益生菌联合铋剂四联疗法对不同分型幽门螺杆菌根除率的影响CSCD

目的 探讨益生菌联合铋剂四联疗法对不同分型幽门螺杆菌(Helicobacter pylori,H. pylori)根除率以及患者肠道菌群的影响,为相关治疗提供参考。方法 收集2021年12月至2022年6月因上腹部不适就诊于湖北医药学院附属随州医院消化内科门诊,证实为H. pylori感染的91例患者作为研究对象。完善胃镜、血清抗体分型检测,采集患者治疗前及治疗后粪便标本进行肠杆菌、肠球菌、双歧杆菌及乳杆菌等优势菌群的培养。根据血清抗体分型结果将患者分为H. pylori Ⅰ型组(54例)和H. pylori Ⅱ型组(37例)。H. pylori Ⅰ型组患者随机分为试验组与对照组,各27例;H. pylori Ⅱ型组患者随机分为试验组(19例)与对照组(18例)。全部对照组患者给予泮托拉唑钠肠溶胶囊、克拉霉素胶囊、阿莫西林胶囊及枸橼酸铋钾胶囊口服,疗程14 d;全部试验组患者在对照组基础上联合服用双歧杆菌三联活菌肠溶胶囊,疗程14 d。治疗结束停药4周后行14C呼气试验,结果为阴性则判定为H. pylori根除成功。比较不同分型H. pylori根除率以及感染者肠道菌群的改变。结果 H. pylori Ⅰ型感染者中试验组患者根除率显著高于对照组(100.0%vs85.2%,P<0.05)。H. pylori Ⅱ型感染者中试验组与对照组根除率比较差异无统计学意义(84.2%vs 55.6%,P> 0.05)。治疗前,H. pylori Ⅰ型组患者肠道双歧杆菌、乳杆菌、肠杆菌及肠球菌的数量均显著高于H. pylori Ⅱ型组(均P<0.05)。治疗后,H. pylori Ⅰ型和H. pylori Ⅱ型试验组中上述菌群均高于治疗前(均P<0.05)。H. pylori Ⅰ型对照组患者治疗后肠道双歧杆菌、乳杆菌及肠球菌数量低于同组治疗前,大肠埃希菌数量高于同组治疗前(均P<0.05)。治疗后,H. pylori Ⅱ型对照组患者肠道双歧杆菌数量低于同组治疗前,乳杆菌、大肠埃希菌、肠球菌数量均高于同组治疗前(均P<0.05)。治疗后,试验组中H. pylori Ⅰ型感染者肠道双歧杆菌、乳杆菌、大肠埃希菌、肠球菌数量均高于H. pylori Ⅱ型感染者(均P<0.05);对照组中H. pylori Ⅰ型感染者肠道双歧杆菌、乳杆菌及大肠埃希菌数量均高于H. pylori Ⅱ型感染者,肠球菌数量低于H. pylori Ⅱ型感染者(均P<0.05)。治疗后,H. pylori Ⅰ型组和H. pylori Ⅱ型组中试验组患者上述菌群均高于对照组(均P<0.05)。结论 在治疗H. pylori Ⅰ型感染者时添加益生菌不仅能提高H. pylori的根除率,而且有利于患者肠道菌群的恢复。在无严重胃部疾病时,对于H. pylori Ⅱ型感染者,选择定期随访有利于患者康复,若合并严重胃部疾病时可添加益生菌,虽不能提高H. pylori根除率但有利于调节肠道菌群,促使肠道微生态恢复平衡。     

