老年胃溃疡抗幽门螺杆菌治疗的预后观察

目的　 探讨老年人胃溃疡抗幽门螺杆菌 (Hp)治疗后的预后情况。　 方法 　将胃溃疡患者分为老年组及青年组 ,予兰索拉唑 (达克普隆 ) ,阿莫西林 ,甲硝唑抗Hp三联治疗。 4周及 1年后复查胃镜及病理学检查 ,了解溃疡的愈合及Hp根除情况。　 结果　老年组平均年龄 65岁 ,青年组平均年龄 32岁。治疗结束后 ,4周后 2组溃疡愈合率分别为 94%、96% ,1年后分别 78%、87% ,Hp根除率 4周后分别为 83%、86% ,1年后分别 76%、70 %。2组差异无显著性 (P >0 0 5 )。Hp根除患者中 ,2组溃疡愈合率 4周后均为 10 0 % ,1年后分别为 89%、95 % ,Hp未根除患者中 ,2组溃疡愈合率 4周后分别为 67%、75 % ,1年后分别为 42 % ,69%。Hp根除与未根除患者溃疡愈合差异有显著性 (P <0 0 5 )。　 结论　老年人胃溃疡患者于抗Hp治疗后 ,溃疡愈合率及Hp根除率与青年人相仿。根除Hp有利于胃溃疡愈合     

根除幽门螺杆菌对胃溃疡愈合质量及复发的影响研究

目的探讨幽门螺杆菌（Helicobacter pylori，Up）对胃溃疡愈合质量及复发的影响。方法120例坳阳性活动期胃溃疡患者，口服泮托拉唑、阿莫西林、甲硝唑一周后，继续口服泮托美拉唑5周。治疗结束后复查胃镜取病理组织学检查并检测Hp根除情况，对比却根除组与却根除失败组内镜下溃疡愈合形态差异和愈合质量（包括内镜下再生黏膜成熟度和再生黏膜组织学成熟度）。所有患者随诊1年以上了解溃疡复发情况。结果治疗后92例胃溃疡患者月p检测阴性，坳根除率为80．43％；却根除组与跏根除失败组在内镜下愈合率方面的差异无显著性意义（P〉0．05），但两组在再生黏膜成熟度和再生黏膜组织学成熟度方面的差异有显著性意义（P〈0．01）。坳根除组1年溃疡复发率为4．35％，却根除失败组为21．43％，两组差异有显著性意义（P〈0．05）。结论根除Hp可提高胃溃疡的愈合质量，减少溃疡病复发。     

幽门螺杆菌相关性胃溃疡治疗前后多胺含量的变化

目的探讨根除幽门螺杆菌(Hp)后,胃黏膜组织中多胺含量的变化及意义。方法Hp阳性胃溃疡患者58例,测定根除Hp前后胃黏膜多胺含量及组织学检查。结果Hp阳性患者多胺含量明显高于阴性者,根除Hp后显著下降。结论根除Hp感染能够降低胃黏膜的增殖活性,从而降低胃癌的危险性。     

幽门螺杆菌感染并发胃溃疡临床特点及规范治疗探讨

目的对幽门螺杆菌感染并发胃溃疡临床特点及规范治疗进行研究探讨。方法随机抽取2013年2月~2014年4月本院消化内科接诊的96例幽门螺杆菌感染并发胃溃疡患者作为研究对象,按照随机数表法将其分为观察组和对照组,每组各48例,对照组采取胶体果胶铋、阿莫西林、奥美拉唑三联疗法治疗,观察组患者在对照组的基础上加用替硝唑,观察并比较两组患者临床疗效及药物不良反应。结果观察组总有效率为97.9%,Hp根除率95.8%明显高于对照组85.4%,70.8%,复发率10.4%明显低于对照组29.2%,组间比较差异具有统计学意义(P0.05),两组患者不良反应发生率比较差异无统计学意义(P0.05)。结论应用质子泵抑制剂、胃黏膜保护剂和两种抗生素联合治疗Hp感染并发胃溃疡可显著提高临床疗效和Hp根除率,降低复发率,且未增加患者不良反应,值得临床推广应用。     

