Successful eradication of Helicobacter pylori prevents relapse of peptic ulcer disease. Combination therapies with a proton pump inhibitor for Helicobacter pylori-infected gastric ulcer patients. Helicobacter pylori eradication as the sole treatment for gastric and duodenal ulcers. Is eradication sufficient to heal gastric ulcers in patients infected with Helicobacter pylori? A randomized, controlled, prospective study. Effect of the eradication of Helicobacter pylori on duodenal ulcer healing and ulcer relapse: randomized controlled study in Japan. Eradication of Helicobacter pylori infection and the recurrence of duodenal ulcers. Randomised double blind controlled study of recurrence of gastric ulcer after treatment for eradication of Helicobacter pylori infection. Eradication of Helicobacter pylori improves the healing rate and reduces the relapse rate of nonbleeding ulcers in patients with bleeding peptic ulcer. The GU-MACH study: the effect of 1-week omeprazole triple therapy on Helicobacter pylori infection in patients with gastric ulcer. Effects of killing Helicobacter pylori quadruple therapy on peptic ulcer: a randomized double-blind clinical trial. Helicobacter pylori eradication versus one-year maintenance therapy: effect on relapse and gastritis outcome. Prospective, randomized study of H2-blocker and triple therapy for duodenal ulcer treatment and the eradication of Helicobacter pylori. Triple therapy for the eradication of Helicobacter pylori and reduction of duodenal ulcer relapse: comparison of 1 week and 2 week regimens and recrudescence rates over 12 months. Cure of gastric ulcer disease after cure of Helicobacter pylori infection--German Gastric Ulcer Study. Effect of treatment of Helicobacter pylori infection on the long-term recurrence of gastric or duodenal ulcer. A randomized, controlled study. Helicobacter pylori eradication in the healing and recurrence of benign gastric ulcer: a two-year, double-blind, placebo controlled study. 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. Does the eradication of Helicobacter pylori cure duodenal ulcer disease in communities with a high prevalence rate? Comparison with long-term acid suppression. One-week antibiotics versus maintenance acid suppression therapy for Helicobacter pylori-associated peptic ulcer bleeding. Short and long term outcome of Helicobacter pylori positive resistant duodenal ulcers treated with colloidal bismuth subcitrate plus antibiotics or sucralfate alone. Randomised controlled trial of short term treatment to eradicate Helicobacter pylori in patients with duodenal ulcer. Helicobacter pylori eradication reduces the rate of rebleeding in ulcer hemorrhage. Treatment of Helicobacter pylori reduces the rate of rebleeding in peptic ulcer disease. The DU-MACH study: eradication of Helicobacter pylori and ulcer healing in patients with acute duodenal ulcer using omeprazole based triple therapy. Eradication of Helicobacter pylori and prevention of recurrence of duodenal ulcer: a randomized, double-blind, multi-centre trial of omeprazole with or without clarithromycin. [Helicobacter pylori eradication heals the duodenal ulcer. Randomized, simple, and controlled study with omeprazole]. Effect of Helicobacter pylori eradication on duodenal ulcer scar in patients with no clinical history of duodenal ulcer. Prospective, randomized, investigator-blind trial of Helicobacter pylori infection treatment in patients with refractory duodenal ulcers. Healing and long-term relapse rates. Antibacterial treatment of gastric ulcers associated with Helicobacter pylori. Lansoprazole reduces ulcer relapse after eradication of Helicobacter pylori in nonsteroidal anti-inflammatory drug users--a randomized trial. Management of Helicobacter pylori eradication--the influence of structured counselling and follow-up. Long-term effects of eradication of Helicobacter pylori on relapse and histology in gastric ulcer patients: a two-year follow-up study. A multicenter, double-blind study on triple therapy with lansoprazole, amoxicillin and clarithromycin for eradication of Helicobacter pylori in Japanese peptic ulcer patients. An alternative non-macrolide, non-imidazole treatment regimen for curing Helicobacter pylori and duodenal ulcers: ranitidine bismuth citrate plus amoxicillin. The RBC H. pylori Study Group. Effect of esomeprazole triple therapy on eradication rates of Helicobacter pylori, gastric ulcer healing and prevention of relapse in gastric ulcer patients. Ranitidine bismuth citrate with clarithromycin for the eradication of Helicobacter pylori and for ulcer healing. Enhancing compliance not a prerequisite for effective eradication of Helicobacter pylori: the HelP Study. Antibiotic versus maintenance therapy in the prevention of duodenal ulcer recurrence. Results of a multicentric double-blind randomized trial. Does treatment of Helicobacter pylori with antibiotics alone heal duodenal ulcer? A randomised double blind placebo controlled study. Effect of ranitidine and amoxicillin plus metronidazole on the eradication of Helicobacter pylori and the recurrence of duodenal ulcer. Low H. pylori reinfection rate after triple therapy in Chilean duodenal ulcer patients. Three treatment schemes with colloidal bismuth subcitrate (Q-ULCER) in peptic ulcer with Helicobacter pylori. Treatment of Helicobacter pylori in patients with duodenal ulcer hemorrhage--a long-term randomized, controlled study. Helicobacter pylori eradication in dyspeptic primary care patients: a randomized controlled trial of a pharmacy intervention. Double-blind, multicenter, placebo-controlled evaluation of clarithromycin and omeprazole for Helicobacter pylori-associated duodenal ulcer. Antimicrobial therapy for Helicobacter pylori infection versus long-term maintenance antisecretion treatment in the prevention of recurrent hemorrhage from peptic ulcer: prospective nonrandomized trial on 125 patients. Refractory duodenal ulcer healing and relapse: comparison of omeprazole with Helicobacter pylori eradication. Cure with omeprazole plus amoxicillin versus long-term ranitidine therapy in Helicobacter pylori-associated peptic ulcer bleeding. Triple versus dual therapy for eradicating Helicobacter pylori and preventing ulcer recurrence: a randomized, double-blind, multicenter study of lansoprazole, clarithromycin, and/or amoxicillin in different dosing regimens.
The NIH consensus conference in 1994 recommended that all patients with peptic ulcers should be tested and treated for Helicobacter pylori. Recent studies have shown that the eradication of H. pylori is associated with a significant reduction in the relapse rate of peptic ulcers, but there are few reports about long-term outcome.
                To evaluate the relapse rate of peptic ulcer in the long-term follow-up of patients after H. pylori eradication therapy.
                Patients infected with H. pylori (445; 88 duodenal ulcer, 357 gastric ulcer) were randomly divided into three groups. In group A, patients received 'conventional treatment' including acid decreasing therapy with a histamine H2-receptor antagonist or proton pump inhibitor (PPI). In group B, patients received 'dual therapy' including one antibiotic plus acid-decreasing therapy. In group C, patients received 'triple therapy' with PPI plus amoxicillin and clarithromycin. Eradication of H. pylori infection was assessed by histology of biopsy specimens from both the antrum and body corpus at 4 weeks, and 6 and 12 months after stopping therapy. Endoscopy was performed at intervals of 6 months for 5 years.
                Intention-to-treat eradication rates for the duodenal ulcer patients were 0% for group A, 46% for group B and 80% for group C; eradication rates for the gastric ulcer patients were 0%, 33% and 83% respectively. No recurrence was noted in the duodenal ulcer patients and only 4% of gastric ulcers recurred after successful eradication during follow-up for 5 years. In contrast, in patients with persistent H. pylori infection all DU and 92% of gastric ulcers recurred.
                Eradication of H. pylori infection changes the natural course of peptic ulcer. We investigated the eradication and recurrence rate of Helicobacter pylori-infected gastric ulcer patients by combination therapies. Eighty-six H. pylori-positive gastric ulcer patients were assigned randomly to one of seven groups: I, omeprazole 20 mg (n = 9); II, lansoprazole (LPZ) 30 mg (n = 16); III, LPZ 30 mg plus plaunotol 480 mg (n = 13); IV, LPZ 30 mg plus ecabet sodium 2 g (n = 11); V, LPZ 30 mg plus clarithromycin 600 mg (the first 2 weeks; n = 11); VI, LPZ 30 mg plus plaunotol 480 mg plus clarithromycin 600 mg (the first 2 weeks; n = 13); and VII, LPZ 30 mg plus ecabet sodium 2 g plus amoxicillin 1,500 mg (the first 2 weeks; n = 13). All therapy was for 8 weeks except where otherwise noted. H. pylori eradication rates as diagnosed by culture, histology, urease test, and [13C]urea breath test 4 weeks after stopping therapy were 0, 0, 8, 45, 6, 46, and 62%, respectively, in groups I-VII. No patient achieving H. pylori eradication suffered recurrence. The combination therapies with proton pump inhibitors in addition to antibiotics and antiulcer agents are safe and effective in H. pylori eradication. It is uncertain whether eradication of Helicobacter pylori--without a prolonged suppression of acid secretion--is sufficient to allow healing of peptic ulcers. We evaluated whether eradication of H. pylori with no following anti-secretory medication then administered is sufficient for treatment of peptic ulcers. We also looked at the impact of non-steroidal anti-inflammatory drug (NSAID) and acetylsalicylic acid (ASA) use on ulcer relapses.
                The effect of eradication on ulcer healing and relapse rate was analysed in 115 patients, randomly allocated to four treatment groups: (1) quadruple therapy (28); (2) dual therapy (n-30); (3) triple therapy (n=27); and (4) lansoprazole and placebo (n=30). Endoscopic assessment was performed at 0, 8, and 52 weeks.