不同基因型幽门螺杆菌感染与消化性溃疡患者血清炎症因子及CD4+T细胞、PINP水平的关系

目的探讨不同基因型H.pylori感染与消化性溃疡(PU)患者血清炎症因子及CD4⁺T细胞、Ⅰ型原胶原N端前肽(PINP)水平的关系,为后续研究提供参考。方法选择2017年8月至2019年3月于我院消化科就诊的122例PU患者为研究对象,其中H.pylori阴性患者50例[HP(-)组],H.pyloriⅠ型感染患者38例[HP(Ⅰ)组],H.pyloriⅡ型感染患者34例[HP(Ⅱ)组],对比各组患者血清炎症因子IL-17、IL-10、TNF-α和PINP及CD4⁺T淋巴细胞水平。采用Logistic回归对不同菌型H.pylori感染患者血清炎症因子及CD4⁺T细胞、PINP水平的相关性进行评估,并结合ROC曲线对其相应诊断价值进行评估。结果HP(-)组患者IL-17、IL-10、TNF-α水平最低,HP(Ⅰ)组患者IL-17、IL-10、TNF-α水平最高,组间差异有统计学意义(均P<0.001)。HP(-)组患者CD4⁺T细胞及PINP水平最低,HP(Ⅰ)组CD4⁺T细胞及PINP水平最高,组间差异有统计学意义(均P<0.001)。多因素Logistic回归显示,血清炎症因子及CD4⁺T细胞、PINP水平与H.pyloriⅠ型、H.pyloriⅡ型感染均有显著正相关性(均P<0.05)。ROC曲线分析显示,IL-17、IL-10、TNF-α、CD4⁺T细胞和PINP诊断H.pyloriⅠ型感染的AUC分别为0.863(95%CI:0.786~0.941)、0.844(95%CI:0.754~0.935)、0.907(95%CI:0.847~0.967)、0.921(95%CI:0.864~0.977)、0.742(95%CI:0.639~0.845),而诊断H.pyloriⅡ型感染的AUC分别为0.711(95%CI:0.599~0.823)、0.747(95%CI:0.641~0.854)、0.930(95%CI:0.874~0.986)、0.918(95%CI:0.861~0.974)、0.736(95%CI:0.631~0.840)。H.pylori阴性与CD4⁺T细胞和PINP水平无明显相关性(r=0.226,P=0.225),H.pyloriⅠ型、H.pyloriⅡ型感染与CD4⁺T细胞和PINP水平具有显著正相关性(r=0.428、0.367,P=0.007、0.033)。结论血清炎症因子及CD4⁺T细胞和PINP水平与PU患者H.pylori感染具有相关性,可作为临床辅助监测指标。     

凝结芽孢杆菌活菌片联合三联方根除幽门螺杆菌的临床研究

目的 观察和评价凝结芽孢杆菌活菌片(商品名:爽舒宝)联合三联方根除幽门螺杆菌(Helicobacter pyori,H.pylori)的疗效.方法 将90例Hpylori感染患者随机分为治疗Ⅰ组、治疗Ⅱ组和对照组,每组30例.治疗I组:常规三联方根除治疗1周的同时,口服凝结芽孢杆菌活菌片(商品名:爽舒宝),根除治疗结束后,继续服用爽舒宝1周.治疗Ⅱ组:常规根除治疗1周的同时,口服爽舒宝,根除治疗结束,继续服用爽舒宝3周.对照组:常规根除治疗1周,不用任何微生态制剂.观察记录三联方根除治疗期间和治疗结束后4周内发生的任何不良反应.结果 治疗Ⅰ组和Ⅱ组H.pylori检测值均显著低于对照组,H.pylori根除率高于对照组,差异有统计学意义(P＜0.05).治疗Ⅱ组H.pylori检测值低于治疗Ⅰ组,H.pylori根除率高于治疗Ⅰ组,差异有统计学意义(P＜0.05).三联方根除治疗中,治疗Ⅱ组和治疗Ⅰ组不良反应发生率低于对照组,差异有统计学意义(P＜0.05),治疗Ⅱ组和治疗Ⅰ组差异无统计学意义(P＞0.05).三联方根除治疗结束后4周内,治疗Ⅱ组不良反应发生率最低,其次是治疗Ⅰ组,对照组不良反应发生率最高,三组之间差异均有统计学意义(P＜0.05).结论 爽舒宝联合三联方根除H.pylori,能够提高H.pylori根除率,减少治疗过程中不良反应的发生.根除治疗结束后再服用3周的益生菌,能彻底恢复肠道菌群平衡,减少三联方根除治疗结束后不良反应的发生,值得临床推广.     

幽门螺杆菌感染的治疗进展

幽门螺杆菌(helicobacter pylori,H.pylori,HP)感染是一个世界性问题。人类感染Hp可导致慢性胃炎、胃和十二指肠溃疡、消化性胃黏膜相关的淋巴样组织淋巴瘤和胃腺癌。根除幽门螺杆菌对胃肠疾病的转归和预防有着重要作用。但是由于抗茵药物的滥用,使得对幽门螺杆茵的治疗变得棘手。本文就Hp的致病机制、耐药性问题及治疗方法等的研究进展作一综述。     

