Omeprazole, clarithromycin and furazolidone for the eradication of Helicobacter pylori in patients with duodenal ulcer

AIM: To evaluate the efficacy of omeprazole plus clarithromycin and furazolidone in Helicobacter pylori eradication and duodenal ulcer healing in Brazilian patients. METHODS: Forty H. pylori-positive patients with duodenal ulcer were randomized to receive 20 mg omeprazole o.m. or b.d. for 1 month plus 500 mg clarithromycin (b.d. ) and 200 mg furazolidone (b.d.) for 1 week. RESULTS: Three months after the end of the treatment the eradication rates were 90% by intention-to-treat analysis, and 97% by per protocol analysis. Mild side-effects were observed in 25 patients, none of whom abandoned the protocol. No difference was observed between the 20 mg and 40 mg omeprazole daily doses. Cure or significant improvement of the symptoms and of the histological alterations were observed after H. pylori eradication. CONCLUSION: Our results demonstrate that clarithromycin and furazolidone in combination with omeprazole are a good alternative for H. pylori eradication in Brazilian patients with duodenal ulcer.     

Short report: short-term triple therapy for H. pylori-associated duodenal ulcer disease

Thirty consecutive patients with endoscopically proven duodenal ulceration who had Helicobacter pylori infection on culture and histology, were treated with tripotassium dicitrato bismuthate (1 tablet q.d.s., 400 mg metronidazole t.d.s. and 500 mg tetracycline t.d.s. for one week, followed by the bismuth salt for a further 3 weeks. All patients were endoscoped at entry and 4 weeks after cessation of treatment, to check for ulcer healing and H. pylori eradication. Two antral biopsies were taken at each endoscopy for histological and microbiological evidence of H. pylori infection. Complete healing of duodenal ulcers was observed in 27/30 patients (90%). Gastritis improved or completely resolved in 26 patients. Eradication of H. pylori was achieved in 27 patients. Of the three patients who failed to heal, two were H. pylori-positive at follow-up and one was H. pylori-negative.     

Recurrence of duodenal ulcer after Helicobacter pylori eradication is related to high acid output

Background : Helicobacter pylori eradication reduces the recurrence of duodenal ulcers. It is unclear why duodenal ulcers rarely recur in the absence of reinfection with H. pylori or NSAID treatment.
Methods : Basal, gastrin-releasing peptide- and pentagastrin-stimulated peak acid outputs in patients with ulcer relapse after H. pylori eradication were measured, and compared with patients without ulcer relapse after H. pylori eradication.
Results : Pentagastrin-stimulated peak acid output was significantly higher in H. pylori -positive patients with duodenal ulcers than in H. pylori -negative controls, and fell significantly after H. pylori eradication. In H. pylori -negative patients with recurrent duodenal ulcers, pentagastrin-stimulated peak acid output was significantly higher than in controls and similar to H. pylori -positive patients with duodenal ulcers.
Conclusions : These findings suggest that duodenal ulcer relapse after eradication of H. pylori may be related to high pentagastrin-stimulated peak acid output. In this subset of patients with duodenal ulcers, maintenance anti-secretory treatment may be necessary to prevent relapse.     

Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection

BACKGROUND: Helicobacter pylori infection, gastric acid hypersecretion and NSAID consumption may cause peptic ulcer. AIM: To investigate the respective roles of H. pylori and acid secretion in bleeding duodenal ulcer. PATIENTS AND METHODS: A total of 99 duodenal ulcer patients were referred for evaluation of acid secretion: seven with Zollinger-Ellison Syndrome; 14 with hypersecretory duodenal ulcer, defined by the coexistence of elevated basal acid output and pentagastrin acid output; and 78 duodenal ulcer patients with normal acid output. All non-Zollinger-Ellison Syndrome patients were H. pylori-positive and cured of infection. All patients were followed-up for a 36-month period, to assess the occurrence of bleeding episodes. RESULTS: Twenty-nine patients had at least one bleeding episode in the 4 years before the study. Bleeding was more frequent in males and in patients on NSAIDs. The mean basal acid output was not higher among bleeders. In the 21 patients (14 hypersecretory duodenal ulcer, seven Zollinger-Ellison Syndrome) with basal acid output > 10 meg/h and pentagastrin acid output > 44.5 meg/h, the risk of bleeding was higher (OR 6.5; 95% CI: 2-21). In the follow-up period, three out of 83 (3.3%) non-Zollinger-Ellison Syndrome patients had a H. pylori-negative duodenal ulcer with bleeding. The risk of bleeding after H. pylori cure was not higher in hypersecretory duodenal ulcer patients (P > 0.3), nor among patients with previous bleeding episodes (P > 0.2). CONCLUSIONS: In H. pylori-positive duodenal ulcer patients, the coexistence of elevated basal acid output and pentagastrin acid output leads to a sixfold increase in the risk of bleeding. After H. pylori cure, gastric acid hypersecretion is not a risk factor for bleeding. However, duodenal ulcer recurrence with bleeding may occasionally occur in patients cured of H. pylori, even if acid output is normal.     

Diagnosis of Helicobacter pylori after triple therapy in uncomplicated duodenal ulcers--a cost-effectiveness analysis

BACKGROUND: The cost-effectiveness of determining Helicobacter pylori status after treatment remains to be established. AIM: To determine the benefit of post-treatment assessment of H. pylori eradication in patients with uncomplicated duodenal ulcer. MATERIALS AND METHODS: A decision analysis was performed in patients with uncomplicated duodenal ulcer who were H. pylori-positive and had received eradication therapy. A decision tree was devised to compare the costs per patient of two different strategies: (a) systematic performance of post-treatment urea breath test and new treatment if positive; and (b) clinical follow-up, 13C-urea breath test if dyspeptic symptoms recurred and eradication treatment if the test was positive. RESULTS: Post-eradication 13C-urea breath test was notably more expensive than clinical follow-up, both in a low-cost per care setting (197 vs. 132 Euros) and in a high-cost per care (614 vs. 340 US $) scenario. This conclusion remained stable for a wide range of variations of the variables included in the decision tree (e.g. cure rates of eradication treatment, cost of the urea breath test or sensitivity, and specificity of urea breath test to detect eradication). CONCLUSION: In patients with uncomplicated duodenal ulcer, evaluation of eradication after H. pylori treatment markedly increases costs with no clear improvement in results and therefore should not be performed routinely.     

Systematic review: the effect of Helicobacter pylori and its eradication on gastro-oesophageal reflux disease in patients with duodenal ulcers or reflux oesophagitis

BACKGROUND: The effect of Helicobacter pylori in provoking or protecting against gastro-oesophageal reflux disease is unclear and studies have given conflicting results. Recent guidelines recommend H. pylori eradication in patients on long-term proton pump inhibitors. AIM: To ascertain the effect of H. pylori eradication on gastro-oesophageal reflux disease outcomes (reflux oesophagitis and heartburn) in patients with duodenal ulcer disease, and to ascertain the effect of H. pylori infection on reflux oesophagitis concerning heartburn, pH, severity, healing and relapse rates. METHODS: A systematic review of electronic databases was undertaken to September 2003. Experts in the field, pharmaceutical companies and journals were contacted about unpublished trials. Studies were reviewed according to predefined eligibility and quality criteria. Twenty-seven studies/trials were included in the systematic review. RESULTS: Study variation rather than therapy-influenced results in relation to the presence or absence of oesophagitis in patients with duodenal ulcer who underwent H. pylori eradication at 6-48 months follow-up. In patients with reflux oesophagitis no obvious differences were discovered in heartburn scores, 24-h pH values, healing and relapse rates between H. pylori-positive and -negative cases. CONCLUSION: There is no evidence to indicate that H. pylori eradication in duodenal ulcer disease provokes reflux oesophagitis or worsens heartburn; (ii) there are insufficient data to draw firm conclusions about the impact of H. pylori in patients with reflux oesophagitis.     