                The ulcer healing rate was 100% [95% confidence interval (CI), 95-100%] in H. pylori-negative and 83% (95% CI, 67-94%) in H. pylori-positive patients (P<0.01). In patients who used NSAIDS or ASA, the healing rates was 100% (95% CI, 73-100%) and 75% (95% CI, 19-99%) in H. pylori-negative (12 patients) and H. pylori-positive patients (four patients) (P = not significant). Ulcer relapses occurred in 5% (95% CI, 1-13%) of H. pylori-negative and in 36% (95% CI, 19-56%) of H. pylori-positive patients (P < 0.01). In H. pylori-negative patients who used NSAIDs or ASA the ulcer relapse rate was 30% (95% CI, 7-65%), whereas the ulcer relapse rate was 2% (95% CI, 0.4-10%) in patients who did not use NSAIDs or ASA (P < 0.05). No difference in ulcer relapse rate in H. pylori-positive patients who used or did not use NSAIDs or ASA was found. The eradication rate of H. pylori was 93% (95% CI, 76-99%) in the quadruple therapy group, 83% (95% CI, 64-94%) in the dual therapy group, 100% (95% CI, 87-100%) in the triple therapy group, and 0% (95% CI, 0-12%) in the lansoprazole and placebo group.
                Eradication treatment for H. pylori-positive gastric or duodenal ulcer is sufficient, with no need to follow it with anti-secretory medication. Cure of the infection reduces ulcer relapses in patients who did not use NSAIDs or ASA. In Helicobacter pylori infection, the effect of short-term triple therapy with proton pump inhibitor plus two antibiotics on gastric ulcer healing is not well known.
                To compare 1-week triple therapy with 8-week proton pump inhibitor therapy on gastric ulcer healing in infected patients.
                We randomly assigned 120 patients with H. pylori and gastric ulcers to proton pump inhibitor plus amoxicillin and clarithromycin for 1 week (n = 61) or proton pump inhibitor alone for 8 weeks (n = 59), with endoscopic assessment of ulcer healing 8 weeks after the start of treatment.
                Triple therapy eradicated H. pylori in 51 patients [intention-to-treat, 84%; 95% confidence interval (CI), 75-93%]. At 8 weeks, gastric ulcers were healed in 30 patients given triple therapy (49%; 95% CI, 37-62%) and in 49 patients given proton pump inhibitor (83%; 95% CI, 73-93%, P < 0.001). Healing rates in the triple therapy and proton pump inhibitor-only groups were 89% and 100%, respectively, for ulcers of < 1.0 cm in diameter, 54% and 77% for ulcers of 1.0 to < 1.5 cm in diameter, and 5% and 77% (P < 0.001) for ulcers of > or = 1.5 cm in diameter.
                One-week triple therapy healed most ulcers of < 1.0 cm, but not ulcers of > or = 1.5 cm. Short-term therapy is effective for gastric ulcers of < 1.0 cm, but, for larger ulcers, follow-up therapy to suppress acid is needed. To investigate the effect of the eradication of Helicobacter pylori on the healing and relapse of duodenal ulcers. 50 patients with active duodenal ulcer and H. pylori infection were randomly allocated to two treatment groups. One group (cimetidine group) received cimetidine 400 mg twice daily for 6 weeks and the other group (double-therapy group) received 300 mg amoxicillin granules and 250 mg metronidazole thrice daily for 2 weeks, in addition to the same regimen of cimetidine as the cimetidine group. Forty-two patients completed the study. After confirmation of ulcer scar, all patients were followed up for 6 months while receiving treatment with teprenone, an agent that does not affect acid secretion or the eradication of H. pylori. The healing rates at 6 weeks were 90% in the cimetidine group and 95.5% in the double-therapy group. H. pylori eradication occurred in 0% of the cimetidine group and in 73.7% of the double-therapy group (P = 0.004). The cumulative relapse rates in the two groups at 6 months were 64.3% and 11.1%, respectively (P = 0.0007). In the double-therapy group, the cumulative relapse rate at 6 months in the patients in whom H. pylori persisted was 50% (2/4); the rate was 0% (0/14) in the patients in whom H. pylori had been eradicated (P = 0.005). Histological gastritis significantly improved compared with the baseline in the double-therapy group, but no such improvement was seen in the cimetidine group. White scarring was found in 7.1% of the cimetidine group and in 83.3% of the double-therapy group after 6 months (P < 0.0001). The eradication of H. pylori markedly decreased the relapse rate in duodenal ulcer patients, and it significantly improved both the grade of gastritis and the quality of the ulcer scar. The purpose of this study was to compare the performance of different regimens on Helicobacter pylori (H. pylori) eradication and duodenal ulcer recurrence. During a four-week period, 59 patients with duodenal ulcers who were positive for H. pylori infection were randomly treated with one of three regimens. Seventeen patients were treated with ranitidine, 19 with colloidal bismuth subcitrate (CBS), and 23 with triple therapy (CBS, tetracycline and metronidazole). Forty-six patients with healed ulcers after treatment received follow-up for six months without maintenance therapy. The recurrence rates of duodenal ulcers confirmed by endoscopy in these three groups were 64%, 33% and 0% at the third month, and 73%, 67% and 5% at the sixth month, respectively. In the ranitidine therapy group, H. pylori infection was still present at the final follow-up. In the CBS therapy group, H. pylori was suppressed initially, but recurred in all cases. In the triple therapy group, there was only one case in which H. pylori infection persisted and where ulcer recurrence occurred after 3.5 months. The remaining cases were all H. pylori negative and had no recurrence of duodenal ulcers during the six months of follow-up. Overall, 19/27 (70%) patients positive for H. pylori had a recurrence of duodenal ulcers, while none of the 19 patients who were negative for H. pylori had a recurrence of ulcers at the sixth month. This study shows that triple therapy is more effective than the other two regimens in the eradication of H. pylori and in reducing the recurrence of ulcers. H. pylori may play a role in the recurrence of the duodenal ulcer. To determine whether eradication of Helicobacter pylori infection reduces recurrence of benign gastric ulceration.
                Randomised, double blind, controlled study. Patients were randomised in a 1:2 ratio to either omeprazole 40 mg once daily for eight weeks or the same treatment plus amoxycillin 750 mg twice daily for weeks 7 and 8. A 12 month untreated follow up ensued.
                Teaching and district general hospitals between 1991 and 1994.
                107 patients with benign gastric ulcer associated with H pylori.
                Endoscopically confirmed relapse with gastric ulcer (analysed with life table methods), H pylori eradication, and healing of gastric ulcers (Mantel-Haenszel test).
                172 patients were enrolled. Malignancy was diagnosed in 19; 24 were not infected with H pylori; four withdrew because of adverse events; and 18 failed to attend for start of treatment, leaving 107 patients eligible for analysis (35 omeprazole alone; 72 omeprazole plus amoxycillin). In the omeprazole/amoxycillin group 93% (67/72; 95% confidence interval 84% to 98%) of gastric ulcers healed and 83% (29/35; 66% to 94%) in the omeprazole group (P = 0.103). Eradication of H pylori was 58% (42/72; 46% to 70%) and 6% (2/35; 1% to 19%) (P < 0.001) and relapse after treatment was 22% (16/72) and 49% (17/35) (life table analysis, P < 0.001), in the two groups, respectively. The recurrence rates were 7% (3/44) after successful H pylori eradication and 48% (30/63) in those who continued to be infected (P < 0.001).
                Eradication of H pylori reduces relapse with gastric ulcer over one year. Eradication rates achieved with this regimen, however, are too low for it to be recommended for routine use. A causal relationship between Helicobacter pylori (H. pylori) and peptic ulcer complications remains obscure. The aim of this study was to determine the importance of H. pylori and other risk factors for healing rate, ulcer recurrence, and rebleeding in patients with bleeding peptic ulcer.
                A total of 223 patients with H. pylori positive bleeding peptic ulcer were randomly allocated to three treatment groups: 1) quadruple therapy (QT) (88 patients); 2) dual therapy (DT) (88 patients); and 3) omeprazole and placebo therapy (OPl) (47 patients). Endoscopic assessment was performed initially and at 8 and 52 wk. Ulcer healing and eradication rates were assessed; endpoints were ulcer relapse and ulcer rebleeding during 52 wk.
                Results after 8 and 52 wk were available for 211 and 179 patients, respectively. Eradication rate was 100% (95% CI = 96-100%) in the QT, 84% (95% CI = 74-91%) in the DT, and 4% (95% CI = 1-15%) in the OPl group. Ulcer healing rate was 95% (95% CI = 91-98%) in H. pylori negative and 8% (95% CI = 70-91%) in H. pylori positive patients. Ulcer relapses occurred in 2% (95% CI = 0.5-6%) of H. pylori negative and in 38% (95% CI = 24-54%) of H. pylori positive patients, and rebleeding occurred in five patients (three H. pylori positive and two negative).
                Eradication of H. pylori infection enhances healing of bleeding peptic ulcers after endoscopic therapy. H. pylori infection is an important independent risk factor for relapsing of nonbleeding ulcers in patients with bleeding peptic ulcer. To study the efficacy of omeprazole triple therapy in the eradication of Helicobacter pylori in patients with active gastric ulcer, and to assess healing and relapse of gastric ulcer.
                A double-blind, randomized study was carried out in 18 centres in Germany, Hungary and Poland. Patients (n = 160) with gastric ulcer and a positive H. pylori screening test were randomized to a 7-day twice daily treatment with omeprazole 20 mg, clarithromycin 500 mg and amoxycillin 1000 mg (OAC) or omeprazole 20 mg, clarithromycin 250 mg and metronidazole 400 mg (OMC), or with omeprazole 20 mg once daily (O). After completion of this 1-week treatment, patients were treated with omeprazole until healing (maximum 12 weeks), and followed for 6 months. H. pylori was assessed by urea breath test (UBT) and histology.
                Eradication rates ITT were OAC 79% (95% CI: 65-90%), OMC 86% (95% CI: 73-94%) and O 4% (95% CI: 0-14%). Eradication rates PP were OAC 83% (95% CI: 68-93%), OMC 93% (95% CI: 80-98%) and O 3% (95% CI: 0-13%). Gastric ulcer relapses occurred in 5, 0 and 11 patients in the groups, respectively.
                The results from the study demonstrate that OMC and OAC 1-week regimens are safe and effective for eradication of H. pylori in gastric ulcer patients, and that ulcer relapse is infrequent after successful eradication. To study the therapeutic efficacy of a Chinese and Western integrated regimen, killing Helicobacter pylori quadruple therapy on H pylori-associated peptic ulcers (PU).
