Cure of Helicobacter pylori-positive active duodenal ulcer patients: a double-blind, multicentre, 12-month study comparing a two-week dual vs a one-week triple therapy. GISU (Interdisciplinary Group for Ulcer Study).

AIMS: To compare a two-week dual therapy to a one-week triple therapy for the healing of duodenal ulcer and the eradication of the Helicobacter pylori infection. PATIENTS AND METHODS: A total of 165 patients with active duodenal ulcer were enrolled in the study. At entry, endoscopy, clinical examination and laboratory tests were performed. Histology and the rapid urease test were used to diagnose Helicobacter pylori infection. Patients received either lansoprazole 30 mg plus amoxycillin 1 g bid for two weeks (two-week, dual therapy) or lansoprazole 30 mg plus amoxycillin 1 g plus tinidazole 500 mg bid for one week plus lansoprazole qd for an additional week (one-week, triple therapy). Two and twelve months after cessation of therapy, endoscopy and clinical assessments were repeated. RESULTS: Duodenal ulcer healing and Helicobacter pylori eradication were both significantly greater (p<0.0001) in the triple therapy group (healing: 98.6%; Helicobacter pylori cure rate: 72.6%) than in the dual therapy group (healing: 77.3%; Helicobacter pylori cure rate: 33.3%). Ulcers healed more frequently in Helicobacter pyloricured than in Helicobacter pylori-not cured patients (94.9% vs. 77.2%; p<0.0022). After one year, Helicobacter pylori eradication was re-confirmed in 46/58 patients previously treated with the triple therapy and in 10/40 patients treated with the dual therapy [p<0.0001]. Only three duodenal ulcer relapses were observed throughout follow-up: all were in Helicobacter pylori-not cured patients. CONCLUSIONS: Triple therapy was more effective than dual both in curing Helicobacter pylori infection and healing active duodenal ulcers. The speed of ulcer healing obtained after only 7 days of antibiotics and 14 days of proton pump inhibitors confirmed that longer periods of anti ulcer therapy were not necessary. Helicobacter pylori -not cured patients had more slowly healing ulcers which were more apt to relapse when left untreated.     

Prolonging proton pump inhibitor-based anti-Helicobacter pylori treatment from one to two weeks in duodenal ulcer: is it worthwhile?

AIMS: To compare the efficacy of one-week versus two-week treatment with lansoprazole, amoxycillin and clarithromycin in inducing healing of Helicobacter pylori-positive duodenal ulcers as well as to investigate the role of several factors, determinant in the ulcer healing process. PATIENTS AND METHODS: Seventy-one active duodenal ulcer patients were randomised to receive one- or two-week treatment with lansoprazole (30 mg bid), clarithromycin (500 mg bid) and amoxycillin (1 g bid), not followed by any additional acid suppressive therapy. Ulcer healing and Helicobacter pylori infection were assessed by endoscopy and urea breath test 4 weeks after the end of treatment. Before entering the trial and four weeks after the end of treatment, dyspeptic symptoms were recorded and scored by a validated questionnaire. The potential effects of a number of clinical variables on the ulcer healing process were evaluated by means of univariate and multivariate analyses. RESULTS: Duodenal ulcer was healed in 80.5% patients treated for one week and in 91.4% patients treated for 2 weeks according to intention-to-treat analysis (p=NS). Ulcer healing was more frequent in the Helicobacter pylori cured patients compared to those with persisting infection (90.9% vs 68.5%; p=0.04). Multivariate analysis did not reveal any significant predictor of duodenal ulcer healing. CONCLUSIONS: Two-week treatment with lansoprazole, amoxycillin and clarithromycin, without continuation of antisecretive therapy, is better, although the difference is not statistically significant, than one-week treatment in healing Helicobacter pylori-positive duodenal ulcer disease. The eradication of Helicobacter pylori is the most important factor related to ulcer healing.     