Triple therapy with clarithromycin, omeprazole, and amoxicillin for eradication of Helicobacter pylori in duodenal ulcer patients in Asia and Africa

BACKGROUND: Studies assessing the efficacy of triple therapy containing clarithromycin and amoxicillin for the eradication of Helicobacter pylori infection and healing of duodenal ulcers in Asian and African countries are limited. AIM: To determine the efficacy and safety of 1-week triple therapy with omeprazole, amoxicillin and clarithromycin for eradicating H. pylori infection in patients with active duodenal ulcer living in Asian and African regions. METHODS: This was an open-label, multicentre study in 11 centres in Asia and Africa. Patients with endoscopy-proven duodenal ulcer and who were H. pylori-positive were treated with clarithromycin 500 mg, omeprazole 20 mg, and amoxicillin 1000 mg, all given twice daily for 7 days. Upper endoscopy was repeated at week 6 to check for ulcer healing and H. pylori status. RESULTS: A total of 117 patients were recruited. H. pylori eradication rates were 85% by per protocol analysis and 80% by intention-to-treat analysis. Ulcer healing was found in 94% of subjects (per protocol analysis). Clinical success, measured by change of pre-treatment ulcer symptoms, was strongly supported by complete resolution or improvement in 100% of the evaluable patients (per protocol analysis). Since treatment-related adverse events, when present, were largely mild or moderate, the triple therapy regimen was considered safe. CONCLUSION: Seven-day triple therapy with omeprazole, amoxicillin, and clarithromycin was efficacious for treating Asian and African patients with duodenal ulcer disease associated with H. pylori infection, and the treatment regimen was well-tolerated.     

Cost-effectiveness analysis of different strategies for treating duodenal ulcer. Helicobacter pylori eradication versus antisecretory treatment

Helicobacter pylori has recently been recognised as a causative agent for duodenal ulcer, and the efficacy of various combinations of antibacterials and antisecretory agents in eradicating this pathogen has been assessed. The objective of this study was to determine the efficiency of 2 treatment strategies for patients with H. pylori-positive duodenal ulcer. Cost effectiveness was analysed for antisecretory therapy (omeprazole 20 mg/day for 4 weeks), and eradication therapy (triple therapy: omeprazole 40 mg/day plus clarithromycin 1 g/day plus amoxicillin 2 g/day for 1 week). In a Markov model, a hypothetical cohort of 5000 patients was followed for 10 years through 6 disease states. Cyclic eradication therapy (i.e. in the first duodenal ulcer episode and in relapses) was the most cost effective [21 Spanish pesetas (Pta) per day free of symptoms (DFS); Pta128 = $US1 (October 1995)] of the eradication options evaluated [antisecretory in the first episode, then eradication for relapses (Pta22.3/DFS), and eradication therapy first, then antisecretory therapy (Pta27.3/DFS)]. Antisecretory therapy alone was less cost-effective (Pta39/DFS) than each of the 3 eradication options. Eradication treatment in the first episode of duodenal ulcer and relapses has savings in direct costs per patient of up to 56% compared with antisecretory therapy alone. Sensitivity analyses showed the model to be very robust. It is, therefore, advisable to treat initial episodes of H. pylori-positive duodenal ulcer and relapses with triple therapy. The improved cost-effectiveness ratio was largely explained by the long term reduction in relapses obtained with the eradication strategies.     