                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.
                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% vs 20% 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).
                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. The aim of this study was to determine ulcer healing and H. pylori eradication rates obtained with triple therapy (omeprazole, amoxicillin and clarithromycin). Ulcer relapsing rate one year after eradication was also assessed. Maintenance therapy with placebo was compared with ranitidine therapy and the effect of eradication on histological variables of the gastric mucosa was studied.
                A prospective, double-blind parallel study was performed in 85 patients endoscopically diagnosed of duodenal ulcer H. pylori positive. Patients were randomized to a 7-days triple therapy (group A) or omeprazole plus antibiotic placebo (group B). All patients were treated only with omeprazole for the next three weeks. Patients with ulcer healing after treatment were entered in a one-year follow up phase with ranitidine placebo (group A) or ranitidine (group B). Endoscopy and biopsies were performed at baseline, after treatment (5 weeks) and after 12 months of follow-up or when relapsing symptoms appeared.
                Healing rate was 90.2% in group A and 85.7% in group B. Eradication rate was 78% in group A and 0% in group B. Out of 37 healed patients in group A, eradication was achieved in 29 and only one relapse was found (3.4%). Three out of eight patients with healing but without eradication relapsed at 12 months (35%) (p < 0.05). Histopathological results showed statistically significant differences (p < 0.05) between eradicated and non eradicated patients in terms of severity of inflammation and intestinal metaplasia, but not in terms of atrophy.
                H. pylori eradication is useful to prevent ulcer relapse and to improve gastric mucosa status. The efficacy of H2-blocker and triple therapy in curing duodenal ulcer was compared and the contribution of the eradication of Helicobacter pylori on ulcer remission was assessed. Forty-two duodenal ulcer patients infected with H. pylori were randomized to receive either H2-blocker therapy with famotidine (n = 21) or triple therapy with bismuth, amoxicillin, and metronidazole (n = 21). All patients received treatment for four weeks. Endoscopic evaluation of ulcer status and bacteriologic identification of H. pylori were performed at two, six and 12 months after therapy. Triple therapy had a similarly high healing rate to H2-blocker therapy (100% vs 90.5%) at two months of follow-up. However, at 12 months of follow-up, the ulcer remission rate in the triple therapy group (94.4%) was significantly higher than that of the H2-blocker therapy group (38.9%) (p < 0.05), resulting in the former therapy having a significantly lower rate of H. pylori infection compared to the latter (5.6% vs 100%, p < 0.005). Patients with persistent H. pylori infection at two months of follow-up had a significantly higher ulcer recurrence rate (64.7%) at 12 months than those without infection (5.3%) (p < 0.05). The success of triple therapy in ulcer remission may be attributed to the high eradication rate of H. pylori. The aim of this study is to assess the relationship between Helicobacter pylori and the relapse of duodenal ulcer, and also to evaluate the differences in efficacy and side effects between 1 week and 2 week triple therapy. Sixty-two patients with active duodenal ulcer, which healed within 8 weeks of nizatidine treatment, were randomly allocated to one of two groups. Group 1 (n = 29) received no drugs, Group II (n = 33) received triple therapy for 1 week (IIa, n = 16) or 2 weeks (IIb, n = 17). Eleven patients whose ulcer did not heal after an 8 week nizatidine treatment period were randomly assigned into Group IIa (n = 5) and IIb (n = 6). Seven patients whose ulcer recurred after discontinuation of nizatidine were allocated to receive 2 weeks of triple therapy. All patients received endoscopy 6 weeks after entry, and again at 3, 6 and 12 months unless both ulcer recurrence and H. pylori infection were found. The frequency of ulcer relapse 6 weeks after the active duodenal ulcer had healed was 83% (24/29 in Group I, 13% in Group 11a and 14% in Group IIb. The cumulative rate of recurrence was significantly higher in Group I than in Group II (90 vs 30% at 12 months, P < 0.01). Ulcer relapse was associated with persistence of H. pylori infection (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS) Helicobacter pylori infection is associated with gastric ulcer disease in about 75% of cases.
                The aim of this study was to determine whether H. pylori eradication reduces gastric ulcer relapse rates.
                The study was randomized, controlled, multicentric and investigator blinded, and was conducted at three university hospitals, two teaching hospitals, and by six practising gastroenterologists.
                During a period of 1 year 152 patients with gastric ulcers were randomly assigned to one of two treatment regimens: omeprazole 20 mg daily in the morning for 8 weeks (74 patients), or bismuth subsalicylate 600 mg three times daily for 8 weeks combined with 500 mg amoxicillin twice daily and 1000 mg tinidazole twice daily for the first 10 days (triple therapy) (78 patients). Follow-up examinations were performed 6, 12 and 18 months after treatment and whenever ulcer symptoms occurred.
                Of the 152 randomized patients five were excluded because of gastric cancer, 10 missed follow-up examinations and seven receiving triple therapy terminated treatment because of side effects. Of the remaining 130 patients, five of 69 (7.2%) in the omeprazole and six of 61 (9.8%) in the triple group were H. pylori negative. After 8 weeks' therapy, the gastric ulcer was healed in 85.9% (omeprazole) and in 81.8% triple) in H. pylori-positive patients, and in 80% (omeprazole) and 16.7% (triple) in H. pylori-negatives. H. pylori was eradicated in 8.1% of the patients who received omeprazole monotherapy and in 78.2% receiving triple therapy, and in 8.1% and 69.4% in an intention-to-treat analysis. The subsequent relapse rates during a follow-up period of 12 months were 50% in the omeprazole group and 4% in the triple group. Gastric ulcer relapse was observed in 49% of patients who were H. pylori positive and in 2% who were H. pylori negative after treatment.
                The data show that the presence of H. pylori is an important predictor of gastric ulcer relapse and that eradication of H. pylori may heal gastric ulcer disease. To determine the effect of treating Helicobacter pylori infection on the recurrence of gastric and duodenal ulcer disease.
                Follow-up of up to 2 years in patients with healed ulcers who had participated in randomized, controlled trials.
                A Veterans Affairs hospital.
                A total of 109 patients infected with H. pylori who had a recently healed duodenal (83 patients) or gastric ulcer (26 patients) as confirmed by endoscopy.
                Patients received ranitidine, 300 mg, or ranitidine plus triple therapy. Triple therapy consisted of tetracycline, 2 g; metronidazole, 750 mg; and bismuth subsalicylate, 5 or 8 tablets (151 mg bismuth per tablet) and was administered for the first 2 weeks of treatment; ranitidine therapy was continued until the ulcer had healed or 16 weeks had elapsed. After ulcer healing, no maintenance antiulcer therapy was given.
                Endoscopy to assess ulcer recurrence was done at 3-month intervals or when a patient developed symptoms, for a maximum of 2 years.
                The probability of recurrence for patients who received triple therapy plus ranitidine was significantly lower than that for patients who received ranitidine alone: for patients with duodenal ulcer, 12% (95% CI, 1% to 24%) compared with 95% (CI, 84% to 100%); for patients with gastric ulcer, 13% (CI, 4% to 31%) compared with 74% (44% to 100%). Fifty percent of patients who received ranitidine alone for healing of duodenal or gastric ulcer had a relapse within 12 weeks of healing. Ulcer recurrence in the triple therapy group was related to the failure to eradicate H. pylori and to the use of nonsteroidal anti-inflammatory drugs.
                Eradication of H. pylori infection markedly changes the natural history of peptic ulcer in patients with duodenal or gastric ulcer. Most peptic ulcers associated with H. pylori infection are curable. Helicobacter pylori infection is associated with idiopathic gastric ulcer in about 90% of the cases, but only a few controlled studies aimed at evaluating gastric ulcer healing and the natural history after Helicobacter pylori-eradication have been carried out.
                The aim of the present study was to evaluate the efficacy of omeprazole coupled with amoxicillin in the eradication of Helicobacter pylori and healing and prevention of gastric ulcer recurrence.
                Fifty-nine patients with active gastric ulcer were randomized under double-blind conditions to receive either omeprazole 20 mg twice daily for four weeks plus amoxicillin 3 g daily during the first and second week (29 patients, Group A) or omeprazole .20 mg twice daily for 4 weeks plus placebo for two weeks (30 patients, Group B).
                Endoscopic studies were carried out at the end of the 4 weeks treatment (or after 8 weeks in non-healed patients) as well as 2, 6 and 12 months later. A total of 3 biopsies in the antrum, 3 in the gastric body and at least seven at the edge of the crater were taken at each endoscopic control for exclusion, of malignancy, histological detection of Helicobacter pylori and for evaluation of gastric histology according to the Sydney system.
                With intention to treat analysis, the percentage of healing after 4 and 8 weeks was 86% and 100% in Group A patients and 86% and 93% in Group B, respectively. Two patients dropped out in Group B for non medical reasons. The percentage of eradication was 63% in Group A and 7% in Group B. During a 12-month follow-up gastric ulcer relapsed in 20/32 (63%) of the persistently Helicobacter pylori positive patients. Only two out 20 (10%) Helicobacter pylori cured patients showed a gastric ulcer relapse and Helicobacter pylori reinfection. Twenty out of 30 patients, still healed after 12 months, underwent endoscopic control after two years. A gastric ulcer relapse was observed in three out of nine (33%) patients with persisting infection after treatment. No gastric lesions, but one case of erosive oesophagitis were observed in the 11 Helicobacter pylori-eradicated patients.
                In our experience, Helicobacter pylori eradication does not favour gastric ulcer healing but does positively influence the subsequent natural history. 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.
                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.
                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.
                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).