Factors influencing Helicobacter pylori eradication with 2 week combination therapy of lansoprazole and amoxycillin: Intragastric distribution of colonization and gastric mucosal atrophy

In Japan, gastric ulcers are often accompanied by marked gastric mucosal atrophy. We evaluated the dual therapy of double-dose lansoprazole and amoxycillin for Helicobacter pylori eradication in Japanese ulcer patients and investigated the effects of intragastric distribution of H. pylori colonization and gastric mucosal atrophy on eradication with this combination therapy. Seventy-six H. pylori-positive ulcer patients received lansoprazole (30 mg) plus amoxycillin (500 mg) twice daily for 2 weeks (LA-60 group), lansoprazole (30 mg once daily) plus amoxycillin (500 mg twice daily) for 2 weeks (LA-30 group) or lansoprazole (30 mg once daily) for 6 or 8 weeks (LPZ group). Infection was evaluated by light microscopy, culture and biopsy urease tests. Helicobacter pylori colonization was classified as localized to the corpus (localized type) or involving the antrum and corpus (whole type). Fundic mucosal atrophy was graded according to endoscopic and histological features. Eradication was achieved in 67.6% in the LA-60 group, 31.6% in the LA-30 group, and 0% in the LPZ group, and moderate or severe histological gastritis was improved in the LA-60 group. Eradication was better in localized-type colonization (92%) than whole-type (56%), and better with fundic mucosal atrophy (84%) than without, but poor in both whole-type colonization and scanty mucosal atrophy (47%). The LA-60 therapy achieves better eradication in Japanese ulcer patients with localized H. pylori colonization and/or gastric mucosal atrophy, which are likely to be important predictors for the successful eradication with dual therapy.     

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease

Background. It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid.Aims. To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions.Methods. Duodenal (anterior, superior, inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and ¹³C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment.Results. Duodenal gastric metaplasia regression was observed in all ( ) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0.001).Conclusions. The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.     

Hypersecretory duodenal ulcer and Helicobacter pylori infection: for-year follow-up study

Background. About 10% of duodenal ulcer patients are characterized by gastric acid hypersecretion with normal gastrin values. Relapsing duodenal ulcer after Helicobacter pylori cure has been related to high acid output and maintenance antisecretory therapy has been suggested in hypersecretory duodenal ulcer patients. The role of Helicobacter pylori infection and the effects of Helicobacter pylori cure in hypersecretory duodenal ulcer patients still remain to be fully studied.Aim. To study: a) whether gastric acid hypersecretion “per se” is a risk factor for duodenal ulcer recurrence; b) whether maintenance antisecretory therapy is necessary after eradication in hypersecretory duodenal ulcer patients.Patients. The study population comprised 8 hypersecretory duodenal ulcer patients, selected from a population of 79 Helicobacter pylori-positive duodenal ulcer patients.Methods. Hypersecretory duodenal ulcer patients were followed-up for at least 4 years after eradication. Gastric acid secretion was measured again 12 months after Helicobacter pylori eradication. Gastroscopy with histology was performed 3, 6, 12 and 36 months after treatment, ¹³C-urea breath test after 42 months; clinical questionnaires were completed every 6 months.Results. After eradication, despite a not significantly reduced high acid output (median value of basal acid output and pentagastrin-stimulated acid output, respectively, 23.1 mEg/h and 64. 1 mEg/h before treatment vs 16 mEg/h and 49.7 mEq/h 12 months after treatment), all patients were free from symptoms, none of them had duodenal ulcer relapse or complications (7/8 before treatment), or needed antisecretory maintenance therapy, except for one patient taking non-steroidal anti-inflammatory drugs.Conclusions. These findings, obtained in a selected population of hypersecretory duodenal ulcer patients with long-term follow-up, suggest that after successful Helicobacter pylori eradication gastric acid hypersecretion “per se” is not able to determine the recurrence of duodenal ulcer.     