Recurrent symptoms and gastro-oesophageal reflux disease in patients with duodenal ulcer treated for Helicobacter pylori infection

BACKGROUND: Eradication of Helicobacter pylori has been shown to prevent relapse of endoscopically detected duodenal ulcers. There is controversy regarding symptom improvement after therapy. Some studies have suggested that a substantial number of patients remain symptomatic after eradication therapy. Other studies suggest that gastro-oesophageal reflux disease (GERD) may develop as a result of H. pylori eradication. AIM: To determine the relationship between symptoms and H. pylori eradication and to determine whether H. pylori eradication results in symptoms or endoscopic findings of GERD. METHODS: Two hundred and forty-two patients with endoscopically documented duodenal ulcer disease and evidence of H. pylori infection by rapid urease testing and histology were studied in four randomized, placebo-controlled, double-blind trials of H. pylori eradication therapy. All patients underwent symptom assessment and endoscopy with biopsy before therapy and 1 and 6 months after completing therapy. The rapid urease test and histology were used to determine H. pylori status. Interviewers were blinded to H. pylori status after eradication and were unaware of the endoscopic findings (interviews were performed prior to repeat endoscopy). RESULTS: The presence of epigastric pain was significantly associated with persistent H. pylori infection 1 month after therapy (odds ratio 2.3, 95% CI: 1.02-5.2; P=0.041), as was nausea (OR 7.1, 95% CI: 0.93-55.6; P=0.029). The presence of epigastric pain was significantly associated with ulcer relapse at 6 months (OR 7.5, 95% CI: 3.6-15.7; P < 0.001) as was nausea (OR 5.1, 95% CI: 1.7-16.0; P=0.002). Heartburn was not associated with eradication of H. pylori or ulcer relapse. New onset reflux symptoms were reported by 17% (17 of 101 patients) at 6 months and were not significantly different in patients with (15%) and without (22%) persistent H. pylori infection (P=0.47). Erosive oesophagitis was present at endoscopy in one of the 17 cases that developed new heartburn. CONCLUSIONS: One month after completion of therapy, the presence of epigastric pain or nausea is associated with persistent infection and these symptoms at 6 months are suggestive of duodenal ulcer relapse. The incidence of GERD is not increased in patients who have eradication of H. pylori.     

clinical aspects of Helicobacter pylori eradication therapy in peptic ulcer disease

Background and aims : Although the role of H. pylori in peptic ulcer disease is no longer in dispute, certain aspects of eradication therapy in this condition have yet to be settled. Uncertainties still surround the relationship between Helicobacter pylori status and ulcer healing, the efficacy of eradication therapy in alleviating acute symptoms and healing ulcers, and the prognosis after eradication with respect to recurrence of symptoms, ulcers and complications. The present literature review, encompassing studies published up to October 1995, specifically addresses these issues.
Results : Pooled data show that eradication therapy heals 90% of duodenal ulcers and 85% of gastric ulcers, while individual studies repeatedly confirm that it is more effective at healing ulcers than conventional treatment with anti-secretory drugs. Recent reports indicate that triple therapy regimens for 1 week, provided they include an anti-secretory drug, are sufficient to achieve high rates of healing and rapid symptom relief. A detailed analysis of the data, particularly those from studies reporting healing rates in relation to H. pylori status after eradication therapy, provides strong evidence that eradication of H. pylori produces ulcer healing. Follow-up studies show that ulcer recurrence and complications are rare after eradication treatment in patients with either gastric or duodenal ulcer disease. However, while ulcer symptoms are infrequent during follow-up, a proportion of patients appear to develop gastrooesophageal reflux after eradication.
Conclusions : H. pylori eradication is highly effective in promoting ulcer healing and preventing subsequent ulcer recurrence. These beneficial effects of eradication therapy are observed in patients with either gastric or duodenal ulcers which are associated with H. pylori infection.     

Comparison of lansoprazole-based triple and dual therapy for treatment of Helicobacter pylori-related duodenal ulcer: an Asian multicentre double-blind randomized placebo controlled study