                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. The long-term effect of Helicobacter pylori eradication on the natural history of duodenal ulcer has been investigated and compared with long-term acid suppression treatment in an endemic community for infection. Seventy-three patients with endoscopically verified H. pylori positive active duodenal ulcer disease were included in this prospective study. Patients were divided into two groups. Group A patients (n = 39) were given an omeprazole-based triple eradication regimen, while group B patients (n = 34) were given omeprazole alone followed by long-term famotidine 20 mg daily as maintenance treatment. A control endoscopy was performed at the third month of treatment. The bacterium was eradicated in 32 (82%) of group A patients. All patients were followed up for two years and an endoscopy performed at the end of each year. H. pylori recurred in 13 patients and the reinfection rate was 44.8% over two years. Duodenal ulcer recurred in seven of these patients at two years (24.1%). There was a close association between H. pylori reinfection and ulcer relapse. Group B patients remained H. pylori positive during the study and the ulcer recurred in five of these patients (6.6%) despite continuous famotidine treatment. There was no statistically significant difference in ulcer relapse rate between the groups. These results suggested that H. pylori eradication is not an absolute solution for duodenal ulcer disease in high endemic regions and continuous maintenance treatment with H2-receptor antagonists is still an alternative approach in some chronic recurrent cases. Bleeding peptic ulcer is the most important cause of upper gastrointestinal bleeding. Our aim was to compare the effect of anti-Helicobacter therapy with maintenance treatment of H2-receptor antagonist in the prevention of relapses of ulcer and bleeding. Patients with bleeding duodenal or gastric ulcers and H. pylori infection were randomized to receive either a one-week course of triple therapy with bismuth subcitrate, metronidazole, and tetracycline plus ranitidine or a six-week course of ranitidine 300 mg/day. After the ulcers healed, the antibiotic-treated patients were not given any medication, whereas the ranitidine-treated patients continued to receive a maintenance dose of 150 mg/day. One hundred twenty-six patients were randomized to receive anti-Helicobacter therapy and 124 patients to receive long-term ranitidine. H. pylori eradication was achieved in 98.2% in those who received triple therapy and 6.1% in those who received ranitidine (P < 0.0001). At the six-week follow-up, ulcer healing was documented in 88.2% in those who received triple therapy and 86.1% in those who received ranitidine (P = 0.639). Recurrent ulcer developed in nine of the ranitidine-treated patients and three of them presented with recurrent upper gastrointestinal bleeding. One patient in the antibiotic group developed recurrent ulcer without rebleeding (P = 0.01). It is concluded that eradication of H. pylori is sufficient for the prevention of recurrent bleeding ulcers. Thirty two patients with Helicobacter pylori positive duodenal ulcers resistant to treatment were randomly assigned to 4 weeks' treatment with sucralphate 4 g/day or colloidal bismuth subcitrate 480 mg/day plus amoxycillin from days 1 to 7 and tinidazole from days 8 to 14. After 4 weeks, patients with unhealed ulcers were crossed over to the other form of treatment for a further 4 week period. Patients with healed ulcers were followed up for 1 year without maintenance therapy with clinical and endoscopic investigations 3, 6, and 12 months after healing. Complete healing rates at 4 weeks were 88% (15 of 17) in the colloidal bismuth subcitrate plus antibiotics group and 40% (six of 15) in the sucralphate group (p < 0.05). After cross over, overall healing rates were 88% (22 of 25) and 47% (eight of 17), respectively (p < 0.05). H pylori eradication occurred in 83% of patients treated with the triple therapy. Cumulative relapse rates at 12 months were 12% (two of 17) in patients in whom H pylori had been eradicated and 100% (10 of 10) in those with persistent infection after short term therapy (p < 0.05). These results show that a colloidal bismuth subcitrate plus antibiotics regimen is highly effective in the short term treatment of resistant duodenal ulcers and that H pylori eradication can change the natural tendency to early recurrence of these ulcers. To determine whether one week's drug treatment is sufficient to eradicate Helicobacter pylori in patients with duodenal ulcer.
                Single blind, randomised controlled trial.
                Specialised ulcer clinic in a teaching hospital.
                155 patients with H pylori and a duodenal ulcer verified endoscopically which had either bled within the previous 24 hours or was causing dyspepsia.
                Patients were allocated randomly to receive either omeprazole for four weeks plus bismuth 120 mg, tetracycline 500 mg, and metronidazole 400 mg (all four times a day) for the first week (n = 78), or omeprazole alone for four weeks (n = 77). Further endoscopy was performed four weeks after cessation of all drugs.
                Presence or absence of H pylori (by urease testing, microscopy, and culture of antral biopsy specimens), duodenal ulcer, and side effects.
                Eradication of H pylori occurred in 70 (95%) patients taking the four drugs (95% confidence interval 86% to 97%) compared with three (4%) patients taking omeprazole alone (1% to 11%). Duodenal ulcers were found in four (5%) patients taking the four drugs (2% to 12%) and in 16 (22%) patients taking omeprazole alone (14% to 32%). Mild dizziness was the only reported side effect (six patients in each group) and did not affect compliance.
                A one week regimen of bismuth, tetracycline, and metronidazole is safe and effective in eradicating H pylori and reduces the number of duodenal ulcers four weeks after completing treatment. To evaluate whether eradication with omeprazole and amoxicillin results in a reduction of ulcer recurrence and rebleeding in patients with Helicobacter pylori-associated duodenal ulcer hemorrhage, patients with upper gastrointestinal hemorrhage from duodenal ulcers with stigmata of recent hemorrhage, a drop in hemoglobin level of more than 2 g/dL, and documented H. pylori infection (by rapid urease test and histologic findings) were randomly assigned to receive omeprazole, 40 mg every day, and amoxicillin, 1 g twice a day, (Group A) or omeprazole alone, 40 mg every day, (Group B) for 2 weeks. No maintenance antiulcer therapy was given. Patients underwent a second endoscopy 4 weeks after completion of therapy and were followed for 1 year. Endoscopy was performed again at the end of 1 year. All patients showed ulcer healing 4 weeks after completion of therapy. H. pylori eradication rates were 83% (Group A) and 5% (Group B) (p < .001). Ulcer recurrences were significantly lower in Group A (3/29 or 10%) than in Group B (9/22 or 41%; p < .05). Comparison of Group A patients with eradication and Group B patients without eradication also revealed a significant difference in rates of ulcer relapse (1/24 or 4% versus 9/21 or 43%; p < .01). Rebleeding occurred significantly less often in the dual therapy group than in the omeprazole group (0/29 versus 6/22 or 27%; p < .01). Eradication of H. pylori significantly reduces the rates of ulcer recurrence and rebleeding in patients with duodenal ulcer bleeding. Dual therapy with omeprazole and amoxicillin should be considered in all H. pylori-positive patients with hemorrhage from duodenal ulcers. We evaluated whether therapy designed to eradicate Helicobacter pylori infection resulted in a reduction in rebleeding in patients with peptic ulcer disease. Patients presenting because of major upper gastrointestinal hemorrhage from peptic ulcer and whose ulcers healed in a study in which they were randomized to receive ranitidine alone or triple therapy plus ranitidine were followed up regularly with endoscopy. No maintenance anti-ulcer therapy was given after ulcer healing.
                Patients received ranitidine, 300 mg, or ranitidine plus triple therapy. Triple therapy consisted of tetracycline, 2 g; metronidazole, 750 mg; and bismuth subsalicylate, 5 or 8 tablets (151 mg bismuth per tablet), and was administered for the first 2 weeks of treatment; ranitidine therapy was continued until the ulcer had healed or 16 weeks had elapsed. After ulcer healing, no maintenance antiulcer therapy was given. Development of ulcer recurrence with or without recurrent upper gastrointestinal bleeding was evaluated.
                Thirty-one patients with major upper gastrointestinal bleeding from peptic ulcer were studied; 17 received triple therapy and 14 ranitidine alone. Major rebleeding occurred significantly (p = 0.031) more often in those in the ranitidine group (28.6%), compared with none (0%) in the triple therapy group.
                Eradication of H. pylori infection reduces the rate of ulcer recurrence and rebleeding in complicated ulcer disease. To investigate the efficacy of two omeprazole triple therapies for the eradication of Helicobacter pylori, ulcer healing and ulcer relapse during a 6-month treatment-free period in patients with active duodenal ulcer.
                This was a double-blind, randomized study in 15 centres across Canada. Patients (n = 149) were randomized to omeprazole 20 mg once daily (O) or one of two 1-week b. d. eradication regimens: omeprazole 20 mg, metronidazole 400 mg and clarithromycin 250 mg (OMC) or omeprazole 20 mg, amoxycillin 1000 mg and clarithromycin 500 mg (OAC). All patients were treated for three additional weeks with omeprazole 20 mg once daily. Ulcer healing was assessed by endoscopy after 4 weeks of study therapy. H. pylori eradication was determined by a 13C-urea breath test and histology, performed at pre-entry, at 4 weeks after the end of all therapy and at 6 months.
                The intention-to-treat (intention-to-treat) analysis contained 146 patients and the per protocol (per protocol) analysis, 114 patients. The eradication rates were (intention-to-treat/per protocol): OMC-85% and 92%, OAC-78% and 87% and O-0% (O). Ulcer healing (intention-to-treat) was greater than 90% in all groups. The differences in the eradication and relapse rates between O vs. OMC and O vs. OAC were statistically significant (all, P < 0.001). Treatment was well tolerated and compliance was high.
                The OMC and OAC 1-week treatment regimens are safe and effective for eradication, healing and the prevention of relapse in duodenal ulcer patients. Antimicrobial treatment for Helicobacter pylori eradication is currently recommended for all patients with duodenal ulcer disease, but consensus on the best treatment is lacking.
                Patients with active duodenal ulcer and H. pylori were enrolled in a double-blind, randomized, placebo-controlled multi-centre study. Patients received omeprazole 40 mg daily for 28 days and either clarithromycin 500 mg t.d.s. or placebo t.d.s. for the first 14 days. Patients underwent endoscopy before starting treatment, at 2 weeks, immediately after stopping treatment if unhealed at 2 weeks, and at 1, 6 and 12 months after the end of treatment, or at the recurrence of symptoms. Eradication of H. pylori, duodenal ulcer healing and ulcer recurrence were measured.