替普瑞酮辅助治疗老年幽门螺杆菌阳性胃溃疡疗效分析

目的探讨替普瑞酮辅助治疗老年幽门螺杆菌（Hp）阳性胃溃疡患者的疗效。 方法选取2019年6月至2021年6月在谷城县人民医院确诊的100例Hp感染伴胃溃疡患者,其中50例予四联疗法治疗（对照组）,余50例在其基础上联合口服替普瑞酮（观察组）,均持续治疗2周。比较两组临床疗效、胃蛋白酶原Ⅰ（PGⅠ）、胃泌素-17、白细胞介素-8（IL-8）和肿瘤坏死因子-α（TNF-α）水平和不良反应。计数资料比较采用χ²检验,计量资料比较采用t检验。 结果两组患者治疗总有效率的差异无统计学意义（χ²=0.298,P>0.05）。治疗后,两组患者胃蛋白酶原Ⅰ和胃泌素-17均较治疗前升高（观察组：t=15.789、24.325,对照组：t=12.612、13.452,P<0.05）,且观察组较对照组升高更加显著（t=2.299、6.050,P<0.05或0.01）;两组TNF-α和IL-8均较治疗前降低（观察组：t=51.065、16.228,对照组：t=24.701、6.819,P<0.05）,且观察组较对照组降低更加显著（t=29.360、13.767,P<0.01）。治疗期间两组不良反应发生率的差异无统计学意义（χ²=0.444,P>0.05）。 结论对于老年Hp阳性胃溃疡患者,替普瑞酮辅助治疗可降低患者胃黏膜损伤水平和炎症水平,有利于患者康复。     

中西医结合治疗幽门螺杆菌阳性消化性溃疡的临床研究

将幽门螺杆菌（HP）阳性消化性溃疡62例随机分为3组，分别用灭幽丸、抗生素三联和中西药联合进行治疗。结果显示，中药组（灭幽丸）溃疡愈合率为80．95％，HP根除率76.19％；西药组（丽珠得乐＋甲硝唑＋四环素）溃疡愈合率75．00％，HP根除率90．00％；联合组（灭幽丸＋西药组用药）愈合率90．48％，HP根除率95．24％。活动性胃炎消失率中药组（23．80％）和联合组（28．57％）优于西药组（15.00％）。中药组和联合组副作用亦明显少于西药组。     

胃复春联合三联疗法治疗幽门螺杆菌阳性胃溃疡临床观察

[目的]观察胃复春联合三联疗法（枸橼酸铋雷尼替丁片、阿莫西林分散片、克拉霉素缓释片）对幽门螺杆菌（Hp）阳性胃溃疡的临床疗效,及对Hp根除率、胃泌素（GAS）、胃动素（MTL）的影响.[方法]将Hp阳性的胃溃疡患者176例随机分为两组,治疗组92例、对照组84例.对照组使用三联疗法,治疗组在对照组基础上加服胃复春;服药10天后,对照组单独口服枸橼酸铋雷尼替丁片4周;治疗组在服用枸橼酸铋雷尼替丁片基础上加服胃复春片4周.观察两组的临床疗效、Hp根除率、胃泌素、胃动素水平.[结果]治疗组总有效率95.65 ％,优于对照组,差异有统计学意义（P＜0.05）;治疗组Hp根除率91.30％,优于对照组,差异有统计学意义（P＜0.05）;治疗组治疗后胃泌素水平低于治疗前水平,亦低于对照组治疗后水平,其差异均有统计学意义（P＜0.05）.[结论]胃复春联合三联疗法抗Hp治疗方案能有效根除幽门螺杆菌,降低胃泌素水平,对幽门螺杆菌阳性胃溃疡能起到较好的治疗效果.     

幽门螺杆菌的根除及其在十二指肠溃疡愈合和复发中的作用

幽门螺杆菌的根除及其在十二指肠溃疡愈合和复发中的作用胡伏莲，黄志烈，王菊梅，贾博琦，刘新光，谢鹏雁幽门螺杆菌（Ｈｐ）与十二指肠溃疡病关系密切，然而Ｈｐ在十二指肠溃疡发病中的作用目前意见尚不一致。本研究的目的不仅要观察质子泵抑制剂奥美拉唑（ｏｍｅｐｒａ...     

治疗的依从性、年龄、性别对胃溃疡患者使用三联7天疗法根除幽门螺杆菌治疗的影响

目的研究胃溃疡患者使用三联7天疗法治疗幽门螺杆菌（Helicobacter pylori,H.pylori）感染的根除率,评估患者依从性、年龄、性别对于此类人群根除H.pylori治疗的影响。方法将经胃镜检查确诊为新发胃溃疡,并经活组织病理学检查明确有H.py-lori感染的1 075例患者纳入研究范围,所有入选患者均接受三联（洛赛克或耐信20 mg/次、2次/天,联合克拉霉素500 mg/次、2次/天,与阿莫西林1 000 mg/次、2次/天）7天疗法行根除H.pylori治疗,之后予以耐信或洛赛克20 mg/次、1次/天、治疗49天。所有入选患者系统治疗完成后6-8周复查胃镜。结果40-59岁与60岁以上人群的胃溃疡患者对治疗的依从性差异无显著性,而40岁以下人群对治疗的依从性较差（P〈0.05）。〈40岁、40-59岁和≥60岁胃溃疡患者的H.pylori根除率分别为61.0%、72.7%和81.9%。〈40岁与40-59岁和≥60岁患者的H.pylori根除率差异有统计学意义（P〈0.05）。不同性别胃溃疡患者的H.pylori根除率差异无显著性（P〉0.05）。结论使用三联7天疗法治疗胃溃疡患者的H.pylori感染,H.pylori的根除率较低,患者对治疗的依从性、年龄是影响胃溃疡患者H.pylori根除率的重要因素,而性别对此无影响。     