BAKCGROUND: In Asian countries with limited resources, clarithromycin-based triple therapy may not be readily available. There are also few direct comparisons of different regimens in Asia. AIM: To compare two lansoprazole-based non-clarithromycin triple therapies and one dual therapy in a prospective double-blind placebo-controlled study of Helicobacter pylori eradication and duodenal ulcer healing. METHODS: Fourteen centres in Asia participated in this study. Patients with acute duodenal ulcer who were H. pylori-positive were recruited. They were randomized to receive: (a) lansoprazole 30 mg b.d., amoxycillin 1 g b.d. and metronidazole 500 mg b.d. for 2 weeks (LAM-2 W), or (b) LAM for 1 week and placebo (LAM-1 W), or (c) lansoprazole 30 mg b.d., amoxycillin 1 g b.d. and placebo for 2 weeks (LA-2 W). Upper endoscopy was repeated at week 6 to check for duodenal ulcer healing. Symptoms and side-effects were recorded. RESULTS: A total of 228 patients were recruited, and two patients took less than 50% of the drugs. H. pylori eradication rates (intention-to-treat) were 68 out of 82 (83%) with LAM-2 W, 55 out of 71 (78%) with LAM-1 W and 43 out of 75 (57%) with LA-2 W. There were significant differences (P=0. 001) in eradication rates when comparing either LAM-2 W or LAM-1 W with LA-2 W. The eradication rate in patients with metronidazole resistant H. pylori strains were significantly lower than those with metronidazole sensitive strains (P=0.0001). The duodenal ulcer healing rates at week 6 were 85%, 85% and 72% in LAM-2 W, LAM-1 W and LA-2 W, respectively (P=0.065). Side-effects occurred in 13%, 11% and 9% in LAM-2 W, LAM-1 W and LA-2 W, respectively. H. pylori eradication and initial ulcer size were factors affecting duodenal ulcer healing. CONCLUSIONS: This Asian multicentre study showed that 1-week lansoprazole-based triple therapy without clarithromycin has similar efficacy in H. pylori eradication and ulcer healing compared with a 2-week regimen. Both triple therapies were significantly better than dual therapy in H. pylori eradication. Therefore, 1-week lansoprazole-based triple therapy is as safe and effective as 2-week therapy in eradication of H. pylori infection and healing of duodenal ulcer in these Asian centres.     

Triple therapy with sucralfate, amoxycillin and metronidazole for healing duodenal ulcer and eradicating Helicobacter pylori infection

Methods: Seventy-seven chronic duodenal ulcer patients (50 male) were entered into this study. Treatment was started with sucralfate suspension (2 g b.d.) for 8 weeks. After 2 weeks the patients also received 750 mg amoxycillin t.d.s. plus 500 mg metronidazole t.d.s. for 12 days. Endoscopy with six antral biopsies (urease test, Gram staining, culture and histology) was performed before commencement of sucralfate therapy, 4 weeks after the end of antibiotic therapy, and during the follow-up examinations at 6 and 12 months.
Results: Seven patients were excluded prematurely from the study. Helicobacter pylori in five patients had primary resistance to metronidazole and these patients were also excluded. The ulcer healing rate 4 weeks after the end of antibiotic therapy was 92% and the H. pylori eradication rate was 82% (all per protocol). In all patients who were still H. pylori- positive, the bacterium became resistant to metronidazole and histologically the inflammatory state of the mucosa was the same as before treatment. All H. pylori- eradicated patients (n=53) were re-examined after 6 and 12 months; no ulcer recurrence was observed and each time only one reinfection was found.
Conclusions: In an open study, sucralfate with amoxycillin and metronidazole appeared to act together to eradicate H. pylori infection and to speed duodenal ulcer healing.     

Triple therapy for Helicobacter pylori eradication is more effective than long-term maintenance antisecretory treatment in the prevention of recurrence of duodenal ulcer: a prospective long-term follow-up study

