Effect of the eradication of Helicobacter pylori on peptic ulcer healing

Acid suppressive therapy with H2 receptor antagonist or proton pump inhibitor can hardly shift peptic ulcers to S2 stage (white scar). As a result, judgement of ulcer healing has been made at S1 stage (red scar). However, it has been a problem that many ulcer scars relapse. Helicobacter pylori eradication therapy can prevent peptic ulcers from relapsing. The eradication therapy shifted 92% gastric ulcers from all stages to S2 stage after 24 months. We has divided S1 stage categorized by conventional endoscopy into H3-C stage (with small defect of mucosa) and S1-C stage by dye contrast method. The ulcers at H3-C stage relapse more frequently than those at S1-C stage. The acid suppressive therapy shifted only 7%, 15% gastric ulcers at H3-C stage, S1-C stage to S2-C stage after 6 months, respectedly. On the other hand, the eradication therapy shifted 56%, 65% gastric ulcers at H3-C stage, S1-C stage to S2-C stage, respectedly. It may be one reason why the eradication therapy prevents peptic ulcers from relapsing that the therapy shifts almost peptic ulcers to S2 stage.     

A randomized comparison of triple therapy Helicobacter pylori eradication regimens in children with peptic ulcers

An open, randomized trial was performed to compare the efficacy of three Helicobacter pylori eradication regimens in children with peptic ulcer disease. A total of 106 children (5 - 15 years) were treated for 1 week with metronidazole, 30 - 40 mg/kg per day depending on age, amoxycillin, 750 mg/day, and one of three anti-secretory agents: proprietary omeprazole, 20 - 40 mg/day depending on age; generic omeprazole, 20 - 40 mg/day; or ranitidine, 150 mg twice daily. The H. pylori eradication rate was significantly higher in patients receiving proprietary omeprazole (88.9%) than in those receiving generic omeprazole (80.0%) or ranitidine (74.3%), and this was associated with a trend towards faster ulcer healing. It is concluded that triple therapy consisting of an anti-secretory agent and two antimicrobials produces effective eradication of H. pylori and ulcer healing in children with peptic ulcer disease, and that proprietary omeprazole is more effective than both ranitidine and the generic formulation used in this study.     

Strategies for peptic ulcer healing after 1 week proton pump inhibitor-based triple Helicobacter pylori eradication therapy in Japanese patients: differences of gastric ulcers and duodenal ulcers

Helicobacter pylori (H. pylori) eradication therapy alone is insufficient to ensure healing of large ulcers with H. pylori-positive gastric ulcer (GU). The question of what is the optimum antiulcer treatment following H. pylori eradication therapy has not been fully elucidated. Furthermore, the ulcer healing effects of eradication therapy itself with H. pylori-positive duodenal ulcer (DU) have not been investigated. In GU study, the eradication therapy + proton pump inhibitor (PPI) group (group A) were administered eradication therapy followed by 7 weeks of a PPI, and the eradication therapy + gastroprotective drug (GP) group (group B) eradication therapy followed by 7 weeks of a GP. In DU study, the eradication therapy + PPI group (group C) were administered eradication therapy followed by 5 weeks of a PPI, and the eradication therapy only group (group D) was eradication therapy alone. In GU study, healing rates for ulcer of ≥15 mm in diameter were significant greater in the group A. In DU study, high healing rates were seen both the group C and D. In conclusion, a PPI could significantly heal GU than a GP after eradication therapy in GU. Meanwhile, the eradication alone is sufficient for DU.     