幽门螺杆菌相关胃溃疡的细胞增殖与凋亡研究

目的观察Ｈｐ感染对胃溃疡（ＧＵ）患者胃粘膜上皮细胞增殖与凋亡的影响,进而对溃疡发生机制进行探讨．方法标本取自内镜下胃粘膜活检,细胞凋亡检测采用Ｔｕｎｅｌ方法,细胞增殖检测采用免疫组化ＬＳＡＢ方法测定增殖细胞核抗原（ＰＣＮＡ）．结果ＧＵＨｐ＋患者细胞凋亡指数（ＡＩ）明显高于Ｈｐ－患者（Ｐ＜００５）,但比较两者的增殖细胞指数（ＰＣＮＡＬＩ）,无显著性差异（Ｐ＞００５）;慢性浅表性胃炎Ｈｐ＋患者ＡＩ,ＰＣＮＡＬＩ明显高于Ｈｐ－患者（Ｐ＜００５）,ＧＵＨｐ＋患者的ＡＩ／ＰＣＮＡＬＩ比值为１５４１,明显高于其他各组（Ｐ＜００５）．结论Ｈｐ感染能诱导ＧＵ患者胃粘膜上皮细胞凋亡增加,出现细胞凋亡与细胞增殖平衡失调,促进溃疡形成     

消化性溃疡患者Hp感染与粘膜血流量

目的研究幽门螺杆菌（Ｈｐ）感染与消化性溃疡（ＰＵ）胃肠粘膜血流量（ＧＤＭＢＦ）的关系．福建省立医院消化内科福建省福州市３５０００１方法采用多普勒激光血流仪测定内镜检查患者的非病灶区贲门、胃体、胃窦部及溃疡或胃炎病灶区的ＧＤＭＢＦ．结果非病灶区ＧＤＭＢＦ以贲门部最高，胃体部次之，胃窦部较低，分别为１．６８±０５５Ｖ，１７０±０４２Ｖ和１３５±０３７Ｖ，均明显高于ＰＵ病灶区０８９±０３３Ｖ（Ｐ＜００１）；伴有Ｈｐ感染的ＰＵ患者病灶区及其它非病灶区ＧＤＭＢＦ均显著低于不伴Ｈｐ感染者．结论Ｈｐ感染可造成胃肠粘膜血流量降低，可能是溃疡病灶难愈或复发的原因之一．     

幽门螺杆菌根除疗法治疗慢性特发性血小板减少性紫癜的疗效预测

目的:观察抗幽门螺杆菌三联疗法治疗Hp阳性的慢性特发性血小板减少性紫癜的疗效,并分析抗Hp治疗后,血小板应答的预测因子.方法:59例Hp阳性的慢性特发性血小板减少性紫癜患者,随机分组为抗Hp组和安慰剂对照组,对照组在随访3个月后给予三联抗Hp治疗.每例患者治疗前检测血清CagA蛋白浓度.结果:抗Hp组有效率明显高于对照...     

胃癌与十二指肠溃疡患者血清胃蛋白酶原比较

目的 比较胃癌患者与十二指肠溃疡患者血清胃蛋白酶原水平的差异及探讨其与H．pylori感染的关系。方法 采用时间分辨荧光免疫分析方法检测108例胃癌和96例十二指肠溃疡患者血清胃蛋白酶原Ⅰ、Ⅱ（PGⅠ，PGⅡ），ELISA方法检测血清H．pylori抗体。结果 胃癌和十二指肠溃疡患者之间PGⅠ水平有显著性差异，胃癌组和十二指肠溃疡组中H．pylori阳性和阴性间PGⅠ、PGⅡ、PGⅠ，PGⅡ水平等无显著性差异。结论 胃癌患者血清PGⅠ水平显著低于十二指肠溃疡患者，H．pylori感染对胃癌和十二指肠溃疡患者血清胃蛋白酶原水平和PGⅠ，PGⅡ比值均无影响。     

A pilot study to evaluate a new combination therapy for gastric ulcer: Helicobacter pylori eradication therapy followed by gastroprotective treatment with rebamipide