BACKGROUND: The effectiveness of Helicobacter pylori eradication treatment and long term acid suppression maintenance in the natural course of duodenal ulcer has not been directly compared. AIM: To compare in a prospective randomized study the effectiveness of H. pylori eradication on the prevention of recurrence of duodenal ulcer with long-term maintenance acid suppression therapy. METHODS: One hundred and fourteen duodenal ulcer patients were randomized to the treatment over a 12-month period. Fifty-seven of them received triple therapy consisting of 1 g sucralfate q.d.s. for 28 days, 300 mg metronidazole q.d.s. for 14 days and 250 mg clarithromycin q.d.s. for 14 days. Another 57 received 20 mg omeprazole q.d.s. for 12 months. An upper endoscopy was performed before treatment, at 6 weeks, and 2, 6 and 12 months after the first endoscopy. Side-effects were self-recorded and clinical follow-ups were arranged for up to 4.25 years. RESULTS: The ulcer healing rate was 90.2% (95% confidence interval (95% CI): 79-97%) in the omeprazole group at 6 weeks as compared to 83.3% (95% CI: 70-93%) in the triple therapy group (P = 0.38). There was a higher success rate of pain control in the omeprazole group. Side-effects were more frequently reported and compliance was poorer in the triple therapy group during the first 4 weeks. During follow-up, more relapses were seen in the omeprazole group (9.8%, 95% CI: 3-21%) than the triple therapy group (4.2%, 95% CI: 1-13%) at 1 year (P = 0.44). All relapses were due to the persistence of H. pylori infection. At the 1 year follow-up, none of the patients who were H. pylori negative had an endoscopic relapse compared to 7 out of 56 patients who remained H. pylori positive (12.5%, 95% CI: 5-24%, P = 0.018). After a mean follow-up of 4.07 years, none of those who remained H. pylori negative had an ulcer relapse while the 11 out of 41 who remained H. pylori positive had an ulcer relapse (26.8%, 95% CI 14-43, P = 0. 0005). CONCLUSIONS: Both regimens were highly effective in healing ulcers. The eradication of H. pylori infection was associated with more side-effects and poor compliance but was more effective than the maintenance therapy in reducing the recurrence of duodenal ulcers. For the prevention of ulcer recurrence, testing of H. pylori status after triple therapy is more important than maintenance therapy.     

Dose-response of omeprazole combined with amoxycillin on duodenal ulcer healing and eradication of Helicobacter pylori.

BACKGROUND: Combination therapy using omeprazole and amoxycillin can cure Helicobacter pylori infection, but data are controversial concerning the efficacy of this regimen. The present study investigated varying doses of omeprazole combined with a standard amoxycillin dose on duodenal ulcer healing and eradication of H. pylori, in order to find an optimal dose regimen. METHODS: H. pylori-positive out-patients (n = 231) with duodenal ulcers were treated randomly and double-blind with either omeprazole 20, 40 or 80 mg b.d. plus amoxycillin 1 g b.d. for 14 days. Patients with an unhealed ulcer after this therapy took omeprazole 20 mg o.m. for another month. RESULTS: After 2 weeks, ulcer healing rates in the three treatment groups were not statistically different (85, 82 and 93%, respectively). Treatment with omeprazole 80 mg b.d. was significantly better in curing H. pylori infection (eradication rate 69%) than treatment with omeprazole 20 and 40 mg b.d. (47 and 53%). CONCLUSIONS: Combination of either omeprazole 20 or 40 mg b.d. plus amoxycillin 1 g b.d., is not sufficiently effective to be recommended as an anti-H. pylori therapy. Omeprazole 80 mg b.d. combined with amoxycillin is more efficient and well tolerated, but better treatment options now exist to cure H. pylori infection.     

埃索美拉唑短程三联疗法治疗老年消化性溃疡的临床观察

目的观察埃索美拉唑短程三联疗法对幽门螺杆菌(Hp)相关性老年消化性溃疡病的治疗效果。方法选取55例Hp阳性,年龄在60岁以上的消化性溃疡患者,随机分成两组。第1组:Hp阳性的十二指肠溃疡患者,第2组:Hp阳性的胃溃疡患者。分别予以埃索美拉唑20 mg,阿莫西林1 000 mg,呋喃唑酮100 mg,每日2次,疗程7 d。观察各组患者症状缓解情况,Hp根除率,不良反应及溃疡愈合率。结果各组患者症状在1~3d内缓解,Hp根除率第1组、第2组分别为91%、94%。溃疡愈合率分别为95%、91%。结论埃索美拉唑联合治疗老年性消化性溃疡1周方案,Hp根除率高,顺从性和耐受性好。     