四逆汤加减联合复方嗜酸乳杆菌对幽门螺杆菌阳性十二指肠球部溃疡患者的作用

目的探讨四逆汤加减联合复方嗜酸乳杆菌对幽门螺杆菌(H.pylori)阳性十二指肠球部溃疡(DU)患者H.pylori根除率及相关指标的影响。方法选取2017年9月至2019年5月我院收治的144例H.pylori阳性DU患者,随机分为对照组(n=72)和观察组(n=72)。两组患者均给予标准四联疗法治疗,对照组患者给予复方嗜酸乳杆菌,观察组患者在对照组基础上给予四逆汤加减。统计两组患者疗效、H.pylori根除率、不良反应情况,同时对比两组患者治疗前后中医证候积分、肠黏膜功能[甘露醇(MAN)、乳果糖(LAC)、L/M]、Toll样受体5(TLR5)、干扰素γ(IFN-γ)、白细胞介素-6(IL-6)水平,并于治疗后6个月随访两组患者复发率。结果 (1)观察组患者治疗总有效率(94.44%)、H.pylori根除率(91.67%)均高于对照组(79.17%,77.78%)(均P0.05)。(2)治疗后观察组患者舌象、泛吐清水、胃痛评分均低于对照组(均P0.05)。(3)治疗后观察组患者MAN、LAC、L/M比值、TLR5、IFN-γ、IL-6水平均低于对照组(均P0.05)。(4)观察组患者不良反应发生率(5.56%)及随访6个月复发率(4.29%)与对照组(8.33%,5.80%)比较差异无统计学意义(均P0.05)。结论四逆汤加减联合复方嗜酸乳杆菌治疗H.pylori阳性DU患者的疗效确切,能有效提高H.pylori根除率,减轻患者临床症状,改善患者肠黏膜功能,降低炎症反应,安全性较高。     

益生菌辅助埃索美拉唑镁四联疗法对幽门螺杆菌阳性十二指肠溃疡患者肠道菌群分布及血清IFN\|γ、IL\|10的调节作用

目的探讨益生菌辅助埃索美拉唑镁四联疗法在幽门螺杆菌(H.pylori)阳性十二指肠溃疡中的应用价值。方法按照随机数字表将我院116例H.pylori阳性十二指肠溃疡患者(2017年12月至2019年2月收治)分为观察组与对照组,各58例。对照组患者给予常规埃索美拉唑镁四联疗法治疗,观察组患者于对照组基础上联合益生菌(双歧杆菌三联活菌胶囊)辅助治疗,两组患者均治疗4周。对比两组患者临床疗效、治疗前后肠道菌群(双歧杆菌、乳杆菌)数量及血清免疫炎症介质[干扰素-γ(IFN-γ)、白细胞介素-10(IL-10)]水平、H.pylori根除率及治疗安全性。结果 (1)观察组患者治疗有效率为93.10%(54/58),显著高于对照组的79.31%(46/58)。(2)治疗后两组患者肠道双歧杆菌、乳杆菌数量较治疗前增加,且观察组高于对照组(均P0.05)。(3)治疗后两组患者血清IFN-γ、IL-10水平均较治疗前降低,且观察组低于对照组(均P0.05)。(4)观察组患者H.pylori根除率为91.38%(53/58),显著高于对照组的70.69%(41/58)。(5)治疗期间观察组不良反应发生率为12.07%(7/58),与对照组的13.79%(8/58)比较差异无统计学意义(χ~2=0.077,P=0.782)。结论益生菌辅助埃索美拉唑镁四联疗法治疗H.pylori阳性十二指肠溃疡患者效果确切,有利于提高H.pylori根除率,其机制可能与其能改善肠道菌群分布、下调血清免疫炎症介质表达有关。     

布拉酵母对服用抗血小板药物老年幽门螺杆菌阳性患者肠道菌群及消化道出血的影响CSCD

目的评价布拉酵母(Saccharomyces boulardii,S.boulardii)联合四联疗法根除幽门螺杆菌(Helicobacter pylori,H.pylori)对服用阿司匹林老年患者的影响,并从免疫炎症及肠道菌群的角度,探讨S.boulardii治疗H.pylori感染的机制。方法选择180例年龄60~75岁且服用阿司匹林的H.pylori阳性患者,随机分为两组,其中四联组应用铋剂四联疗法,S.boulardii组在铋剂四联疗法基础上加用S.boulardii。观察两组患者H.pylori根除率、血清白细胞介素(IL)-8和IL-17水平、临床疗效评分、不良反应、肠道菌群变化。随访12个月,观察H.pylori根除成功者和H.pylori根除失败者消化道出血情况。结果(1)四联组和S.boulardii组患者H.pylori根除率按方案(PP)分析分别为85.4%、86.7%(χ^(2)=0.066,P=0.826),按意向性(ITT)分析分别为77.8%、80.0%(χ^(2)=0.133,P=0.855),差异无统计学意义。(2)S.boulardii组患者不良反应发生率低于四联组(χ^(2)=1.925,P=0.009)。(3)治疗后,两组患者血清IL-8、IL-17水平,临床症状评分均低于治疗前,且S.boulardii组低于四联组(均P<0.05)。(4)治疗后,四联组患者肠道内乳杆菌数量、双歧杆菌数量、双歧杆菌/肠杆菌值(B/E值)较治疗前降低,而S.boulardii组较治疗前增加(均P<0.05);四联组患者肠道内肠杆菌、肠球菌数量较治疗前增加(均P<0.05),而S.boulardii组较治疗前无显著变化(均P>0.05)。(5)随访12个月,H.pylori根除成功患者消化道出血发生率低于H.pylori根除失败者(χ^(2)=3.825,P<0.001)。结论S.boulardii联合四联疗法不能提高服用抗血小板药物老年患者的H.pylori根除率,但可改善患者临床症状,降低不良反应,其机制可能与S.boulardii改善肠道菌群,减轻免疫炎症反应有关。此外,成功根除H.pylori可有效降低服用抗血小板药物老年患者消化道出血的风险。     