Dual therapy versus triple therapy forHelicobacter pylori-associated duodenal ulcers

We compared the ulcer healing effect and eradication ofH. pylori by one-week triple therapy of bismuth, metronidazole, and tetracycline with two-week dual therapy of amoxicillin and omeprazole. One hundred twelve patients with confirmedH. pylori infection and duodenal ulcers were recruited in a prospective, randomized, single-blinded trial. Ulcer healing, eradication ofH. pylori in the stomach six weeks after randomization, and side effects reported by patients during the therapy. Duodenal ulcers were healed in 44 of 49 (89.8%, 95% CI 81.3–98.3%) patients receiving triple therapy and in 44 of 53 (83.0%, 95% CI 72.9–93.1%) patients receiving dual therapy (P=0.32).H. pylori was successfully eradicated in 41 of 49 (83.6%, 95% CI 73.4–94%) patients and in 40 of 53 (75.5%, 95% CI 63.9–87.1%) patients in the triple therapy group and the dual therapy group respectively (P=0.31). Side effects experienced by patients who received triple therapy were significantly more frequent than those who received dual therapy (P=0.0076). In conclusion, a two-week course of omeprazole and amoxicillin achieves a comparable rate ofH. pylori eradication and ulcer healing with fewer side effects.     

Medium- and high-dose omeprazole plus amoxicillin for eradication ofHelicobacter pylori in duodenal ulcer disease

The purpose of the present study was to investigate theHelicobacter pylori eradication potency of combined amoxicillin-omeprazole treatment in patients with duodenal ulcer disease and to compare the efficacy of two omeprazole and amoxicillin doses concerningH. pylori eradication, ulcer healing, pain relief, and safety. Ninety patients with activeH. pylori-positive (culture and/or histology) duodenal ulcer disease were randomly treated with either omeprazole 20 mg twice a day plus amoxicillin 1 g twice a day (group I,N=30), omeprazole 40 mg twice a day plus amoxicillin 1 g twice a day (group II,N=30), or omeprazole 40 mg twice a day plus amoxicillin 1 g three times a day (group III,N=30) over two weeks, followed by ranitidine at bedtime for another four weeks. The overall proportion ofH. pylori eradication was 83% and of ulcer healing 92% without statistically significant differences between the study groups. Complete pain relief occurred after a median of one day in all groups. Six patients complained of side effects during the therapy phase, which led to therapy discontinuation in one female patient. In conclusion, omeprazole plus amoxicillin is a highly effective and well-tolerated therapy regimen to eradicateH. pylori in duodenal ulcer disease. In addition, the results suggest that there is no clear dose-response relation between the dosages of omeprazole and amoxicillin used in this study on the one hand and theH. pylori eradication rates on the other.     

A prospective randomized study of amoxycillin and omeprazole with and without metronidazole in the eradication treatment of Helicobacter pylori

A combination of amoxycillin and omeprazole is often used to treat Helicobacter pylori infection. A three-drug regimen comprising metronidazole, amoxycillin and omeprazole has been proposed as an alternative therapy. In a prospective, randomized, comparative study, we evaluated these two regimens with respect to safety and ef?cacy in patients with H. pylori infection. Sixty patients with peptic ulcer (gastric, 32 patients; duodenal, 28 patients) who had a history of ulcer recurrence were randomly assigned to dual therapy with amoxycillin (500 mg three times daily for 2 weeks) and omeprazole (20 mg once daily for 8 weeks) or to triple therapy with metronidazole (500 mg twice daily for 2 weeks) plus amoxycillin and omeprazole, given in the same dosages as dual therapy. Forty-eight patients completed the protocol; treatment was discontinued because of side effects in nine patients, and three patients dropped out of the study. On the basis of all patients treated, the rate of H. pylori eradication was signi?cantly higher for triple therapy 20/23 cases, 87.0%; 95% con?dence interval (CI), 0.664–0.972) than for dual therapy 13/25, 52.0%; 0.313–0.722; P < 0.05). On an intention-to-treat basis, the difference between the groups in the rate of H. pylori eradication was marginally signi?cant (P= 0.06 [0.028–0.512]). Side effects were reported by ?ve patients receiving triple therapy (skin rash, one; nausea, two; headache, one; abdominal pain, one), and four patients receiving dual therapy (skin rash, two; abdominal pain, one; diarrhoea, one). All side effects resolved spontaneously after termination of treatment. There was no signi?cant difference in safety between the two regimens. Triple therapy with metronidazole, amoxycillin, and omeprazole was signi?cantly more effective for the eradication of H. pylori than dual therapy with amoxycillin and omeprazole alone. The safety of these regimens was similar, and triple therapy was found to be clinically acceptable.     

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.     