铝镁加混悬液联用埃索美拉唑治疗幽门螺杆菌阳性十二指肠溃疡的疗效观察

目的 观察铝镁加混悬液联用埃索美拉唑治疗幽门螺杆菌阳性十二指肠溃疡的临床疗效.方法 将幽门螺杆菌感染阳性的十二指肠溃疡患者124例随机分为两组：对照组用埃索美拉唑＋阿莫西林＋克拉霉素抗Hp治疗,7天后单用埃索美拉唑;治疗组用埃索美拉唑＋阿莫西林＋克拉霉素抗Hp治疗,7天后应用埃索美拉唑联合铝镁加混悬液;治疗4周后复查胃镜,观察十二指肠溃疡愈合情况,停药4周后复查14C呼气试验,比较两组患者溃疡愈合率、治疗有效率及Hp根除率.结果 对照组和治疗组溃疡愈合率分别为61.29％和66.13％,差异无统计学意义（P＞0.05）;对照组和治疗组溃疡有效率分别为82.26％和95.16％,差异有统计学意义（x 2=5.153,P＜0.05）;对照组和治疗组Hp清除率分别为82.26％和79.03％,差异无统计学意义（P＞0.05）.结论 铝镁加混悬液联用埃索美拉唑治疗幽门螺杆菌阳性十二指肠溃疡的疗效优于单用埃索美拉唑.     

Helicobacter pylori eradication as a surrogate marker for the reduction of duodenal ulcer recurrence

Objectives:

An abundance of data exists documenting the association of H. pylori eradication with the reduction in duodenal ulcer recurrence.

Aim:

To evaluate the validity of using H. pylori eradication as a surrogate marker for the reduction in duodenal ulcer recurrence using rigorously controlled studies.

Methods:

Three controlled clinical trials were conducted in patients with uncomplicated, active duodenal ulcers. Patients were treated with various combinations of omeprazole and amoxycillin. Ulcer healing and H. pylori eradication were assessed. For patients whose duodenal ulcer healed, duodenal ulcer recurrence was determined over a 6-month period in patients with H. pylori eradication and those remaining positive for H. pylori at least 4 weeks after treatment. To support the data obtained from these clinical trials, a search of the medical literature was conducted to identify additional human clinical trials in which duodenal ulcer recurrence rates were measured and categorized by H. pylori status at least 1 month post-treatment.

Results:

In 11 controlled trials, the overall 6–18-month duodenal ulcer recurrence rate was 54% among patients remaining positive for H. pylori at least 4 weeks after treatment compared to 6% among patients with H. pylori eradication following treatment. This finding was corroborated by the uncontrolled trials, in which the duodenal ulcer recurrence rate was 64% among patients found to be H. pylori-positive and 6% for patients found to be H. pylori-negative at least 4 weeks after treatment. A time course of duodenal ulcer recurrence rates using pooled data from both controlled and uncontrolled studies demonstrated that duodenal ulcer recurrence rates for H. pylori-negative patients persisted for up to 4 years following treatment. Duodenal ulcer recurrence rates for H. pylori-positive patients increased for the first year, then levelled off. A comparison of the duodenal ulcer recurrence rates for different treatment regimens revealed that eradication regimens based on omeprazole plus antibiotics and bismuth plus antibiotics exhibited similar duodenal ulcer recurrence rates for H. pylori-positive and -negative patients.

Conclusion:

Regardless of treatment regimens, H. pylori eradication produced a consistent and significant reduction in duodenal ulcer recurrence. Therefore H. pylori eradication, 4 weeks post-therapy, can be used as a surrogate marker for reduced duodenal ulcer recurrence in investigational clinical trials.