Improvement in gastric histology following Helicobacter pylori eradication therapy in Japanese peptic ulcer patients

We aimed to determine if successful or failed eradication of Helicobacter pylori with triple therapy causes any difference in gastric mucosal histology. Japanese H. pylori-positive patients with a healed peptic ulcer received high (n = 112) or low (n = 113) doses of triple therapy (omeprazole, amoxicillin and clarithromycin) for 1 week. Biopsies from the greater curvature of the central antrum and upper corpus were taken 6 weeks and 30 weeks after treatment completion, and gastric mucosal histology compared between successful (n = 171) and failed (n = 34) eradication groups. Morphological variables of gastritis were graded according to the updated Sydney System. Successful eradication therapy was defined as improvement in inflammation, neutrophil activity and atrophy; failed eradication therapy as improvement in inflammation and neutrophil activity only. Gastric mucosal atrophy gradually improved (in addition to improvements in inflammation and neutrophil activity) with successful eradication of H. pylori infection.     

Anti-ulcer therapy after eradication of Helicobacter pylori

Helicobacter pylori (H. pylori) infection is the cause of the frequent relapse of peptic ulcer disease. Successful eradication therapy of H. pylori is associated with a decline in the recurrence of peptic ulcer. In this paper, we discussed the significance of anti-ulcer therapy after H. pylori eradication therapy. In patients with duodenal ulcer, maintenance therapy for preventing ulcer recurrence is not necessary because the rate of ulcer recurrence after eradication therapy is very low. However, in patients with gastric ulcer, the rate of ulcer relapse and reflux esophagitis ranges between 5-10% in the Japanese population even after successful eradication therapy; therefore, maintenance therapy for 1 year may be permissible in patients with gastric ulcer even after successful eradication therapy.     

Side effects of Helicobacter pylori eradication therapy

The authors found that antihelicobacter therapy is accompanied by various side-effects, such as allergic reactions, gastrointestinal disturbances, dysbacteriosis, hematological disorders, and sometimes toxic hepatic lesions, depending on what antibiotic and in what doses is applied, as well as on the duration of antibiotic therapy.     

Tailor-made medicine in Helicobacter pylori eradication therapy

Pharmacokinetic profiles of omeprazole and lansoprazole were well correlated with the CYP2C19 genotype. The heterozygous extensive metabolizer was slightly different from the homozygote, but there was no statistically significant difference. The CYP2C19 genotype dependence found for lansoprazole was not obvious compared with omeprazole. As for rabeprazole, the pharmacokinetic profile was independent of the CYP2C19 genotype. CYP2C19 genotyping can provide a new strategy to choose an optimal regimen, and this genotyping is especially useful for Japanese, as the frequency of poor metabolizers is five times greater than that found among Caucasians. However, we should be aware that the increase of antimicrobial-resistant strains of H. pylori may force us to examine antimicrobial susceptibility of all patients in order to achieve a more than 80% eradication rate at first-line therapy in the near future. We should also have proper knowledge of the influence of the CYP2C19 genetic polymorphism on treatment efficacy according to the variety of PPI and the combination with other drugs.     

左克胶囊三联疗法根除幽门螺杆菌感染

目的观察左氧氟沙星短程三联疗法根除幽门螺杆菌（Hp）感染的疗效。方法100例Hp阳性患者[A组，男62例，女38例；年龄（59±11）岁；十二指肠球部溃疡（DU）62例，胃溃疡（GU）38例]给予泮托拉唑40mg，po，bid，左氧氟沙星200mg及阿莫西林1000mg，po，bid。另102例Hp阳性患者[B组，男59例，女43例；年龄（57±9）岁；DU58例，GU44例]给予泮托拉唑40mg，克拉霉素500mg及阿莫西林1000mg，po，bid。疗程均为1周。疗程结束后4～6周复查胃镜及Hp。结果A、B两组抗Hp治疗结束后4—6周停用PPI2周后，Hp根除率各为87％、79％（P〉0．05），均无严重不良反应。结论Hp耐药菌株多见，左旋氧氟沙星联合奥美拉唑和阿莫西林是一种安全、疗效高、耐受性好的治疗Hp感染的方案。     

Effects of eradication therapy on gastric emptying in patients with Helicobacter pylori-positive duodenal ulcers