Randomised study ofefficacy of Omeprazole and clarithromycin with either amoxycillin or metronidazole in the eradication of Helicobacter pylori in screened primary care patients

Background. Population Helicobacter pylori screening and treatment has been advocated as a means of reducing mortality from gastric cancer. The optimum Helicobacter pylori eradication therapy to use in this setting is uncertain.Aims. To compare efficacy of seven days of omeprazole, clarithromycin and either metronidazole, or amoxycillin in Helicobacter pylori positive subjects detected by population screening.Patients. Helicobacter pylori positive patients from the placebo group of a population screening and treatment trial were invited to take part in the investigation.Methods. Patients were randomised to receive either omeprazole, clarithromycin and metronidazole or omeprazole, clarithromycin and amoxycillin, and Helicobacter pylori eradication was verified with a ¹³C-urea breath test at least four weeks after completion of therapy.Results. A total of 221 patients took part in the study and 210 completed the protocol. Treatment was successful in 93/111 (84%) patients allocated to omeprazole, clarithromycin and metronidazole and in 96/110 (87%) allocated to omeprazole, clarithromycin and amoxycillin in an intention-to-treat analysis (p=0.46). Per protocol eradication rates were 93/107 (87%) in the metronidazole, and 96/103 (93%) amoxycillin group (p=0.129).Conclusions. There was no significant difference between the two regimens. The eradication rates achieved are comparable with previous studies in both dyspepsia and peptic ulcer patients.     

Impairment of gastric secretion modulation in duodenal ulcer and in long-term PPI treatment: quantitative morphologic findings and pathophysiologic implications

Helicobacter pylori affects gastric secretion. This functional effect might have a morphometric counterpart. Therefore, the gastric cell secretory compartment was morphometrically assessed in different pathophysiologic conditions related to Helicobacter pylori infection. Nineteen Helicobacter pylori-positive nonduodenal ulcer subjects, 15 omeprazole chronically treated subjects, and 19 duodenal ulcer patients were studied against 19 controls. Somatostatin, gastrin, enterochromaffin-like, and parietal cell density was assessed in gastric biopsies. No differences in any cell type density were found between Helicobacter pylori-positive nonduodenal ulcer subjects and controls. On the contrary, differences were significant when comparing omeprazole and duodenal ulcer patients to controls (higher density of gastrin, enterochromaffin-like, and parietal cells, lower density of somatostatin cells). In duodenal ulcer a reversion to control values followed Helicobacter pylori eradication and ulcer healing. A direct linear correlation between enterochromaffin-like, gastrin, and parietal cell density was demonstrated. An almost complete map of mucosal cells involved in gastric secretion is provided by this study. The cell density pattern, identical to the omeprazole group, points to an impaired feedback control of secretion in duodenal ulcer. The reversion to control values after Helicobacter pylori eradication and ulcer healing demonstrates the pathogenetic role of Helicobacter pylori–host interaction in these changes.     

Omeprazole-amoxycillin therapy for eradication ofHelicobacter pylori in duodenal ulcer bleeding: Preliminary results of a pilot study

Thirty-five patients with duodenal ulcer bleeding andHelicobacter pylori-colonization were assigned to receive 2×20 mg omeprazole and 3×750 mg amoxycillin daily for 2 weeks. Eradication was defined as no evidence ofH. pylori infection by urease test and by histology 4 weeks after completion of therapy. Two patients were lost to follow up. All ulcers healed completely (100% ulcer healing rate). Twenty-nine out of the 33 patients wereH. pylori-negative (87.9% eradication rate). Three patients complained of typical side effects of amoxycillin (9.1% side effect rate). The patients were prospectively followed for 12 months. After ulcer healing, no maintenance therapy was given. One of the 29 patients in whomH. pylori eradication had been successful suffered a second ulcer hemorrhage withH. pylori re-infection (3.4% relapse rate of ulcer bleeding), and this was managed endoscopically. Recurrent ulcer hemorrhage occurred in 2 out of 4H. pylori-resistant patients. At the end of the follow-up period, of the patients in whomH. pylori eradication had been initially successful, only the patient with re-bleeding remained re-infected. The 4H. pylori-resistant patients showed persistentH. pylori colonization. In conclusion, omeprazole plus amoxycillin is a safe and effective treatment for eradicatingH. pylori; this treatment reduces the relapse rate of duodenal ulcer bleeding.     