Background and Aim: Controversies remain over the need for antiulcer treatment following 1‐week eradication triple therapy for Helicobacter pylori‐positive peptic ulcers. The usefulness of combination therapy for gastric ulcers in Japanese patients, which consists of H. pylori eradication followed by gastroprotective therapy with rebamipide, was therefore evaluated. Methods: The study was conducted in 52 H. pylori‐positive patients with an endoscopically‐proven open gastric ulcer. All patients received 1‐week triple therapy (lansoprazole, amoxicillin and clarithromycin) followed by 7‐week rebamipide therapy. After completion of the combination therapy, all patients underwent evaluation of ulcer healing by endoscopy, gastric ulcer symptoms and H. pylori eradication by rapid urease test and ¹³C‐urea breath test. Results: The ulcer healing rates were 85.7% (36/42) at 8 weeks, 83.3% (30/36) in eradicated patients and 100% (6/6) in non‐eradicated patients. The overall gastrointestinal symptom‐free rate improved from 19.0% at baseline to 88.1% at 8 weeks. H. pylori was effectively eradicated in 85.7% (36/42) of patients. Conclusions: The results suggested that the combination therapy for open gastric ulcer was safe, well‐tolerated and effective. However, data from a double‐blind placebo‐controlled study is necessary to confirm these findings.     

兰索拉唑、羟氨苄青霉素、替硝唑联合根除幽门螺杆菌的疗效观察

目的评价兰索拉唑（达克普隆）、羟氨苄青霉素、替硝唑三联疗法对幽门螺杆菌（Ｈｐ）相关性消化性溃疡的疗效。方法将８７例Ｈｐ阳性的十二指肠和（或）胃溃疡患者随机分为２组：第１组４３例,每次口服兰索拉唑３０ｍｇ、羟氨苄青霉素１０００ｍｇ、替硝唑５００ｍｇ,均每日２次,２周为一疗程;第２组４４例,给药方式同第１组,只是疗程缩短为１周,疗程结束后继续每日口服兰索拉唑３０ｍｇ,持续１周。疗程结束达４周时复查胃镜及Ｈｐ。３５例Ｈｐ根除后６个月行１４Ｃ－尿素呼气试验（ＵＢＴ）。结果第１组有３例因过敏性皮疹而退出观察,４０例用于统计学分析。第１组和第２组的Ｈｐ根除率分别为９００％和８１８％,十二指肠溃疡和胃溃疡的愈合率分别为９２５％和８８６％。６个月的Ｈｐ再感染率为８６％。结论第１组Ｈｐ根除率和溃疡愈合率均略高于第２组,两组相比差异无显著性（Ｐ＞００５）。两组均有较理想的溃疡愈合率和Ｈｐ根除率。     

Lewis blood genotypes of peptic ulcer and gastric cancer patients in Taiwan

AIM: The Lewis b (Leb) antigen has been implicated as a possible binding site for attachment of Helicobacter pylori (H pylori) to gastric mucosa. However, studies both supporting and denying this association have been reported in the literature. Differences in secretor (Se) genotype have been suggested as a possible reason for previous discrepancies. Therefore, we investigated the relationship between Le and Se genotypes and H pylori infection rates in people with peptic ulcer or gastric cancer. METHODS: Peripheral blood samples were obtained from 347 patients with endoscopic evidence of peptic ulcer disease (235 cases of duodenal ulcer, 62 of gastric ulcer, and 50 of combined duodenal ulcer/ gastric ulcer) and 51 patients with gastric cancer on endoscopy. Peripheral blood specimens from 101 unrelated normal volunteers were used as controls. Lewis phenotype was determined using an antibody method, whereas Le and Se genotypes were determined by DNA amplification and restriction enzyme analysis. Gastric or duodenal biopsies taken from patients with endoscopic evidence of peptic ulcer or gastric cancer were cultured for H pylori. Isolates were identified as H pylori by morphology and production of urease and catalase. The H pylori infection status was also evaluated by rapid urease test (CLO test), and urea breath test (13C-UBT). Results of studies were analyzed by chi-square test (taken as significant). RESULTS: H pylori was isolated from 83.7% (303/347) of patients with peptic ulcer disease. Statistical analysis did not show any significant difference in Lewis phenotype or genotype between patients with and without H pylori infection. No significant association was found between Lewis genotype and peptic ulcer or gastric cancer. CONCLUSION: Lewis blood genotype or phenotype may not play a role in the pathogenesis of H pylori infection. However, bacterial strain differences and the presence of more than one attachment mechanism may limit the value of epidemiological studies in elucidating this matter.     

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.