In this study 28 patients with Helicobacter pylori-positive duodenal ulcers were treated with a 7-day triple-therapy regimen (omeprazole, clarithromycin, amoxycillin). Gastric emptying time was measured scintigraphically before and after therapy. Only 13 patients attended regularly for their endoscopic and scintigraphic follow-ups. Gastric emptying time was 57.6+/-16.5 min in 28 patients before therapy, and 44.4+/-13.9 min after therapy (44.7+/-7.9 min in the control group). The present study demonstrated gastric emptying time to be longer in the ulcer patients compared with healthy controls and that, after eradication therapy, gastric emptying time became almost normal in the ulcer patients.     

消化性溃疡患者根治幽门螺杆菌和反流性食管炎的关系

目的　通过对消化性溃疡 (PU)患者根治幽门螺杆菌 (Hp)前后胃窦和食管下段黏膜病理及感染情况的分析 ,探讨Hp和反流性食管炎 (RE)的关系。方法　随机复查 10 5例PU患者 ,其中 74例用三联方案 (铋剂 +阿莫西林 +甲硝唑或呋喃唑酮 )根治Hp ,3个月后取胃窦和食管下段黏膜标本作组织学和Hp检查。RE按中国烟台试行标准进行分级。结果　 10 5例PU治疗前合并RE(I级 ) 2例 ,胃窦黏膜Hp阳性 74例 ,经抗Hp治疗后胃窦黏膜Hp转阴者 4 5例 ,发生胃镜RE(I级 ) 5例 ,组织学RE(轻度 ) 7例 ;胃窦黏膜Hp持续阳性者 2 9例 ,发生胃镜RE(I级 ) 2例 ,组织学RE(轻度 ) 4例。食管下段黏膜两组Hp均为阴性。虽然Hp转阴组发生胃镜RE和组织学RE数略高 ,但两组RE发生率差异无统计学意义 (P >0 .0 5 )。此外 ,检测 112例各级RE患者食管下段黏膜Hp感染情况 ,Ⅰ、Ⅱ、Ⅲ级RE的阳性率分别为 0 %、15 .5 5 %和 30 .77% ,三者间差异有统计学意义 (P <0 .0 1)。结论　PU根治Hp后转阴患者RE的发生率无明显升高 ,提示PU抗Hp治疗后RE的发生与胃窦黏膜是否感染Hp无明显关系。而RE的病变程度与食管下段黏膜Hp感染有一定关联     

Role of Helicobacter pylori eradication in the prevention of peptic ulcer in NSAID users

Helicobacter pylori (H. pylori) and non-steroidal anti-inflammatory drug (NSAID) are independent risk factors for peptic ulcers and ulcer complications and they have additive or synergistic effects. A meta-analysis showed that the OR for the incidence of peptic ulcer was 61.1 in patients infected with H. pylori and also taking NSAID when compared to patients uninfected with H. pylori and not taking NSAID. H. pylori eradication may prevent NSAID-induced ulcers in NSAID naive patients. In patients receiving long-term NSAID, proton pump inhibitor(PPI) is more effective in the prevention of ulcer recurrence and bleeding. However, H. pylori eradication should be considered in patients receiving long -term PPI maintenance treatment to prevent the development of corpus gastritis and gastric atrophy.     

Helicobacter pylori eradication therapy for gastric ulcer in elderly

Sixty-five-years or older person accounts for 23% of the population in Japan. Hence, Helicobacter pylori (H. pylori) eradication therapy is performed in many elderly patients. Urea breath test and H. pylori stool antigen test for diagnosis of H. pylori infection before and after eradication therapy are recommended from the point of being a noninvasive test and providing accurate diagnosis. H. pylori eradication therapy in Japan consists of the PPI/AMPC/CAM as the first therapy, and PPI/AMPC/MNZ as the second therapy. Eradication therapy rate and adverse effect rate of H. pylori eradication therapy for elderly patients are the same as for young people. It is not necessary to avoid H. pylori eradication therapy merely because of high age in elderly patients. However, it is necessary to be careful regarding drug interactions in patients who are taking multiple drugs.     