Follow-up survey of a large-scale multicenter,double-blind study of triple therapy with lansoprazole,amoxicillin, and clarithromycin for eradication of Helicobacter pylori in Japanese peptic ulcer patients

Background: To evaluate histopathological changes and effects on inhibition of ulcer recurrence, a follow-up survey was performed in Japanese patients with Helicobacter pylori-positive active peptic ulcers. These patients had previously participated in a large-scale multicenter trial of triple therapy with lansoprazole (LPZ)/amoxicillin (AMPC)/clarithromycin (CAM) for eradication of H. pylori. Methods: Patients who had been treated with LPZ only or a combination of LPZ, AMPC, and CAM for a period of 7 days and in whom ulcer healing had been confirmed after treatment were grouped according to successful or failed eradication of H. pylori. They were examined endoscopically to determine whether ulcers had recurred. The updated Sydney system was applied to study histological changes after H. pylori eradication therapy, compared with baseline. Results: Twelve months after treatment for H. pylori eradication, gastric ulcers had recurred in 11.4% of those with successful H. pylori eradication and in 64.5% of those with unsuccessful H. pylori eradication. Duodenal ulcers had recurred in 6.8% of patients for whom H. pylori eradication was successful and in 85.3% of patients in whom eradication failed. These findings proved that H. pylori eradication significantly reduced ulcer recurrence (P < 0.0001 for both types of ulcers). Histopathological findings of inflammation and activity grade in both gastric and duodenal ulcers were more favorable in patients with successful eradication than in those with unsuccessful eradication. Conclusions: H. pylori eradication significantly inhibited ulcer recurrence in Japanese peptic ulcer patients. Histopathological findings were also improved with regard to inflammation and activity (neutrophils) in patients in whom H. pylori eradication was successful. Received: May 13, 2002 / Accepted: September 6, 2002 Reprint requests to: M. Asaka Editorial on page 410     

Prospective,randomized, investigator-blind trial ofHelicobacter pylori infection treatment in patients with refractory duodenal ulcers

In this study, 26 patients with duodenal ulcers refractory to treatment with H₂-receptor antagonists for 8–12 weeks were randomly assigned to eight weeks of treatment with colloidal bismuth subcitrate (120 mg four times a day) alone (N=12) or in combination with tetracycline hydrochloride (500 mg four times a day, days 0–14) and metronidazole (500 mg three times a day, days 15–28). Symptoms were scored and endoscopy, histology, and CLO tests were performed before, on completion of treatment, and 3, 6, 12, and 18 months after treatment. Treatment was considered successful whenHelicobacter pylori was not detected by CLO tests and Warthin-Starry stains on gastric biopsies taken from antrum, body, and fundus. On triple therapy, ulcers healed in 12/14 patients (85.71%) and 10/14 (71.42%) patients becameHelicobacter pylori-negative. On bismuth, only one patient becameHelicobacter pylori-negative (8.33%,P<0.0001), but ulcers healed in 8/12 patients (67%,P=NS). Six patients on bismuth, whose ulcers remained unhealed or relapsed early after healing, were offered triple therapy, which resulted in ulcer healing in three and Helicobacter pylori clearance in two patients. At 18 months, none of theHelicobacter pylori-negative patients had ulcer relapse. On the contrary, ulcers relapsed in all but one patient, who remainedHelicobacter pylori-positive. Smoking and drinking did not influence the therapeutic outcome. The data confirm previous reports that many duodenal ulcers are infectious and therefore curable.     

Effects of Omeprazole and Eradication of Helicobacter pylori on Gastric and Duodenal Mucosal Enzyme Activities and DNA in Duodenal Ulcer Patients

Vetvik K, Schrumpf E, Mowinckel P, Aase S, Andersen K-J. Effects of omeprazole and eradication of Helicobacter pylori on gastric and duodenal mucosal enzyme activities and DNA in duodenal ulcer patients. Scand J Gastroenterol 1994;29:995-1000.