     

Increased thrombin generation and circulating levels of tumour necrosis factor-alpha in patients with chronic Helicobacter pylori-positive gastritis

BACKGROUND: Conflicting data have been reported concerning the relationship between Helicobacter pylori infection and coronary heart disease. AIM: To evaluate clotting system activation and plasma levels of tumour necrosis factor-alpha, a procoagulant cytokine, in patients with H. pylori-positive and -negative gastritis. METHODS: Three groups of patients were identified: 38 with H. pylori-positive gastritis, 18 with H. pylori-negative gastritis, and 40 H. pylori-negative controls with normal gastric mucosa. Plasma levels of prothrombin fragment 1 + 2 (F1 + 2) and tumour necrosis factor-alpha were assayed. Patients were also controlled after 2 and 6 months following standard H. pylori eradication treatment. RESULTS: At baseline, fragment 1 + 2 and tumour necrosis factor-alpha levels in H. pylori-positive patients were significantly higher than those in H. pylori-negative patients with gastritis (P < 0.05 and P < 0.01, respectively). After H. pylori eradication, fragment 1 + 2 and tumour necrosis factor-alpha levels showed a significant decrease at 2 months (P = 0.03 and P = 0.02, respectively) and a further reduction at 6 months, reaching levels observed in H. pylori-negative patients and controls. CONCLUSIONS: The increase thrombin generation rate and the correlation of plasma fragment 1 + 2 and tumour necrosis factor-alpha levels in H. pylori-positive patients suggest a role for inflammation in mediating the relationship between H. pylori infection and activation of the clotting system.     

Management of Helicobacter pylori in duodenal ulcer: a cost-effectiveness analysis

BACKGROUND: Empirical eradication therapy of H. pylori has been proposed as a therapeutic alternative for duodenal ulcer. AIM: To identify the cost-effectiveness of empirical eradication therapy vs. test-and-treatment for the management of patients already diagnosed with a duodenal ulcer. METHODS: A decision analysis was performed to compare the cost-effectiveness of empirical eradication therapy of H. pylori diagnosed duodenal ulcer vs. eradication therapy after confirmatory diagnosis of Helicobacter pylori infection by means of several diagnostic tests. RESULTS: The empirical eradication therapy of duodenal ulcer was found to be the most effective and cost-effective strategy of all the alternatives. Amongst the alternatives, which included the previous performance of confirmatory diagnostic tests, the best cost-effectiveness ratio used a serology test. The model was robust in the face of changes in the values of therapeutic effectiveness, sensitivity and specificity of the diagnostic tests, prevalence of H. pylori infection in duodenal ulcer, duration of the antisecretory therapy, and number of medical visits. CONCLUSIONS: Based on our cost-effectiveness analysis, a treat approach is more effective and cost-effective than a test-and-treat approach in the clinical management of already diagnosed duodenal ulcer.     

A meta-analysis comparing eradication, healing and relapse rates in patients with Helicobacter pylori-associated gastric or duodenal ulcer

AIM: To compare the effectiveness of Helicobacter pylori eradication in curing peptic ulcer disease in trials involving both gastric ulcer and duodenal ulcer. METHODS: Twenty-four relevant randomized controlled trials and randomized comparative trials met the predefined selection criteria. Only proton pump inhibitor-based eradication trials were considered for the evaluation of eradication efficacy and ulcer healing. For the determination of relapse rates, all trials independent of the eradication therapy regimen were considered. RESULTS: Data from 2102 patients were analysed comparing gastric ulcer with duodenal ulcer. No statistical differences between gastric ulcer and duodenal ulcer patients were found with regard to eradication rates (summarized odds ratio, 1.23; 95% confidence interval, 0.98-1.55) or ulcer relapse rates, whether in successfully H. pylori eradicated patients (summarized odds ratio, 0.69; 95% confidence interval, 0.26-1.84) or unsuccessfully H. pylori eradicated patients (summarized odds ratio, 1.48; 95% confidence interval, 0.85-2.56). Owing to heterogeneity, healing rates were not comparable. CONCLUSIONS: The eradication of H. pylori infection cures both gastric and duodenal ulcer, and the cure rates are similar. This suggests that H. pylori is the key factor in peptic ulcer disease independent of the ulcer site.