芪芍安胃胶囊/黄柴安胃胶囊治疗消化性溃疡伴HP感染的疗效及对胃蛋白酶原、胃泌素-17的影响

目的:探讨芪芍安胃胶囊/黄柴安胃胶囊用于治疗消化性溃疡伴幽门螺杆菌(HP)感染患者的疗效,分析其对血清胃蛋白酶原(PG)和胃泌素-17(G-17)的影响。方法:选取我院于2017年10月到2019年1月收治的消化性溃疡伴HP感染患者114例,分成观察组(n=57)和对照组(n=57)。给予对照组三联疗法,观察组在对照组的基础上予以芪芍安胃胶囊或黄柴安胃胶囊,疗程均为35 d。于治疗前后检测两组血清PGⅠ、PGⅡ、PGⅠ/PGⅡ比值(PGR)和G-17水平。治疗后,两组行疗效评价,比较两组HP转阴率和1年内复发率,记录不良反应。结果:观察组总有效率94.74%,高于对照组总有效率82.46%(P0.05)。观察组HP转阴率89.47%,高于对照组HP转阴率73.68%(P0.05)。观察组1年内复发率11.11%,低于对照组1年内复发率27.66%(P0.05)。观察组不良反应发生率低于对照组(P0.05)。治疗后,两组血清PGⅠ、PGⅡ、G-17水平均低于治疗前,PGR高于治疗前,且观察组血清PGⅠ、PGⅡ、G-17水平均低于对照组,PGR高于对照组(P0.05)。结论:芪芍安胃胶囊/黄柴安胃胶囊治疗消化性溃疡伴HP感染患者具有良好的临床疗效,能够提高HP转阴率,降低1年内复发率和不良反应,并改善血清PGⅠ、PGⅡ、PGR和G-17水平。     

不同疗程布拉酵母菌在根除幽门螺杆菌中的疗效分析

目的探讨不同疗程标准三联疗法复合布拉酵母菌对根除幽门螺杆菌(Helicobacter pylori,H.pylori)疗效的影响及其对治疗中不良反应的改善情况进行系统评价。方法 H.pylori阳性的慢性胃炎、消化性溃疡患者240例,随机分为对照组、短疗程组、中疗程组、长疗程组,每组60例。对照组给予克拉霉素、阿莫西林、潘托拉唑三联治疗14 d,短疗程组、中疗程组、长疗程组在上述标准三联、14 d疗法开始治疗的同时分别加用布拉酵母菌,分别服用2、3、4周,在完成根除H.pylori治疗后第5周进行14C-UBT复查,比较各组H.pylori根除率、药物不良反应发生率,试验结果阴性患者在治疗结束后第3、6、9、12个月复查14C-尿素呼气试验。结果 213按试验设计完成治疗,194例患者按试验设计完成随访。短疗程组H.pylori根除率(73.5%)与对照组(65.9%)比较差异无统计学意义(P0.05),中疗程组(91.4%)、长疗程组(93.1%)根除率均高于对照组,差异有统计学意义(P0.05),中疗程组根除率略低于长疗程组,但差异无统计学意义。各疗程组不良反应发生率均较对照组显著降低(P0.05),但组间比较差异无统计学意义;4组方案中以中等剂量成本-效果比最低(6.56),对照组最高(7.59);各疗程组累积复发率均低于对照组低(P0.05,P0.01,P0.01),各疗程组累积复发率比较差异无统计学意义。结论联用布拉酵母菌能显著提高H.pylori根除率,降低其不良反应,3周疗程为最佳选择治疗周期。数字与后文不符。     