Background: Duodenal and gastric content of mucosal enzymes in duodenal ulcer (DU) patients differs from that of controls. The purpose of this study has been to examine the effect of omeprazole and eradication of Helicobacter pylori on mucosal enzymes in DU patients

Methods: The enzyme activities of seven gastric and duodenal mucosal marker enzymes from the brush border, lysosomes, and mitochondria have been studied. In study I the measurements were made in 29 patients with an active DU before and after 14 days of omeprazole treatment. In study II 22 duodenal ulcer patients were given bismuth subnitrate, oxytetracycline, and metronidazole (triple therapy) for 2 weeks to eradicate H. pylori. Biopsy specimens were taken from the duodenum and the stomach for enzyme measurements and histologic assessment. In study II additional specimens were obtained from the prepyloric region for urease tests and culture of H. pylori.

Results: The ulcer healing rates were more than 90% after both omeprazole and triple therapy. H. pylori was eradicated in 86% after triple therapy. The activities of the brush-border enzymes lactase, neutral-α-glucosidase, alkaline phosphatase, leucyl-β-naphthylami-dase, and γ-glutamyltransferase (γ-GT) increased significantly in the duodenal bulb and the descending duodenum during treatment with omeprazole. No changes in duodenal enzyme activity were detected after triple therapy, whereas a significant fall in γ-GT and acid phosphatase activities was seen in the stomach. The mucosal DNA in the gastric antrum decreased both after treatment with omeprazole and after triple therapy.

Conclusions: A similar decrease in mucosal DNA of the gastric antrum was demonstrated after both omeprazole and triple therapy with bismuth subnitrate, oxytetracycline, and metronidazole. Omeprazole also affects the content of duodenal mucosal enzymes, whereas triple therapy particularly affects the gastric mucosal enzyme activity.     

Helicobacter heilmannii infection in a child after successful eradication of Helicobacter pylori: case report and review of literature

An 11-year-old boy with Helicobacter pylori-associated duodenal ulcer was successfully treated with a combination of lansoprazole, amoxicillin, and clarithromycin. Endoscopy and gastric biopsies were repeated 2 and 12 months later, showing ulcer healing and eradication of H. pylori. However, a 3-year follow-up study demonstrated H. heilmannii in the antral mucosa based on its characteristic morphology and positive urease test and negative culture. The patient had no contact with domestic animals such as cats and dogs. A 7-day course with lansoprazole, amoxicillin, and clarithromycin was performed again, resulting in successful eradication of the organism. Pediatric cases with H. heilmannii infection reported are reviewed.     

Rebamipide, a gastro-protective and anti-inflammatory drug, promotes gastric ulcer healing following eradication therapy for Helicobacter pylori in a Japanese population: a randomized, double-blind, placebo-controlled trial

Background One week of Helicobacter pylori eradication therapy is insufficient for healing of gastric ulcers. We examined the efficacy of rebamipide in gastric ulcer healing following 1 week of eradication therapy in a randomized, double-blind, placebo-controlled trial. Methods Patients with H. pylori-positive gastric ulcer were enrolled and received 1 week of eradication therapy, followed by 100 mg of rebamipide or placebo for 7 weeks. The primary end point was the gastric ulcer healing rate. Results Of the 309 patients entered in the trial, 301 completed H. pylori eradication therapy; 154 patients took rebamipide, and 147 took placebo. The healing rate in the rebamipide group was higher than that in the placebo group in the per-protocol analysis—80.0% (104/130) versus 66.1% (82/124) [95% confidence interval (CI), 3.1–24.7; P = 0.013)—and in a full analysis—70.1% (108/154) versus 60.5% (89/147) (95% CI, −1.1 to 20.3; P = 0.080). Conclusions Compared with placebo, rebamipide significantly promoted gastric ulcer healing following 1 week of eradication therapy.     

