Lansoprazole and secnidazole with clarithromycin, amoxycillin or pefloxacin in the eradication of Helicobacter pylori in a developing country

Background:

A number of triple drug regimens using proton pump inhibitors and two antibiotics have been evaluated in the West and reported to achieve Helicobacter pylori eradication rates of over 90%. In developing countries however, these combinations have neither been well evaluated, nor the optimum treatment for H. pylori infection well defined.

Aim:

To compare the combination of a proton pump inhibitor with a nitroimidazole and another antibiotic in eradicating H. pylori infection and healing duodenal ulcer.

Methods:

Sixty consecutive patients with active duodenal ulcer who were positive for H. pylori (by rapid urease test and ¹⁴C-urea breath test) were randomized into three treatments groups: (1) LAS (n = 21): lansoprazole 30 mg o.m., amoxycillin 500 mg q.d.s. and secnidazole 2 g on alternate days for 2 weeks; (2) LCS (n = 18): lansoprazole 30 mg o.m., clarithromycin 500 mg b.d. and secnidazole 2 g on alternate days for 1 week; (3) LPS (n = 21): lansoprazole 30 mg o.m., pefloxacin 400 mg o.m. and secnidazole 2 g on alternate days for 2 weeks. Urease and breath tests were performed at 0, 6 and 12 weeks to check for H. pylori eradication.

Results:

Intention-to-treat eradication rates were as follows: LAS 86%, LCS 83%, LPS 71%; the overall ulcer healing rate was 90% at 6 weeks.

Conclusions:

High H. pylori eradication rates were achieved using the amoxycillin- and clarithromycin-based therapies. Fewer side-effects, better compliance and low cost favoured the amoxycillin-based therapy.

     

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

Objectives:

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

Aim:

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

Methods:

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

Results:

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

Conclusion:

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

     

Incidence of duodenal ulcer healing after 1 week of proton pump inhibitor triple therapy for eradication of Helicobacter pylori

Background:

A number of clinical studies have assessed the efficacy of short-term twice-daily Helicobacter pylori eradication regimens but few have investigated the proportion of patients in whom duodenal ulcer disease was healed with these regimens.

Aim:

To compare the safety and efficacy of four 1-week H. pylori eradication regimens in the healing of H. pylori associated duodenal ulcer disease.

Methods:

Following endoscopic confirmation of duodenal ulcer disease and a positive CLO test, patients underwent a ¹³C-urea breath test to confirm H. pylori status. Treatment with one of four regimens: LAC, LAM, LCM or OAM, where L is lansoprazole 30 mg b.d., A is amoxycillin 1 g b.d., M is metronidazole 400 mg b.d., C is clarithromycin 250 mg b.d., and O is omeprazole 20 mg b.d., was assigned randomly to those patients who were H. pylori positive, with 62 (LAC), 64 (LAM), 61 (LCM) and 75 (OAM) patients in each treatment group. Follow-up breath tests and endoscopies were performed at least 28 days after the end of treatment.

Results:

Duodenal ulcer disease was healed 28 days after treatment in 53/62 (85.5%) patients who were treated with LAC, 52/64 (81.3%) of patients treated with LAM, 49/61 (80.3%) of patients treated with LCM and 60/75 (80.0%) of patients treated with OAM (intention-to-treat analysis, n=262, assumed unhealed if no follow-up endoscopy was performed). All the treatments were of similar efficacy (P=0.85, chi-squared test) with regard to the healing of duodenal ulcer disease.

Conclusions:

The four 1-week treatment regimens were equally effective in healing H. pylori associated duodenal ulcer disease.

     

H2-antagonist maintenance therapy versus Helicobacter pylori eradication in patients with chronic duodenal ulcer disease: a prospective study

Background:

Few outcome studies directly compare Helicobacter pylori eradication therapy with maintenance H₂-antagonist therapy in duodenal ulcer disease.

Aim:

To examine prospectively the efficacy of H. pylori eradication therapy with ranitidine maintenance therapy over 1 year in patients with confirmed chronic duodenal ulcer.

Methods:

One hundred and nineteen patients with active H. pylori infection were randomized to receive ranitidine, 150 mg/day initially (58 patients), or omeprazole, 40 mg/day, amoxycillin 2 g/day and metronidazole 1.2 g/day for 14 days, or omeprazole 40 mg/day and clarithromycin 1.5 g/day, for 14 days (if penicillin-allergic). Symptoms were assessed using the Gastro-intestinal System Rating Scale (GSRS) and SF36 quality of life index.

Results:

¹³C urea breath testing confirmed overall treatment success in 100% of patients (58/58) per protocol and 95.1% (58/61) on an intention-to-treat basis. At 4 and 12 months there were no differences in any GSRS symptoms between treatment groups. SF36 analysis showed a perceived health improvement at 4 and 12 months in patients who received H. pylori eradication. However, despite successful H. pylori eradication, one-fifth of patients still required antisecretory therapy.

Conclusion:

Following successful H. pylori eradication, chronic duodenal ulcer patients were at least as well symptomatically as when taking maintenance ranitidine. They perceived that their health had improved, but a subgroup was still acid-suppression dependent.

     

Eradication of Helicobacter pylori with lansoprazole, roxithromycin and metronidazole—an open pilot study

Background:

The most extensively studied Helicobacter pylori eradication regimen comprises omeprazole, clarithromycin and metronidazole. Macrolide antibiotics other than clarithromycin should achieve similar efficacy, but they have not yet been thoroughly tested.