抗坏血酸对幽门螺杆菌相关萎缩性胃炎小鼠的干预

目的研究不同浓度抗坏血酸(ascorbic acid)溶液对幽门螺杆菌(Helicobacter pylori,H.pylori)相关萎缩性胃炎小鼠模型的作用。方法将C57BL/6小鼠随机分为5组,每组10只。组1为空白对照组,余4组小鼠用幽门螺杆菌悉尼菌株(Helicobacter pylori-Sydney strain 1,H.pylori-SS1)感染2周,快速尿素酶法和免疫组织化学法检测H.pylori-SS1的定植;组3、组4和组5小鼠分别给予抗坏血酸低倍剂量(0.1 g/L)、中倍剂量(0.5 g/L)和高倍剂量(1.0 g/L)灌胃22周。灌胃结束后,处死所有小鼠取胃组织和血清,H&E染色观察组织学变化,ELISA检测血清胃泌素(gastrin)和白介素8(IL-8)水平。结果与H.pylori组相比,抗坏血酸干预组胃组织萎缩程度减轻、血清胃泌素水平升高、炎症因子水平降低(组2 vs组3:F=21.730,P=0.029;组2 vs组3:F=42.781,P=0.015;组2 vs组3:F=35.720,P=0.021),中倍剂量组较低倍剂量组有更显著的作用(组3 vs组4:F=21.730,P=0.041;组3 vs组4:F=42.781,P=0.034;组3 vs组4:F=35.720,P=0.043),但高倍剂量组与中倍剂量组差异无统计学意义(组4 vs组5:F=21.730,P=0.125;组4 vs组5:F=42.781,P=0.391;组4 vs组5:F=35.720,P=0.450)。结论抗坏血酸干预可减轻小鼠H.pylori相关萎缩性胃炎症状,高剂量抗坏血酸与中低剂量比无显著差异。     

Effect of Helicobacter pylori eradication on peptic ulcer disease complicated with outlet obstruction

Background. At present, the prevalence of Helicobacter pylori ( H. pylori ) in complicated peptic ulcer and the effect of H. pylori eradication on complicated peptic ulcer have not been fully established. In this study, we report the prevalence of H. pylori in peptic ulcer patients complicated with gastric outlet obstruction, effectiveness of oral eradication therapy on these patients, and their long-term follow up.
Patients and Methods. Ten consecutive patients presenting with clinically and endoscopically significant obstructed peptic ulcers were included in this study. During each endoscopy, seven gastric biopsy specimens were obtained and analyzed for H. pylori colonization.
Results. The antral mucosal biopsy specimens were positive for H. pylori in nine patients. H. pylori infection was eradicated and complete ulcer healing was observed in all patients. The mean follow-up period was 14 (7–24) months. One patient had duodenal perforation and underwent surgical intervention following medical treatment, despite the eradication of H. pylori. Ulcer recurrence was noted in two (22.2%) of nine patients, and in one of them the recurrent ulcer was complicated with obstruction (11.1%). The mean time to ulcer recurrence was 17 months (range, 10–24 months). The biopsies and CLOtests were H. pylori negative at the time of ulcer or erosion recurrence in two patients.
Conclusion. We suggest that H. pylori eradication may improve the resolution in obstructive ulcer cases with colonization.     

Implication of gastrin in cyclooxygenase-2 expression in Helicobacter pylori infected gastric ulceration

Gastroduodenal ulcerations have worldwide distribution and the infection with Helicobacter pylori (HP) has been implicated in pathogenesis of this disease. The HP infection is usually accompanied by hypergastrinemia and enhanced generation of prostaglandins (PG), both implicated in the pathogenesis of peptic ulcerations but no study has been undertaken to assess the relationship between the HP infection and coexpression of gastrin and cyclooxygenases (COX), the rate limiting enzymes in the PG production. Since HP infection, usually accompanying peptic ulcerations, results in increased release of gastrin, a potent gastric mitogen that might be capable to induce COX-2 and to generate PG, we decided 1) to compare the seroprevalence of HP and its cytotoxic protein, CagA, in gastric ulcer patients with those in age- and gender-matched controls; 2) to determine the gene expression of gastrin and its receptors (CCK(B)-R) at the margin of gastric ulcer and in the mucosa of antrum and corpus before and after successful eradication of HP, 3) to assess the plasma levels and gastric luminal contents of gastrin before and after HP eradication and 4) to examine the mRNA and enzyme protein expression of COX-1 and COX-2 as well as the PGE2 generation in ulcer margin tissue and gastric antral and fundic mucosa before and after the HP eradication. The trial material included 20 patients with gastric ulcer and 40 age- and gender-matched controls. Anti-HP and anti-CagA IgG seroprevalence was estimated by specific antisera using ELISA tests. Gene expressions of gastrin, CCK(B)-R, COX-1 and COX-2 were examined using RT-PCR with beta-actin as a reference and employing Western blotting for COX-2 expression, while gastrin and PGE2 were measured by RIA. All gastric ulcers were located at smaller curvature within the antral mucosal area. The seroprevalence of HP, especially that expressing CagA, was significantly higher in gastric ulcers (85%) than in controls (62.5%). Both gastrin and CCK(B)-R mRNA were detected by RT-PCR in ulcer margin and gastrin mRNA was overexpressed in remaining antral mucosa, while CCK(B)-R mRNA was overexpressed in fundic mucosa of HP infected patients. Similarly, COX-2 mRNA and protein were found in margin of gastric ulcer and in the HP infected antral and fundic mucosa but not in the mucosa of HP eradicated patients in whom ulcers completely healed and gastrin was expressed only in antrum, CCK(B)-R only in corpus, while COX-1 was detected both in antrum and corpus. HP positive gastric ulcer patients showed about three times higher levels of plasma immunoreactive gastrin and about 50% higher luminal gastrin contents than the HP negative controls and this increased plasma and luminal gastrin was normalized following the HP eradication. A significant fall in gastrin and CCK(B)-R mRNA expression was noticed six weeks after HP eradication in gastric antral and fundic mucosa, while COX-2 mRNA completely disappeared after this treatment. We conclude that 1) HP infected gastric ulcer margin coexpresses gastrin, its receptors (CCK(B)-R), and COX-2; 2) HP infection may be implicated in gastric ulceration via increased release of gastrin that could be responsible for the overexpression of COX-2 that in turn could help ulcer healing through the stimulation of mucosal cell growth, restoration of the glandular structure and angiogenesis in the ulcer area and 3) gastrin produced in HP infected antral mucosa seems to be involved in the induction of COX-2 and PG production by this enzyme and this may contribute to the ulcer healing.     