                One-hundred and fifty-four patients were recruited and randomized to omeprazole plus clarithromycin (n = 74) or to omeprazole plus placebo (n = 80). One month after treatment, H. pylori was eradicated in 57 of 69 (83%; 95% CI: 72-91%) patients receiving omeprazole plus clarithromycin, compared with 1 of 75 (1%; 95% CI: 0-7%) receiving omeprazole alone (P < 0.001). In patients receiving omeprazole plus clarithromycin the ulcer healed at 2 weeks in 83% (95% CI: 71-91%) and at 4 weeks in 100% (95% CI: 95-100%), compared with 77% (95% CI: 66-86%) and 97% (95% CI: 91-100%) in those given omeprazole plus placebo (N.S.). Ulcers recurred at 12 months in 6% (95% CI: 1-16%) of patients given omeprazole plus clarithromycin, compared with 76% (95% CI: 63-86%) of patients given omeprazole plus placebo (P < 0.001). The incidence of side-effects was similar in both treatment groups (38% with clarithromycin dual therapy and 29% with omeprazole plus placebo; P = 0.304). Ninety per cent of patients took at least 90% of their prescribed medication.
                Omeprazole plus clarithromycin dual therapy eradicated H. pylori in 83% of patients with duodenal ulcer and significantly decreased 12-month recurrence from 76% to 6%. 60 patients with Helicobacter pylori (Hp) infection and duodenal ulcer (DU) were randomized to received either: I) Two weeks of bismuth subcitrate, metronidazole and amoxicillin (TG) or II) Omeprazole for four weeks (OG). Endoscopy and antral biopsies were done at entry and four weeks after treatment, control endoscopy was performed 2-4-8 and 12 weeks after inclusion in the trial. Healing was similar in both groups at two four weeks. At twelve weeks DU recurred in OG 65% vs 13.36% in TG and Hp infection was present. Our results showed that Hp eradication healed DU in a similar rate than Omeprazole providing further evidence of a causal link between Hp infection and duodenal ulcer. Helicobacter pylori eradication has become the standard treatment for duodenal ulcer. However, there is no relevant evidence for antibacterial treatment of the white scar stage of duodenal ulcer (duodenal ulcer scar) in patients with no past history of duodenal ulcer.
                To investigate whether H. pylori eradication could decrease duodenal ulcer recurrence in patients with duodenal ulcer scar and no past history of duodenal ulcer.
                We prospectively enrolled 66 patients with duodenal ulcer scar: 53 were H. pylori-positive and 13 were H. pylori-negative. H. pylori-positive patients were randomly assigned into two groups (two-to-one allocation): 36 patients were assigned to the treatment group and 17 to the follow-up group. Thirteen H. pylori-negative patients were followed up according to the study protocol. Follow-up endoscopy was performed to evaluate ulcer scar changes and H. pylori status 6 weeks after anti-H. pylori treatment and then every 6 months for up to 30 months.
                Active duodenal ulcer recurrence was identified in seven of 23 H. pylori-positive/non-cured patients (30%). There was no duodenal ulcer recurrence in 43 H. pylori-negative/cured patients (0%), which was significantly different in terms of duodenal ulcer recurrence (P=0.001).
                H. pylori eradication is effective at preventing active duodenal ulcer recurrence in patients with duodenal ulcer scar and no past history of duodenal ulcer. 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 when Helicobacter 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 became Helicobacter pylori-negative. On bismuth, only one patient became Helicobacter 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 the Helicobacter pylori-negative patients had ulcer relapse. On the contrary, ulcers relapsed in all but one patient, who remained Helicobacter 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. There is a strong association between infection with Helicobacter pylori and gastric ulcers that are unrelated to the use of nonsteroidal antiinflammatory medications. We studied the efficacy of antibacterial therapy without medication to suppress gastric acid for the treatment of patients with H. pylori infection and gastric ulcers unrelated to the use of nonsteroidal agents.
                Patients with gastric ulcers seen on endoscopy and with H. pylori infection confirmed by smear or culture were randomly assigned to receive either a one-week course of antibacterial agents (120 mg of bismuth subcitrate, 500 mg of tetracycline, and 400 mg of metronidazole, each given orally four times a day) or a four-week course of omeprazole (20 mg orally per day). Follow-up endoscopies were performed after five and nine weeks. The patients and their physicians were aware of the treatment assignments, but the endoscopists were not.
                A total of 100 patients were randomly assigned to treatment, and 85 completed the trial. At five weeks, H. pylori had been eradicated in 41 of the 45 patients in the antibacterial-treatment group (91.1 percent; 95 percent confidence interval, 82.9 to 99.3) and in 5 of the 40 in the omeprazole group (12.5 percent; 95 percent confidence interval, 2.3 to 22.7; P < 0.001). The gastric ulcers were healed in 38 of the patients treated with antibacterial drugs (84.4 percent; 95 percent confidence interval, 73.9 to 95.0) and in 29 of those treated with omeprazole (72.5 percent; 95 percent confidence interval, 58.6 to 86.4; P = 0.28). At nine weeks, ulcer healing was confirmed in 43 of the patients receiving antibacterial therapy and in 37 of those receiving omeprazole (P = 1.0). The mean (+/- SD) duration of pain during the first week of treatment was 1.9 +/- 2.6 days in the omeprazole group, as compared with 3.6 +/- 3.0 days in the antibacterial-treatment group (P = 0.004). One year after treatment, recurrent gastric ulcers were detected in 1 of 22 patients (4.5 percent) in the antibacterial-treatment group and in 12 of 23 (52.2 percent) in the omeprazole group (P = 0.001). H. pylori was detected in the 1 patient with a recurrent ulcer who had received antibacterial treatment and in 10 of the 12 patients with recurrent ulcers who had received omeprazole.
                In patients with H. pylori infection and gastric ulcers unrelated to the use of nonsteroidal antiinflammatory drugs, one week of antibacterial therapy without acid suppression heals the ulcers as well as omeprazole and reduces the rate of their recurrence. To study whether prophylaxis with lansoprazole could prevent relapse of ulcers after eradication of Helicobacter pylori in patients with NSAID-related peptic ulcers.
                Patients who presented with peptic ulcers and were found to be infected with H. pylori while receiving NSAIDs were recruited into the study. They received, twice daily, lansoprazole 30 mg, amoxicillin 1 g and clarithromycin 500 mg for 1 week, followed by lansoprazole 30 mg daily for 4 weeks. Patients with healed ulcers and H. pylori eradicated were given naproxen 750 mg daily, and randomly assigned to receive lansoprazole 30 mg daily or no treatment for 8 weeks. The primary endpoint was the cumulative recurrence of symptomatic and complicated ulcers.
                At the end of the 8-week treatment period, significantly fewer patients (1/22, 4.5%, 95% confidence interval [CI] 0-23) in the lansoprazole group compared with the group that received H. pylori eradication alone (9/21, 42.9%, 95% CI 22-66) developed recurrence of symptomatic and complicated ulcers (log rank test P=0.0025).
                Lansoprazole significantly reduced the cumulative relapse of symptomatic and complicated ulcers in patients requiring NSAIDs after eradication of H. pylori. Helicobacter pylori (H. pylori) eradication rate varies according to the treatment regimen used and other factors, e.g. antimicrobial resistance and patient compliance. The aim of the present study was to evaluate the influence of patient counselling and follow-up on H. pylori eradication rates and to document the effectiveness of a 1 week eradication regimen consisting of lansoprazole (30 mg once daily), amoxicillin (1 g twice daily) and clarithromycin (500 mg twice daily).
                Seventy-six dyspeptic patients, who at endoscopy were found to have gastritis, duodenitis or ulceration, and a positive H. pylori urease test, were recruited. Patients were randomly assigned to an intervention group (n = 38) or a control group (n = 38). Intervention patients received their medicines via the hospital pharmacy and were counselled (and followed up) by a hospital pharmacist. Control patients were given a standard advice sheet and referred to their GP who prescribed the same therapy.
                Intervention patients exhibited a statistically significant improvement in the H. pylori eradication rate (94.7% vs 73.7%; P = 0.02) and compliance (92.1% vs 23.7; P < 0.001). Of the 64 H. pylori eradicated patients, 62 were able to eliminate their antisecretory medication compared with only 12 of the H. pylori persistent patients (P < 0.001). A pharmacoeconomic evaluation indicated that counselling and follow-up reduced the direct costs of eradication by approximately 30 UK pounds per patient.
                Structured patient counselling and follow-up can have a significant effect on H. pylori eradication rates and should be a routine part of therapy. The main purpose of this study was to compare omeprazole (ome) plus two antibiotics (OMC) with omeprazole plus placebo (OP) with regard to gastric ulcer relapse for a period of 2 years in patients who were Helicobacter pylori-positive at inclusion.
                Using double-blind randomization 125 patients with gastric ulcer were treated with either OMC (ome 20 mg b.i.d., metronidazole 400 mg b.i.d., clarithromycin 250 mg b.i.d.) (n = 64) or OP (ome 20 mg and placebo) (n = 61) for 1 week, followed by ome 20-40 mg o.d. until healing was confirmed endoscopically after 4, 8 or 12 weeks. Endoscopy and H. pylori diagnostics using culture, histology and serology were performed 6, 12 and 24 months after treatment or at symptomatic relapse. At inclusion, 35% of the OMC group and 38% of the OP group were taking non-steroidal anti-inflammatory drugs (NSAIDs). Nine percent (11/125) of the ulcers were malignant.
                The prevalence of H. pylori was 82% and the eradication rate 88% in the OMC group and 3% in the OP group. More than 90% of the ulcers were healed after 12 weeks. After 2 years, 76% of patients in the OMC group were in remission compared with 28% in the OP group (ITT) (P < 0.001). Sixty percent of patients in the OMC group that continued to take NSAIDs were in remission after 2 years compared with none in the OP group. Atrophy but not intestinal metaplasia decreased after treatment.
