0.41 vs group B:1.12 ± 0.29,P = 0.035).CONCLUSION:H pylori-associated chronic gastritis expressed the mutant-type p53,which was significantly associated with more severe atrophic and metaplastic changes.H pylori eradication led to a significant reduction in the expression of the mutant-type p53.It is considered that H pylori-infected chronic gastritis is associated with a genetic instability that leads to gastric carcinogenesis,and H pylori eradication may prevent gastric cancer.     

胃粘膜萎缩与Hp感染淋巴组织增生的关系

目的研究幽门螺杆菌（Ｈｐ）诱生的胃粘膜相关淋巴组织（ＭＡＬＴ）增生与萎缩关系及Ｈｐ根除后淋巴滤泡（ＬＦ）消失情况．方法光镜观察２５８例Ｈｐ阳性的慢性胃炎三联（奥美拉唑、克拉霉素、痢特灵，７ｄ）药治疗前后（１ｍｏ及１ａ）及正常胃粘膜２５例的ＬＦ检出率和聚集强度．结果慢性胃炎ＬＦ总检出率为７２５％；萎缩性胃炎＞浅表性胃炎，而正常胃粘膜ＬＦ检出率为４％；慢性胃炎ＬＦ聚集强度与粘膜炎症程度呈正相关（ｒ＝０６５，Ｐ＜００１）；但与粘膜萎缩程度呈负相关（ｒ＝－０６９，Ｐ＜００１）；治疗后慢性胃炎ＬＦ检出率和聚集强度明显减低（Ｐ＜００１）；腺上皮萎缩与ＬＦ形成关系密切．结论胃ＭＡＬＴ增生及相伴的免疫反应，可能是引起Ｈｐ相关性胃炎出现胃粘膜萎缩的重要原因之一．     

Effect of Helicobacter pylori eradication on chronic gastritis during omeprazole therapy

BACKGROUND: We have previously observed that profound acid suppressive therapy in Helicobacter pylori positive patients with gastro-oesophageal reflux disease is associated with increased corpus inflammation and accelerated development of atrophic gastritis. AIM: To investigate if H pylori eradication at the start of acid suppressive therapy prevents the development of these histological changes. PATIENTS/METHODS: In a prospective randomised case control study, patients with reflux oesophagitis were treated with omeprazole 40 mg once daily for 12 months. H pylori positive patients were randomised to additional double blind treatment with omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg twice daily or placebo for one week. Biopsy sampling for histology, scored according to the updated Sydney classification, and culture were performed at baseline, and at three and 12 months. RESULTS: In the persistently H pylori positive group (n=24), active inflammation increased in the corpus and decreased in the antrum during therapy (p=0.032 and p=0.002, respectively). In contrast, in the H pylori positive group that became H pylori negative as a result of treatment (n=33), active and chronic inflammation in both the corpus and antrum decreased (p相似文献   

内镜下射频消融配合胃三联治疗慢性胃炎隆起糜烂型的临床观察

目的:探讨射频局部消融配合胃三联治疗慢性胃炎隆起糜烂型的疗效．方法:内镜下符合慢性胃炎隆起糜烂型诊断,H pylori阳性的患者106例,随机分为治疗组:射频消融 洛赛克omeprazole、阿莫西林 Amoxicillin、克拉霉素Clarithromycin(简称胃三联)治疗,对照组:单纯胃三联治疗．结果:治疗组隆起糜烂病灶平复率、临床症状有效率分别为100％和94．1％,对照组隆起糜烂病灶平复率、临床症状有效率分别为 27．2％和58．2％,优于对照组(P<0．05)．H pylori 根除率治疗组88．2％,对照组85．7％,二者之间无显著差异(P>0．05)．结论:射频局部消融配合胃三联治疗慢性胃炎隆起糜烂型疗效确切、操作简单、安全．     

Systemic and local immune responses against Helicobacter pylori urease in patients with chronic gastritis: distinct IgA and IgG productive sites