Long-term effects of Helicobacter pylori infection on acid and pepsin secretion.

Chronic Helicobacter pylori infection causes a slight postprandial hypergastinemia, generally referred to as exaggerated or inappropriate gastrin release. This can be ablated by eradication of this infective agent. The expectations that this would further unravel the mysteries of the pathogenesis of peptic ulcer disease have not been fulfilled. It is now well established that of conventional acid secretory patterns such as basal acid secretion, maximum gastrin-stimulated acid secretion, and of sensitivity of the parietal cell to gastrin, only basal acid is modified by chronic H. pylori colonization. This particularly relates to basal secretion in duodenal ulcer patients, as basal secretion of otherwise healthy, chronically H. pylori-infected subjects appears to be affected in only a small proportion of subjects. It is of particular interest, however, that chronic H. pylori infection supplies a solid explanation why acid inhibitory pathways are deficient in duodenal ulcer disease, since this is reversible following H. pylori eradication as demonstrated by elegant studies with gastrin-releasing, peptide-stimulated acid secretion. Furthermore, it has gradually become apparent that exaggerated gastrin response is probably no more than an innocent bystander of chronic H. pylori infection. Paradoxically, in a small subset of patients, hypo-or anacidity accompanying chronic H. pylori infection can be reverted by H. pylori eradication, for currently unknown reasons.     

Long-term follow-up after eradication of Helicobacter pylori with omeprazole, clarithromycin, and tinidazole (OCT regimen) in a Japanese population

BACKGROUND: The long-term benefit of Helicobacter pylori eradication treatment that includes metronidazole on peptic ulcer disease in Japan is unclear. We investigated the rate of H. pylori re-infection and ulcer relapse after H. pylori eradication. MATERIALS AND METHODS: A total of 266 patients with endoscopically confirmed peptic ulcer disease and H. pylori infection were treated with triple therapy of omeprazole 40 mg (20 mg b.i.d.), clarithromycin 800 mg (400 mg b.i.d.), and tinidazole 1000 mg (500 mg b.i.d.) for 7 days. Endoscopy with gastric biopsy was performed before and 1 month, 6 months, 1.5 years, and 3.5 years after therapy. H. pylori status was determined by H. pylori culture, rapid urease test, and histopathology. 13C-urea breath test was done at 6 months after eradication therapy. Treatment was deemed successful when all tests were negative at 6 months after therapy by endoscopic biopsy. RESULTS: Successful H. pylori eradication was achieved in 262/266 (98.5%) patients with peptic ulcer. Total relapse of peptic ulcer occurred in 8/262 (3%) patients after eradication, with 3/262 (1.1%) occurring within 1.5 years after treatment and 5/262 (1.9%) within 3.5 years. All relapsed patients were found to be H. pylori-positive at the time of relapse. Of the 262 patients who experienced eradication, 20 (7.6%) were subsequently re-infected, six (2.3%) within 1.5 years and 14 (5.3%) within 3.5 years. CONCLUSION: Triple therapy with omeprazole, clarithromycin, and tinidazole (OCT) is useful for H. pylori eradication in Japan, but there is an appreciable re-infection rate in this population.     