                Gastric ulcers are mainly caused by H. pylori, and relapse is effectively prevented by H. pylori eradication, even in patients on NSAIDs. Two triple therapies with lansoprazole (LPZ)/amoxicillin (AMPC)/clarithromycin (CAM) for eradication of Helicobacter pylori were studied in multicenter, double-blind fashion to evaluate the eradication rate of H. pylori and safety of eradiation treatment in Japanese patients with H. pylori-positive active gastric ulcers or duodenal ulcers.
                Patients were randomly chosen for the control treatment of LPZ 30 mg twice a day (b.i.d.; Group A-LPZ-only) or the test treatments of LPZ 30 mg plus AMPC 750 mg and CAM 200 mg b.i.d. (Group B-LAC200) and LPZ 30 mg, AMPC 750 mg and CAM 400 mg b.i.d. (Group C-LAC400). All eradication treatments lasted for a period of 7 days. Successful eradication was assessed by culture and gastric histology 1 month after completion of the ulcer treatment.
                The eradication rates of H. pylori in the full analysis set were 0% in Group A-LPZ-only, 87.5% in Group B-LAC200 and 89.2% in Group C-LAC400 for gastric ulcer and, 4.4% in Group A-LPZ-only, 91.1% in Group B-LAC200 and 83.7% in Group C-LAC400 for duodenal ulcer. The eradication rates of Group B-LAC200 and Group C-LAC400 were 89.2% (95% CI: 84.8-93.7%) and 86.4% (95%CI: 81.5-91.3%) in total in the full analysis set, 89% (95% CI: 84.3-93.7%) and 85.3% (95%CI: 80.1-90.5%) in the per protocol set. The eradication rates in Groups B-LAC200 and group C-LAC400 were statistically significantly higher than the rate in Group A-LPZ-only for both gastric ulcer and duodenal ulcer patients (p <.0001 for both).
                A satisfactorily high H. pylori eradication rate was obtained in Japanese ulcer patients with the triple therapy regimen consisting of LPZ 30 mg, AMPC 750 mg, and CAM 200 mg b.i.d. Because patients who fail to be cured of H. pylori infection following macrolide or imidazole therapy are difficult to treat, there is a clear need for a reasonably effective and simple second-line treatment regimen. The purpose of these two studies was to evaluate the efficacy of ranitidine bismuth citrate (RBC) plus amoxicillin for the cure of H. pylori infection and for healing duodenal ulcers and preventing ulcer relapse.
                Two identically designed randomized, double-blind, double-dummy studies were conducted in patients with an H. pylori-associated duodenal ulcer. Patients were treated with either RBC 400 mg bid for 4 weeks plus amoxicillin 500 mg qid for 2 weeks, RBC 400 mg bid for 4 weeks and placebo qid for 2 weeks, placebo bid for 4 weeks and amoxicillin 500 mg qid for 2 weeks, or placebo bid for 4 weeks and placebo qid for 2 weeks. Patients with healed ulcers after 4 weeks of treatment were eligible for entry into a 24-week observation phase for the assessment of H. pylori status (culture, histology, and CLOtest) and ulcer relapse.
                A total of 229 patients with confirmed H. pylori infection at baseline were evaluated. Of these, 132 whose ulcers had healed entered the 24-week posttreatment observation phase. The combination of RBC plus amoxicillin resulted in higher H. pylori cure rates (55%) and higher duodenal ulcer healing (74%) than did either treatment alone. All treatment were well tolerated.
                The combination of ranitidine bismuth citrate plus amoxicillin cures H. pylori infection in more than half of the patients treated. This treatment regimen shows promise as the basis for future non-macrolide, non-imidazole triple therapy regimens for curing H. pylori infection. Such regimens may be appropriate second-line treatment for patients who are resistant to or who are unable to tolerate macrolide- or imidazole-containing therapies. To compare esomeprazole-based triple therapy with esomeprazole alone for the eradication of Helicobacter pylori (H. pylori), healing of ulcer and prevention of relapse in H. pylori-related gastric ulcer (GU) diseases.
                In this double-blind study, 401 H. pylori-positive patients with more than or equal to two GUs were randomized to: esomeprazole (20 mg) twice daily (bid) and amoxicillin (1000 mg) bid and clarithromycin (500 mg) bid (EAC) for 1 week, followed by placebo for 3 weeks (EAC and placebo); EAC for 1 week, followed by esomeprazole (20 mg) once daily (E20) for 3 weeks (EAC and E20); or esomeprazole (20 mg) bid and placebo antimicrobials for 1 week, followed by E20 for 3 weeks (E20 bid and E20). Patients with unhealed GUs at 4 weeks received E20 for an additional 4 weeks. Healed patients were followed up for 12 months.
                Eradication rates at 4 weeks or 8 weeks were 82% for EAC and E20, 77% for EAC and placebo and 9.5% for E20 bid and E20 (intention-to-treat analysis). Significantly more patients receiving EAC than those receiving esomeprazole alone remained free of GUs during follow-up [EAC and E20, 90%; EAC and placebo, 87%; P=0.0005 for combined group vs. esomeprazole alone [E20 bid and E20 (74%)]. All treatments were well tolerated.
                Esomeprazole-based triple therapy is effective for the eradication of H. pylori, healing of GU and prevention of relapse. Esomeprazole monotherapy for 3 weeks after triple therapy may be beneficial in terms of healing. In a pilot study, ranitidine bismuth citrate (RBC; Pylorid, Tritec) in coprescription with clarithromycin achieved a Helicobacter pylori eradication rate (based on 13C urea breath test alone) of 83%. The aim of the current study was to validate this finding by using three diagnostic tests and a larger group of H. pylori-positive patients with active duodenal ulcer.
                In a blinded study, 95 patients were given either 4 weeks of treatment with RBC, 400 mg bid, alone (RBC400, n = 31) or RBC, 400 mg bid or 800 mg bid, in coprescription with clarithromycin, 250 mg qid for 14 days, followed by 14 days of RBC, 400 mg bid, alone (RBC400 + CLAR and RBC800 + CLAR, respectively; n = 32 for each). Rates of ulcer healing at week 4 and of H. pylori eradication (assessed by antral and corpus urease tests and histology and by 13C urea breath test) at week 8 were compared, together with the incidence of adverse events.
                All three regimens were effective at duodenal ulcer healing and were tolerated well. The coprescription regimens gave significantly higher observed H. pylori eradication rates (82% and 74% for RBC400 + CLAR and RBC800 + CLAR) compared with RBC400 (0%; p < .001).
                RBC in dual therapy with clarithromycin provides excellent H. pylori eradication therapy and is an effective duodenal ulcer healing drug. The aim of this study was to compare cure rates of Helicobacter pylori (H. pylori) infection, compliance, and side effects in patients given 10 days of omeprazole 20 mg b.d., amoxycillin 500 mg t.d.s., and metronidazole 400 mg t.d.s. (OAM) or 10 days OAM plus compliance enhancing measures.
                A total of 119 H. pylori-positive patients were prospectively randomized to receive either 10 days OAM or 10 days OAM plus compliance enhancing measures (medication in a dose dispensing unit, medication chart, an information sheet about H. pylori treatment, and phone call 2 days after starting therapy). H. pylori eradication was assessed by 13C-UBT at least 4 wk after cessation of therapy, compliance by phone interview on the last day of therapy and returned pill count, and side effects by phone interview and returned side effects form.
                In 113 patients attending 13C-UBT H. pylori was eradicated in 51 of 57 patients (89.5%) after 10 days OAM and in 48 of 56 (85.7%) after 10 days OAM plus compliance enhancing measures (p = 0.54). In both groups 97% of medications were taken. Side effects were common (82% of patients). Both side effects (p = 0.001) and ulcer versus nonulcer at endoscopy (p = 0.016) were independent predictors of treatment failure; side effects also predicted noncompliance (p = 0.02).
                Ten days of OAM was effective for H. pylori eradication in our clinical population. Patient compliance was excellent and attempts to increase compliance had no impact on outcome or compliance. Side effects were very common and were significantly associated with treatment failure and decreased compliance. Reduction of gastric acid secretion by maintenance therapy and eradication of Helicobacter pylori by antibiotic treatment have been shown to reduce duodenal ulcer relapse. This study compared the effect of two regimens, a 6-month maintenance on an H2 receptor antagonist versus a one-week antibiotic therapy, on the rate of duodenal ulcer relapse in duodenal ulcer patients with gastric H. pylori infection.
                We conducted a 30-week, double-blind, double-dummy, multicentric clinical trial involving 119 patients (97 M, 22 F, mean age 39 +/- 14 years) randomly assigned to a daily dose of 40 mg famotidine for 6 weeks supplemented with, during the first week, either antibiotics (500 mg amoxicillin q.i.d. and 500 mg tinidazole t.i.d.-antibiotic group) or their placebo (maintenance group). Healed patients after 6 weeks entered the 6-month maintenance phase: the maintenance group received 20 mg famotidine at bedtime and the antibiotic group, a placebo. Endoscopy with antral biopsies was performed to allow a rapid urease test, culture and histological examination upon entry, after 6 weeks, 3 months, and 6 months and, whenever symptoms recurred. H. pylori status was regarded as positive if any one of these three tests was positive, and negative if all tests were negative.
                The 2 treatment groups were well balanced for all baseline characteristics. After 6 weeks, H. pylori was eradicated in 25 (45%) patients in the antibiotic group, and in 1 (2%) in the maintenance group (P < 0.01). In term of intention-to-treat, there was no significant difference in the healing rate after 6 weeks (93 and 83% in the antibiotic and maintenance groups, respectively; P = 0.15) or in the relapse rate after 6 months (13 and 28% in the antibiotic and maintenance groups, respectively; P = 0.17 Log-rank test). However, the overall failure rate (absence of healing, relapse) was lower (P = 0.04, Log-rank test) in the antibiotic group in which all relapses but one were observed in H. pylori positive patients. The rate of ulcer relapse (1/20) in patients of antibiotic group who remained free of H. pylori during the study, was significantly (P < 0.01) lower compared with that of H. pylori positive patients in the maintenance group (11/44). During the first 6-week period, more side effects were observed in the antibiotic group than in the maintenance group (4 vs 1 patient, respectively).