BACKGROUND: Helicobacter pylori urease is a major target for immune responses among various bacterial components in H pylori infected patients. AIMS: To analyse the relation between systemic and local humoral immune responses to H pylori urease and grades of chronic gastritis. PATIENTS: Seventy five patients with chronic gastritis associated with H pylori infection were classified into three groups (grade I, superficial gastritis; II, atrophic gastritis, quiescent; or III, atrophic gastritis, active). METHODS: Anti-H pylori urease specific antibodies in the serum, gastric juice, and biopsy specimens were determined by ELISA or western blotting analysis. The sites for H pylori urease and its specific antibody producing B lymphocytes were confirmed by immunohistochemical analysis. RESULTS: In the sera of patients with grade I gastritis, weak IgG but relatively strong IgG responses to H pylori urease were observed; dominant strong IgG responses were detected in grade II gastritis. In grade III gastritis, significant IgG and IgA responses were obtained. A similar pattern of IgA and IgG responses was detected in gastric juice and tissue. H pylori urease specific, antibody producing B cells were not found in the gastric mucosa of patients with grade I gastritis despite the presence of such B cells in the duodenal bulb. Specific B cells were observed in the gastric mucosa of patients with grade II and III gastritis with atrophy. CONCLUSIONS: Purified H pylori urease, together with localisation of its specific antibody producing B cells, are useful for serological testing and histopathological analysis for determining the stage of chronic gastritis and studying the pathogenesis of H pylori infection.     

萎缩性胃炎患者幽门螺杆菌根除后表皮生长因子及其受体的变化

目的　研究幽门螺杆菌 (Helicobacterpylori,H .pylori)感染对胃黏膜表皮生长因子受体 (epidermalgrowthfactorreceptor ,EGFR)、血清表皮生长因子 (epidermalgrowthfactor,EGF)水平的影响。方法　对 60例H pylori检测阳性的慢性萎缩性胃炎患者进行根除治疗 ,在治疗前及疗程结束 3个月后分别进行胃镜检查 ,并采用免疫组化及放射免疫法测定H pylori根除前后胃黏膜EGFR和血清EGF含量。 3 0例H pylori检测阴性且胃镜检查无明显异常者作为正常对照组。结果　 60例H pylori检测阳性的CAG患者的胃黏膜EGFR阳性率及血清EGF水平均高于正常对照 ,其差异有显著性 (P <0 0 5 ,P <0 0 1)。有 3 1例在根除治疗 3个月后进行了复查 ,其中 2 4例H pylori得到成功根除。 2 4例H pylori得到根除的CAG患者 ,根除后血清EGF水平明显下降 (P <0 0 1) ,而EGFR阳性率无改变 (P >0 0 5 )。结论　H pylori感染引起胃黏膜EGFR阳性率及血清EGF水平增加 ,根除H pylori后血清EGF可恢复至正常水平 ,而胃黏膜EGFR阳性率在短期内没有明显改变     

序贯疗法和三联疗法联合益生茵根除幽门螺杆菌感染的临床对照研究

背景：近年来,幽门螺杆菌（Hp）对抗菌药物耐药的问题日益突出,研究者正不断尝试调整根除治疗方案以提高根除率。目的：评估序贯疗法和三联疗法联合益生菌根除Hp感染的疗效和安全性。方法：纳入有消化不良症状、RUT和“C-UBT均阳性且既往未接受过Hp根除治疗的患者,进入不同组别。序贯疗法组（A组,n=127）：前5d雷贝拉唑10mgbid＋阿莫西林1．0gbid,后5d雷贝拉唑10mgbid＋克拉霉素500mgbid＋替硝唑400mgbid;三联疗法＋益生菌组（B组,n=117）：（雷贝拉唑10mgbid＋阿莫西林1．0gbid＋克拉霉素500mgbid）×7d,三联活菌胶囊3粒tid×14d;标准三联疗法组（C组,n=106）：PPI和抗菌药物的剂量、用法、疗程同B组,但不加用益生菌。疗程结束后4周复查“C-UBT,同时评估症状改善和溃疡愈合情况。治疗期间观察不良反应发生情况。结果：A、B两组Hp根除率（ITT分析：82．7％、78．6％对63．2％;PP分析：83．3％、79．3％对65．0％）和症状缓解率（82．7％、84．6％对65．1％）均显著高于C组（P〈0．05）,A、B组问差异无统计学意义。三种方案的消化性溃疡痊愈率无明显差异（72．7％、67．6％和45．5％,P〉0．05）。B组不良反应发生率显著低于A、C两组（4．3％对15．0％和20．8％,P〈0．05）。结论：与标准三联疗法相比,序贯疗法和三联疗法联合益生菌能明显提高Hp根除率,其中三联疗法联合益生菌安全性更高,可能更适用于临床。