Helicobacter pylori stool antigen test in patients with bleeding peptic ulcers

BACKGROUND: Helicobacter pylori has been linked to chronic gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma. Invasive tests are less sensitive than noninvasive tests in diagnosing H. pylori infection in patients with bleeding peptic ulcers. The H. pylori stool antigen test has been useful in diagnosing H. pylori in patients with peptic ulcers before and after eradication of H. pylori. The aim of this study was to evaluate the H. pylori stool antigen test in patients with bleeding peptic ulcers. METHODS: Patients with bleeding and nonbleeding peptic ulcers underwent a rapid urease test, histology, bacterial culture and H. pylori stool antigen test. Positive H. pylori infection was defined as a positive culture or both a positive histology and a positive rapid urease test. Helicobacter pylori stool antigen was assessed with a commercial kit (Diagnostec H. pylori antigen EIA Kit, Hong Kong). RESULTS: Between October 2000 and April 2002, 93 patients with bleeding peptic ulcers (men/women: 78/15, gastric ulcer/duodenal ulcer: 58/35) and 59 patients with nonbleeding peptic ulcers (men/women: 47/12, gastric ulcer/duodenal ulcer: 30/29) were enrolled in this study. Forty-seven (50.5%) patients with bleeding peptic ulcers and 30 (50.8%) patients with nonbleeding peptic ulcers, were found to be infected with H. pylori (p > .1). Helicobacter pylori stool antigen tests were positive in 54 (58.1%) and 30 (50.8%) patients with bleeding peptic ulcers and nonbleeding peptic ulcers, respectively (p > .1). The sensitivity (82% vs. 93%), specificity (68% vs. 93%), positive predictive value (74% vs. 93%), negative predictive value (77% vs. 93%) and diagnostic accuracy (75% vs. 93%) were all lower in patients with bleeding vs. nonbleeding peptic ulcers. The specificity, positive predictive value, and diagnostic accuracy of the H. pylori stool antigen test in patients with bleeding peptic ulcers were significantly lower than those in patients with nonbleeding peptic ulcers (p = .01, p = .02 and p = .003, respectively). CONCLUSION: The H. pylori stool antigen test is not reliable for diagnosing H. pylori infection in patients with bleeding peptic ulcers.     

The results of Helicobacter pylori eradication on repeated bleeding in patients with stomach ulcer

The triple therapy of Helicobacter pylori eradication prevents repeated bleeding from stomach ulcer. The aim of this one-way blind prospective study was to evaluate the efficiency of the two-week triple therapy for Helicobacter pylori eradication in preventing renewed bleeding in patients with stomach ulcer within one year. This research included 60 hospitalized patients with bleeding stomach ulcer and positive Helicobacter pylori infection, 34 men and 26 women (average age 59.7 years). The patients were given therapeutic scheme of omeprazol--amoxicilin--metrodinazol (OAM) eradication for 14 days. Eradication of H. pylori infection was defined as lack of proof of the infection one month or several months after therapy suspension. By applying triple OAM therapy within two weeks the eradication was successful in 72%. In the group of 17 H. pylori positive patients there were 8 patients (47.6%) with repeated stomach ulcer and 3 patients (18%) with bleeding. Within the group of 43 H. pylori negative patients there were only 2 patients (4.65%) with repeated stomach ulcer and 1 patient (2%) with bleeding, during the observed period of 12 months. This research confirms the hypothesis about the necessity of eradication of Helicobacter pylori infection in patients with bleeding stomach ulcer as prevention of repeated bleeding.     

Cost effectiveness of screening for and eradication of Helicobacter pylori in management of dyspeptic patients under 45 years of age.

OBJECTIVE--To assess the cost effectiveness of screening for and eradicating Helicobacter pylori in patients under 45 years of age presenting with dyspepsia. DESIGN--A decision analytic model composed of a decision tree to represent the epidemiology of dyspepsia and a Markov process to model the outcomes of treatment. PATIENTS--Patients under the age of 45 years presenting to their general practitioner with (peptic type) dyspepsia. INTERVENTIONS--Conventional empirical treatment with healing and maintenance doses of cimetidine v eradication treatment solely in patients with confirmed peptic ulcer; and conventional empirical treatment for all dyspeptic patients compared with the use of a serology test to identify patients with H pylori, who then receive endoscopy to investigate the presence of peptic ulcer disease and, when disease is found, are given eradication treatment with a breath test to confirm successful eradication. MAIN OUTCOME MEASURES--Expected cumulative costs over a period of 10 years. The proportion of time patients spend without a recurrent ulcer. RESULTS--After receiving eradication treatment, patients with confirmed ulcer spend an average of 99% of their time free from recurrent ulcer disease compared with 95% after treatment with cimetidine. Eradication treatment costs less than that with cimetidine. When the initial cost of identifying appropriate patients to receive eradication treatment is added to the analysis, however, these cost savings take almost eight years to accrue. CONCLUSIONS--Enthusiasm for introducing testing for and eradication of H pylori for dyspeptic patients in general practice should be tempered by an awareness that cost savings may take many years to realise.     