                Our results indicate no significant difference between ulcer relapse rates after 6 months following a one-week antibiotic therapy or long-term maintenance therapy. Short-term antibiotic therapy should be considered as a valuable alternative to the long-term maintenance therapy. Treatment of Helicobacter pylori infection prevents duodenal ulcer relapse. It has not been established if treatment of the infection heals duodenal ulcer.
                To test the hypothesis that treatment of the infection was associated with healing of duodenal ulcer.
                A randomised, double blind placebo controlled trial was performed to study the efficacy of an antibiotic only regimen consisting of 300 mg metronidazole, 500 mg amoxycillin, and 250 mg clarithromycin, each given four times daily for two weeks, in the healing of duodenal ulcer as assessed by endoscopy. Symptoms were controlled with acetaminophen and antacids.
                Of 100 consecutive patients with endoscopically established duodenal ulcer, 97 with positive rapid urease test on antral biopsy specimens were admitted into the study and 81 completed the trial. Of these, 40 were randomised to receive antibiotics and 41 to receive placebo. Treatment with antibiotics resulted in 92.5% (95% confidence interval (95% CI) 84.3-100) healing at four weeks and 100% at eight and 12 weeks; the corresponding healing rates for placebo treatment were respectively, 36.6%, 61%, and 63.4% (95% CIs 21.8-51.3, 46.0-75.9, and 48.7-78.2 respectively). The differences between the two treatment groups were significant at p < 0.001 at each time point and by life table analysis. Clearance of H pylori as assessed by urease test on antral biopsy specimens at four weeks and eradication of the organism as determined by 13C-urea breath test at eight weeks were achieved in 85% and 62.5% of patients respectively. Duodenal ulcer healed at four weeks in 87.2% and 86.2% (95% CIs 76.7-97.7 and 73.7-98.8) of patients in whom H pylori clearance or eradication, was achieved, versus 42.9% and 51.9% (95% CIs 27.9-57.8 and 38.3-65.5; p < 0.001 and < 0.003 respectively) in whom these processes failed. Stepwise discriminant analysis on 32 clinical, personal, and endoscopic characteristics as well as H pylori clearance and eradication identified H pylori clearance as the most discriminative variable for the healing of duodenal ulcer at four weeks, followed by ulcer depth and eradication of the organism.
                Treatment with an antibiotic only regimen was effective for the healing of duodenal ulcer, and clearance as well as eradication of H pylori contributed significantly to the healing. The results constituted the strongest evidence to date that H pylori infection was aetiologically related to duodenal ulceration, and support the concept of treating duodenal ulcer associated with H pylori as an infection and relieving its symptoms with acid reducing agents such as antacids. Persistent infection with Helicobacter pylori is associated with the recurrence of duodenal ulcer. Whether the efficacy of bismuth therapy in reducing the rate of recurrence of duodenal ulcer is due to its antimicrobial effects on H. pylori or to a direct protective action on the mucosa is still a matter of debate.
                To study the effect of the eradication of H. pylori on the recurrence of duodenal ulcer, we treated 104 patients with H. pylori infection and recurrent duodenal ulcer with either amoxicillin (750 mg three times daily) plus metronidazole (500 mg three times daily) or identical-appearing placebos, given orally for 12 days. All patients also received ranitidine (300 mg each night) for 6 or 10 weeks. Endoscopy was performed before treatment and periodically during follow-up for up to 12 months after healing.
                Among the 52 patients given antibiotics, H. pylori was eradicated in 46, as compared with 1 of the 52 given placebo (89 percent vs. 2 percent, P < 0.001). After six weeks, the ulcers were healed in 48 patients given antibiotics and 39 given placebo (92 percent vs. 75 percent, P = 0.011). Side effects, mainly diarrhea, occurred in 15 percent of the patients given antibiotics. Among the patients followed up for 12 months, duodenal ulcers recurred in 4 of 50 patients given antibiotics and 42 of 49 given placebo (8 percent vs. 86 percent, P < 0.001). Ulcers recurred in 1 of 46 patients in whom H. pylori had been eradicated, as compared with 45 of 53 in whom H. pylori persisted (2 percent vs. 85 percent, P < 0.001).
                In patients with recurrent duodenal ulcer, eradication of H. pylori by a regimen that does not have any direct action on the mucosa is followed by a marked reduction in the rate of recurrence, suggesting a causal role for H. pylori in recurrent duodenal ulcer. We studied prospectively in a single-blind controlled manner the efficacy of 4-wk triple-antibiotic therapy, with amoxicillin (500 mg p.o., t.i.d.), metronidazole (250 mg p.o., t.i.d.), and bismuth subsalicylate tablets (524 mg p.o., q.i.d.), plus omeprazole (20 mg p.o., q.d.) and compared it with omeprazole (id) in the treatment of duodenal ulcer (DU) patients colonized with Helicobacter pylori.
                One hundred DU patients were entered prospectively over a 12-month period. Fifty-seven of them received triple therapy plus omeprazole and 43 received omeprazole alone. Clinical, endoscopic, and bacteriological evaluations were performed on admission and at 28 days, 4, 8, and 12 months after treatment.
                After 4-wk treatment (day 28), the ulcer healing rate was high, but there was no significant difference between rates in the triple therapy and omeprazole groups (99% vs. 91%). In contrast, the long-term DU recurrence rate after 12-month follow-up was significantly lower (p > 0.01) for triple therapy (3/57, 5%), compared with omeprazole (34/43, 79%). The difference (higher relapse rate for omeprazole-treated patients) was significant (p < 0.001) by the second evaluation, 4 months after treatment. The eradication rate of H. pylori was also significantly higher among DU patients treated with triple therapy (p < 0.001) during all prospective evaluations, grand mean, 82% (range 82-87%), compared with the omeprazole-treated group, in which there were no cases in which H. pylori was eradicated. Follow-up revealed that 2/47 H. pylori-eradicated patients became reinfected after 1 yr, giving a reinfection rate of 4.2 patient/yr.
                Four-week triple-antibiotic therapy plus omeprazole constitutes an adequate alternative for treatment of Chilean DU patients. Since the discovery, several decades ago, of the infection of the gastric mucosa with Helicobacter pylori and its association with chronic antral gastritis and peptic ulcer, the treatment of ulcer illness has recently been revolutionized.
                In this study, the clinical effectiveness of three schemes of treatment with colloidal bismuth subcitrate (CBS) were compared. Fifty-three patients suffering from gastroduodenal peptic ulcer with Helicobacter pylori were distributed randomly into three groups. Group I (n = 17) received 240 mg CBS every 12 h for 6 weeks. Group II (n = 17) received 240 mg CBS every 12 h for 6 weeks, pus metronidazole 500 mg every 8 h plus tetracycline 500 mg every 8 h for 10 days. Group III (n = 19) received 240 mg CBS every 12 h for 6 weeks, plus metronidazole 500 mg every 8 h plus amoxicillin 750 mg every 12 h for 10 days. A duodenoscopy investigation with antrum biopsy for a morphologic study and detection of the germ was carried out by means of urease test and histological study (Warthin-Sarry and hematoxylin-eosin).
                The three schemes of treatment were effective for ulcerous healing with 70.5%, 82.3%, and 78.2%, respectively, without significant differences. The highest clearing index (52.6%) was obtained in group III.
                With these treatments, the Helicobacter pylori eradication was only observed in 47.3% of the patients studied. Eradication of Helicobacter pylori (H. pylori) in patients with uncomplicated duodenal ulcers prevents long-term recurrence of ulcers. We aimed to study whether treatment of H. pylori prevents the long-term recurrence of duodenal ulcer hemorrhage.
                Patients with duodenal ulcer bleeding and confirmed H. pylori infection were recruited. A total of 120 patients were randomly assigned to triple therapy (DeNoltab 120 mg, amoxycillin 500 mg, and metronidazole 300 mg four times daily) or DeNoltab 120 mg four times daily alone. No maintenance therapy was given during the follow-up period. The endpoints were the cumulative rates of symptomatic and bleeding duodenal ulcer recurrences.
                Of the patients receiving the triple regimen, 85.1% had H. pylori eradicated as compared to 2.0% of patients receiving DeNoltab (p < 0.05). More patients in the DeNoltab group than those in the Triple group had recurrence of ulcer bleeding, but this did not reach statistical significance (12/60 vs 6/60, p = 0.20). Logistic regression analysis on clinical, personal, and endoscopic characteristics identified persistent H. pylori infection as the only independent predictor of recurrence of duodenal ulcer bleeding.
                Treatment of H. pylori alone with the present bismuth-based triple therapy in patients with duodenal ulcer hemorrhage did not result in significant reduction in further bleeding episodes, although a trend was seen for the group that was given triple therapy. On the other hand, posttreatment H. pylori status was found to be an independent predictor of bleeding recurrence. To determine the effectiveness of structured adherence counseling by pharmacists on the eradication of Helicobacter pylori when using a standard drug treatment regimen.
                Randomized controlled clinical trial.
                Nonprofit group-practice health maintenance organization (HMO).
                HMO primary care providers referred 1,393 adult dyspeptic patients for carbon 14 urea breath testing (UBT).
                Those whose tests were positive for H pylori (23.3%) were provided a standard antibiotic regimen and randomly assigned to receive either usual-care counseling from a pharmacist or a longer adherence counseling session and a follow-up phone call from the pharmacist during drug treatment. All subjects were given the same 7-day course of omeprazole, bismuth subsalicylate, metronidazole, and tetracycline hydrochloride (OBMT). Dyspepsia symptoms were recorded at baseline and following therapy.
                The main outcome was eradication of H pylori as measured by UBT at 3-month follow-up. Secondary outcomes were patient satisfaction and dyspepsia symptoms at 3-month follow-up.