Strategy for peptic ulcer therapy in the era of H. pylori eradication therapy

The Japanese guideline for gastric ulcer therapy published 2003 has adopted a policy that eradication therapy for H. pylori as the first line therapy on ulcer patients with positive H. pylori status. For NSAID-induced gastric ulcer patients, cessation should be considered. In patients who cannot stop NSAIDs, proton-pump inhibitors or prostaglandin drugs is recommended. Similar strategy can be applied for duodenal ulcer patients. Implementation of this basic strategy in daily clinical practice, however, require further efforts to wider recognition of the new guideline for gastric ulcer therapy as well as to solve several barriers caused by discrepant health reimbursement policy.     

免疫刺激剂在幽门螺杆菌根除治疗中的疗效评价

目的观察和评价免疫刺激剂联合三联疗法在幽门螺杆菌（Hp）根除治疗中的临床疗效。方法将150例Hp阳性患者随机分为2组,治疗组给予免疫刺激剂（匹多莫德口服液）联合三联疗法（奥美拉唑＋克拉霉素＋阿莫西林）治疗,对照组单纯采用三联疗法治疗,观察2组患者的临床疗效。结果治疗组Hp根除率（92.0%）明显高于对照组（64.0%）,差异有统计学意义（P〈0.01）;治疗组症状缓解率（73.3%）显著高于对照组（56.0%）,差异有统计学意义（P〈0.05）;治疗组不良反应发生率（8.0%）低于对照组（17.3%）,但差异无统计学意义（P〉0.05）。治疗组复发率（21.7%）显著低于对照组（43.8%）,差异有统计学意义（P〈0.05）。结论免疫刺激剂联合三联疗法可提高Hp根除率、临床症状缓解率、Hp复发率,减少抗生素不良反应,可直接用于根除Hp的一线首次治疗。     

Helicobacter pylori eradication: role of individual therapy constituents and therapy duration

Treatment of Helicobacter pylori ( H. pylori ) infection has become a key factor in the management of dyspepsia and is the treatment of choice for peptic ulcer disease. First-line eradication regimens combining a proton pump inhibitor (PPI) with clarithromycin and amoxicillin or metronidazole are considered most effective when given for a minimum period of 1 week. Eradication regimens of shorter duration have shown promising results but clinical experience remains limited. Pharmacological properties such as bioavailability and plasma concentrations of individual PPIs differ between individuals but it remains unclear whether these differences impact on the efficacy of eradication therapy and are influenced by renal or hepatic impairment. Bioavailability of PPIs also differs and is impacted on by factors including intragastric pH, metabolic pathways, potency on an mg-for-mg basis and intrinsic antibacterial activity. Several significant pharmacokinetic differences between the PPIs do not seem to influence overall H. pylori eradication rates for first-line triple therapy. However, comparison of factors including pharmacokinetics and treatment duration may prove important in achieving successful eradication with second- and third-line treatments. Based on the factors which influence therapy outcome, we suggest an algorithm for the use of H. pylori eradication therapies.     

Helicobacter pylori infection and eradication

H. pylori infection is associated with various gastroduodenal diseases such as gastritis, peptic ulcer, gastric cancer, gastric MALT lymphoma. H. pylori infection is suggested that it plays a role as protective factor not promoting factor for reflux esophagitis and GERD. Epidemiological studies showed lower prevalence of H. pylori infection in reflux esophagitis and Barrett's esophagus comparing the control. Increased occurrence of reflux esophagitis after curing of H. pylori infection was reported. However, the relationship between H. pylori infection and reflux esophagitis has not been actually made clear. Also the mechanism of reflux esophagitis occurrence after H. pylori eradication is not obscure.