Effects of killing Helicobacter pyloriquadruple therapy on peptic ulcer： A randomized double-blind clinical trial

AIM: To study the therapeutic efficacy of a Chinese and Western integrated regimen, killing Helicobacter pylori quadruple therapy on H pylori-associated peptic ulcers (PU). METHODS: With prospective and double-blind controlled method, seventy-five active PU patients with H pylori infection were randomized to receive one of the following three regimens: (1) new triple therapy (group A: lansoprazole 30 mg qd, plus clarithromycin 250 mg bid, plus amoxycillin 500 mg tid, each for 10 d); (2) killing Hp quadruple therapy(group B: the three above drugs plus killing H pylori capsule 6 capsules bid for 4 wk) and (3) placebo(group C: gastropine 3 tablets bid for 4 wk). H pylori eradication and ulcer healing quality were evaluated under an endoscope 4 wk after treatment. The patients were followed up for 5 years. RESULTS: Both the healing rate of PU and H pylori eradication rate in group B were significantly higher than those in group C (100% and 96.4% vs20% and 0%, respectively,P<0.005), but there was no significant difference compared to those in group A (88% and 92%, P>0.05). The healing quality of ulcer in group B was superior to that in groups C and A (P<0.05). The recurrence rate of PU in group B (4%) was lower than that in group A (10%) and group C (100%,P<0.01). CONCLUSION: Killing Helicobacter pylori quadruple therapy can not only promote the eradication of H pylori and healing quality of ulcer but also reduce recurrence rate of ulcer.     

Comparison of sequential and 7-, 10-, 14-d triple therapy for Helicobacter pylori infection

AIM: To compare the effectiveness of sequential therapy for Helicobacter pylori (H. pylori) infection with that of triple therapy of varying durations.METHODS: The 460 patients enrolled in this study had H. pylori-associated gastritis or a gastric or duodenal ulcer. After screening, H. pylori-infected patients were randomly assigned to receive either conventional triple therapy for 7, 10 or 14 d, or a new 10-d sequential therapy. Each of the 4 treatment groups included 115 patients. The outcomes of eradication therapy were assessed 4 wk after treatment by the urea breath test and histology.RESULTS: The overall eradication rate was 81.0%, and eradication rates were 75.7% for 7-d conventional triple therapy, 81.9% for 10-d conventional triple therapy, 84.4% for 14-d conventional triple therapy, and 82.0% for 10-d sequential therapy. Neither intention-to-treat analysis nor per protocol analysis showed significant differences in eradication rates using sequential therapy or the standard triple therapy (P = 0.416 and P = 0.405, respectively).CONCLUSION: There are no significant differences between 10-d sequential eradication therapy for H. pylori and any duration of standard triple treatment in Korean patients.     

Nonsteroidal anti-inflammatory drug use does not affect short-term endoscopic and histologic outcomes after Helicobacter pylori eradication in patients with rheumatoid arthritis

We evaluated the effects of the use of nonsteroidal anti-inflammatory drugs (NSAIDs) on endoscopic and histological findings in patients with rheumatoid arthritis (RA) before and after the eradication of Helicobacter pylori infection. Helicobacter pylori (H. pylori) eradication using lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 200 mg twice daily for 1 week was conducted in 44 patients (mean age: 56.5 years) with RA. Using the updated Sydney system, endoscopic and histological findings of the greater curvature of the antrum, the greater curvature of the upper corpus, and the lesser curvature of the lower corpus were compared before and after eradication, for a mean follow-up period of 3.5 months. Overall, H. pylori eradication was successful in 32 patients (72.7%). Of these 32 patients, 23 were NSAID users. In the successful eradication group, (1) there was no significant change on endoscopic findings, including gastric erythema and erosion in all three regions irrespective of NSAIDs use; (2) of 17 active ulcers before eradication in NSAIDs users, all healed except for one duodenal ulcer that persisted, where one patient newly developed a gastric ulcer, one developed erosive duodenitis, and two developed reflux esophagitis, all in NSAID users; (3) neutrophil infiltration and chronic inflammation were significantly improved in all three regions after H. pylori eradication irrespective of use of NSAIDs, while atrophic change and intestinal metaplasia did not change. In the eradication failure group; (1) there was no significant change on endoscopic and histological findings in the three regions; (2) two of three ulcers present before eradication on NSAID users persisted even after eradication, and no new cases of gastric ulcer or erosive duodenitis occurred. In conclusion, over a mean follow-up period of 3.5 months, use of NSAIDs in Japanese patients with RA did not impair the healing process of gastric and duodenal ulcers nor did it affect the endoscopic and histological improvements associated with H. pylori eradication.