                Of the 333 participants randomly assigned to treatment, 90.7% completed the 3-month follow-up UBT and questionnaires. Overall eradication rate with the OBMT regimen was 80.5% with no significant difference in eradication rates between the 2 groups (P=0.98). Conclusions In this study, additional counseling by pharmacists did not affect self-reported adherence to the treatment regimen, eradication rates, or dyspepsia symptoms but did increase patient satisfaction. Eradication of Helicobacter pylori leads to faster ulcer healing and a significant decrease in ulcer recurrence. Clarithromycin is the most effective monotherapy for eradicating H. pylori from the gastric mucosa, and omeprazole frequently is used for the treatment of duodenal ulcer disease, prompting the interest to investigate rigorously the combination of clarithromycin and omeprazole for eradicating H. pylori.
                The aim of this double-blind, randomized, multicenter (n = 30), multinational (n = 10) study was to compare clarithromycin and omeprazole with omeprazole monotherapy for the eradication of H. pylori from the gastric mucosa, endoscopic healing, and reduction of symptoms and ulcer recurrence in patients with active duodenal ulcer. Patients with active duodenal ulcer associated with H. pylori infection were randomized to receive omeprazole, 40 mg every morning for 14 days, with either clarithromycin, 500 mg, or placebo three times daily, which was followed by omeprazole, 20 mg every morning for 14 days. Patients underwent endoscopy before enrolling in the study, immediately after finishing treatment, and at 4- to 6-week and 6-month follow-up evaluations or at the recurrence of symptoms.
                Two hundred and eight patients with active duodenal ulcer associated with confirmed H. pylori infection were randomized to treatment with either clarithromycin and omeprazole (n = 102) or omeprazole and placebo (n = 106). Four to six weeks after treatment was completed, H. pylori was eradicated in 74% (95% confidence interval, 63.0%-82.4%) of patients receiving clarithromycin and omeprazole, compared with 1% (0.0%-6.2%) of patients receiving omeprazole monotherapy (p < .001). Clarithromycin resistance developed in eight patients treated with clarithromycin and omeprazole and in none given omeprazole and placebo. Ulcers, which were healed following treatment in more than 95% of study patients, recurred by the 6-month follow-up visit in 10% (5%-19%) of dual therapy recipients, compared with 50% (39%-61%) of those who took omeprazole alone (p < .001).
                Clarithromycin and omeprazole dual therapy is simple and well-tolerated and leads to consistently high eradication rates for patients with duodenal ulcer associated with H. pylori infection. Our objective was to assess the effectiveness of therapy for Helicobacter pylori (HP) on the prevention of recurrent bleeding in patients with recent upper gastrointestinal hemorrhage from peptic ulcers.
                We performed a prospective follow-up study without randomization on 125 consecutive patients (83 males and 42 females) who had presented with their first major episode of upper gastrointestinal hemorrhage from peptic ulcer (22 gastric and 103 duodenal ulcers). All 125 patients were HP-positive. During the acute phase of bleeding, all patients were treated with standard supportive measures. After the acute bleeding phase, patients were allocated to two treatment groups: 1) antimicrobial therapy-84 patients received one of the following three regimens: 1) amoxicillin 500 mg t.i.d. for 10 days + omeprazole 20 mg b.i.d. for 30 days; 2) clarythromycin 500 mg t.i.d. for 12 days + omeprazole 20 mg b.i.d. for 30 days; or 3) amoxicillin 500 mg t.i.d. for 10 days + metronidazole 500 mg t.i.d. for 10 days + colloidal bismuth subcitrate 240 mg b.i.d. for 30 days. For long-term antisecretion maintenance treatment, 41 patients were allocated to either omeprazole 20 mg once a day or ranitidine 150 mg once a day, for 1 yr.
                During the follow-up period, peptic ulcers recurred in six patients in the antibiotic group (7.14%) and 13 patients in the maintenance group (31.7%) (p < 0.001). The fraction of patients without recurrent bleeding was greater in the antibiotic group than in the maintenance group. Two patients in the antibiotic group (2.3%) and five in the maintenance group (12.1%) had recurrent hemorrhages (p < 0.1).
                Cure of HP infection reduces the recurrence of peptic ulcer and of rebleeding from ulcer disease more effectively than does long-term maintenance therapy. To investigate differences between omeprazole and Helicobacter pylori eradication in patients with duodenal ulcers refractory to H2-receptor antagonists and to compare the recurrence rates after the two treatments.
                Forty-five patients with endoscopically proven duodenal ulcers refractory to H2-receptor antagonists and H. pylori infection were randomly assigned to 8 weeks of treatment with omeprazole 40 mg/day or 4 weeks of treatment with colloidal bismuth subcitrate 480 mg/day plus metronidazole 750 mg/day and tetracycline 1000 mg/day from day 1 to day 14. Patients were evaluated endoscopically and clinically at the end of treatment. Patients with healed ulcers were followed up for 1 year after cessation of the treatment. Endoscopy was performed at 3 and 12 months.
                Ulcer healing occurred in 100% (21/21) of patients on triple therapy and 70.5% (12/17) of those treated with omeprazole alone (P = 0.0123). The relapse rate at the 3rd month was 11.7% (2/17) in the triple therapy group and 60% (6/10) in the omeprazole group (P = 0.0248). Of the patients followed to study endpoint (relapse or endoscopy at 12 months) three of 12 (25%) receiving triple therapy, compared to six of eight (75%) receiving omeprazole, relapsed (P = 0.0648).
                These results show that triple therapy is more effective than omeprazole in the treatment of refractory duodenal ulcers and reduces the rate of ulcer relapse. Long-term prophylaxis with ranitidine reduces the risk of recurrent bleeding in patients with a history of bleeding peptic ulcers. To date, no randomized study has been performed to compare cure of Helicobacter pylori infection versus H2 blocker prophylaxis in patients with bleeding peptic ulcer.
                In a prospective randomized study, 95 consecutive patients with H. pylori-associated peptic ulcer bleeding were randomized to either ranitidine prophylaxis (150 mg at night) for 2 years or to H. pylori-eradication with omeprazole 60 mg twice daily plus amoxicillin 750 mg three times daily for 10 days.
                (Intention-to-treat analysis). Forty-eight patients were enrolled in the ranitidine group; 47 in the omeprazole-plus-amoxicillin group. Mean follow-up was 576 days (77 to 730). Ulcer recurrence rate was 31.3% in the ranitidine group (group 1) versus 6.37% in the eradication group (group 2; p = 0.0018). More patients had recurrent bleeding in group 1 (8.3%) than in group 2 (4.2%) but we were not able to show a statistically significant difference with respect to recurrent bleeding between groups (p = 0.29). Definite cure of H. pylori infection was achieved in 89.3%.
                Cure of H. pylori infection reduces recurrence of peptic ulcer and therefore rebleeding more effectively than does long-term maintenance therapy with an H2 blocker. The efficacy and safety of dual and triple therapies with a proton pump inhibitor and antibiotic(s) for therapy of Helicobacter pylori-associated duodenal ulcer disease have been compared using results from independent studies using different methods and regimens, making interpretation difficult. In a large, double-blind, multicenter study conducted in the United States, we compared a triple therapy regimen with four dual therapy and one monotherapy regimens in the eradication of H. pylori and the prevention of ulcer recurrence.
                Patients with active duodenal ulcer disease or history of duodenal ulcer disease within the past year and H. pylori infection were randomized to receive one of six 14-day treatment regimens: lansoprazole 30 mg, clarithromycin 500 mg, and amoxicillin 1 gm b.i.d.; lansoprazole 30 mg b.id. and either clarithromycin 500 mg b.i.d. or t.i.d.; lansoprazole 30 mg b.i.d. or t.i.d. with amoxicillin 1 gm t.i.d.; or lansoprazole 30 mg t.i.d. alone. No additional acid suppression therapy followed eradication therapy. Primary efficacy endpoints were eradication of H. pylori and ulcer recurrence.
                Of 396 patients enrolled in the study, 352 met the entry criteria for duodenal ulcer status and H. pylori positivity. At 4-6 wk after the end of therapy, H. pylori was eradicated from 94% (44 of 47) of patients receiving lansoprazole, clarithromycin, and amoxicillin triple therapy, 77% (39 of 51) of those receiving lansoprazole t.i.d./amoxicillin t.i.d., 75% (36 of 48) of those receiving lansoprazole b.i.d./clarithromycin t.i.d., 57% (28 of 49) of those receiving lansoprazole b.i.d./clarithromycin b.i.d., 53% (26 of 49) of those receiving lansoprazole b.i.d./amoxicillin t.i.d., and 2% (1 of 53) of those receiving lansoprazole monotherapy (p < or = 0.05, triple therapy vs each dual therapy and each dual therapy vs monotherapy). Of those patients who were documented as free of ulcer at 4-6 wk after treatment, ulcers recurred within 6 months in 7% of patients receiving triple therapy, as compared with 13-23% of patients receiving dual therapy, and 69% of patients receiving lansoprazole monotherapy. Patients who were H. pylori negative at 4-6 wk after treatment were less likely to have an ulcer recurrence than were patients who were H. pylori positive (11% [10 of 95] vs 47% [20 of 43], respectively, across treatment groups). For triple therapy and dual therapy, a similar proportion of patients reported a drug-related adverse event (23% vs 17-33%, respectively).
                In patients with active or a recent history of duodenal ulcer, a 14-day course of lansoprazole-based triple therapy without additional acid suppression therapy is highly effective in the eradication of H. pylori and in preventing ulcer recurrence. Among the dual therapies, higher eradication rates occurred when lansoprazole (with amoxicillin) or clarithromycin (with lansoprazole) was administered t.i.d. vs b.i.d., but the rates were still significantly lower than with lansoprazole triple therapy with all three drugs administered b.i.d.
A one to two weeks course of H. pylori eradication therapy is an effective treatment for H. pylori positive peptic ulcer disease.