中西医结合治疗消化性溃疡并H.yilori感染的效果分析

目的：研究消化性溃疡并幽门螺杆菌(H3pylori )感染初治失败患者血浆网膜素-1 (Omentin-1)水平的变化及中西医结合干预 治疗的效果。方法：选择2011 年9 月～2015 年9 月在我院进行诊治的消化性溃疡患者82 例观察组,采用阿莫西林,奥美拉唑、拉 霉素和清幽口服液等中西医结合治疗,并选择20 例健康体检者为对照组。采用ELISA 法检测血浆Omentin-1 水平,分析血浆 Omentin-1 水平与一氧化氮（NO）、白细胞介素-2（IL-2）、内皮素-1(ET-1)、肿瘤坏死因子alpha（TNF-alpha）的关系。观察中西医结合治疗 前后病例组血浆Omentin-1 水平的变化并评价根除的疗效及安全性。结果：进行中西医结合治疗后, H.pylori根除率达 88.6%;有34 例溃疡痊愈,22 例显效,33 例有效,3 例无效,愈合率为68.29% (56 /82),有效率为96.34% (79/82);观察组血浆 Omentin-1 水平为(18.15 ± 3.96) ng/mL,明显低于对照组的(23.12 ± 6.03) ng /mL(P<0.05);与对照组相比,观察组的NO、IL-2 水 平明显降低(P<0.05),ET-1,TNF-alpha和IL-6 水平明显升高(P<0.05);与治疗前相比,经中西医结合治疗后NO、IL-2 水平明显降低 (P<0.05),ET-1,TNF-琢和IL-6 水平明显升高(P<0.05);观察组血浆Omentin-1 与IL-2、NO 呈明显正相关( r = 0.412,P<0.05 和r = 0.382,P<0.05),与IL-6 和TNF-琢呈明显负相关( r =-0.246,P<0.05 和r = -0.258,P<0.05)。结论：中西医结合治疗能升高血浆 Omentin-1 水平,有效提高溃疡愈合率及H.pylori根除率,抑制炎性因子的分泌,增强内源性NO保护作用和机体免疫功能。     

Characteristics of Helicobacter pylori-induced gastritis and the effect of H. pylori eradication in patients with chronic idiopathic thrombocytopenic purpura

BACKGROUND: The association between Helicobacter pylori infection and idiopathic thrombocytopenic purpura (ITP) has been reported widely. We investigated the prevalence of H. pylori infection, its virulence profile and the effectiveness of its eradication in patients with ITP. MATERIALS AND METHODS: Twenty patients with ITP, 20 with peptic ulcer (10 gastric ulcer (GU), 10 duodenal ulcer (DU)) and 20 with NUD were studied. The virulence profile of the strains was assessed by genotyping for cagA, vacA, iceA, and hpyIIIR/hrgA and by assaying for IL-8 and DNA fragmentation after incubation with AGS cells. Infected patients and two uninfected ITP patients received triple therapy and platelets were counted before and 1 month, 6 months, 1 year, and 2 years after eradication therapy. RESULTS: H. pylori infection was found in 17 ITP (85%), 20 ulcer (100%) and 13 NUD (65%) patients. Biopsies and strains were collected from five ITP, 20 ulcer and 13 NUD patients. The ITP patients had a pangastritis or corpus-predominant gastritis pattern. All H. pylori isolates, from ITP, ulcer and NUD patients, were cagA(+) and vacA s1/m1, and did not differ in levels of IL-8 induction or DNA fragmentation. Fifteen ITP (88%) and 17 ulcer (85%) patients had successful eradication of H. pylori. Ten of these 15 (67%) H. pylori-eradicated ITP patients had platelet recovery. There was no significant change in platelet count in the two ITP patients in whom eradication failed or in the two originally H. pylori-uninfected ITP patients, or in the treated ulcer patients. Age at onset of ITP was the main determinant of platelet recovery: 100% of patients diagnosed after the age of 60 recovered compared with only 22% of those diagnosed before 50. CONCLUSIONS: H. pylori-infected ITP patients have a corpus-predominant pattern of gastritis but the virulence profile of their strains does not differ from that of ulcer or NUD patients. Eradication of H. pylori infection is a good therapeutic option for some patients with chronic ITP, especially for those who develop ITP in older age.