Aim:

To determine the efficacy and safety of a triple therapy regimen using lansoprazole, roxithromycin, and metronidazole on the basis of multicentre out-patient care in an open pilot study.

Methods:

163 patients with duodenal ulcer and proven H. pylori infection received lansoprazole 30 mg b.d., roxithromycin 300 mg b.d. and metronidazole 500 mg b.d. for 7 days followed by another 7 days of lansoprazole 30 mg once daily. H. pylori status was determined by urease quick test, histology, microbiology and ¹³C-urea breath test before starting and at least 4 weeks after completing treatment.

Results:

150 patients were available for evaluation; H. pylori was successfully eradicated in 84.7% (127/150) as determined by urease quick test, 78.0% (117/150) by histology, 81.3% (109/134) by ¹³C-urea breath test; and in 75.3% (113/150), at least two tests were negative. Side-effects were reported in 34 patients (most commonly diarrhoea and changes in liver function tests), in two cases the study medication was interrupted. Prior to treatment, 23% of the H. pylori isolates were resistant against metronidazole and 3.4% against roxithromycin. After unsuccessful treatment, 84% of the isolates were resistant against metronidazole and 21% against roxithromycin. Primary resistance to metronidazole increased the chance of treatment failure approximately sevenfold (7% vs. 53%).

Conclusions:

For H. pylori eradication, the combination of lansoprazole, roxithromycin and metronidazole proved to be as safe as other current triple therapy regimens, while a comparison of efficacy rates yet remains to be assessed in prospective controlled trials. The metronidazole-resistant H. pylori is not rare in Germany and, in the present study, has strongly influenced treatment success.

     

Comparison of omeprazole and lansoprazole in short-term triple therapy for Helicobacter pylori infection

Background:

Effective anti-Helicobacter pylori therapies with few side-effects are needed.

Aim:

To study the effectiveness of short-term triple therapy with amoxycillin, clarithromycin and either omeprazole or lansoprazole for eradication and healing of peptic ulcers.

Methods:

Patients with gastric or duodenal ulcers received amoxycillin (1 g b.d.), clarithromycin (500 mg b.d.) and lansoprazole (30 mg b.d.) (LAC) or omeprazole (20 mg b.d.) (OAC) for 7 days. Endoscopic examinations were performed before treatment and at least 4 weeks after completion of therapy. H. pylori status was confirmed by rapid urease test and histological examination (Giemsa stain) from gastric biopsies taken from both the antrum and the body.

Results:

A total of 356 patients were randomized in this single-blind study. On a per protocol basis, H. pylori was eradicated in 134 of 170 patients (79%) in the lansoprazole group and in 105 of 146 (72%) in the omeprazole group (P = 0.189); and in intention-to-treat analysis 72% and 62%, respectively (P = 0.043). Healing of the ulcers was obtained in 166 of 186 (98%), and in 139 of 146 patients (95%), respectively (P = 0.357). Side-effects occurred in two patients in the LAC group and in six in the OAC group B (four stopped therapy).

Conclusions:

This study has shown that the two regimens are highly effective in healing duodenal ulcers and are well tolerated. Neither treatment achieves the ideal cure rate for H. pylori. Lansoprazole does not appear to have a significant advantage over omeprazole either in ulcer healing or in H. pylori eradication.

     

Short-term low-dose pantoprazole-based triple therapy for cure of Helicobacter pylori infection in duodenal ulcer patients

Background:

The eradication of Helicobacter pylori infection has been achieved using various therapy regimens, but the efficacy of the proton-pump inhibitor pantoprazole as part of these regimens has not yet been widely tested.

Aim:

To evaluate the efficacy and tolerability of a 1-week low-dose pantoprazole-based triple therapy in patients with H. pylori-positive duodenal ulcer.

Methods:

In an open single-centre prospective study, 71 patients with endoscopically proven active duodenal ulcer and H. pylori infection received pantoprazole 40 mg o.m. for 4 weeks, and during the first week a combination antimicrobial treatment comprising tinidazole 500 mg b.d. plus clarithomycin 250 mg b.d. H.?pylori eradication was defined as concordant negative histology and rapid urease test performed at endoscopy 4–6 weeks after the end of treatment, confirmed 4 weeks later by ¹³C-urea breath test.

Results:

Sixty-six patients (93%) completed the trial and five patients were lost to follow-up. H. pylori infection was cured in 61 out of the 66 patients who completed the trial (per-protocol analysis: 92.4%, 95% CI: 83.2–97.5%; intention-to-treat analysis: 85.9%, 95% CI: 75.7–93.0%). At final endoscopy, 65 out of 66 patients had healed ulcer (98.5%). Mild adverse events occurred in six patients (9.1%).

Conclusions:

One-week low-dose pantoprazole-based triple therapy is a simple, effective and well-tolerated regimen for ulcer healing and H. pylori eradication in patients with duodenal ulcer.

     

Triple regimens using lansoprazole or ranitidine bismuth citrate for Helicobacter pylori eradication

Background:

A combination of an antisecretory agent with two antibiotics is considered the ‘gold standard’ for Helicobacter pylori eradication.

Objectives:

To compare the eradication rates and the safety profile of two short-term triple therapies containing lansoprazole (L) or ranitidine bismuth citrate (RBC) as antisecretory agents.

Methods:

One hundred and twelve H. pylori-positive patients either with peptic ulcer (56 duodenal ulcers: 25 active and 31 with a history of ulcer; 13 gastric ulcers: nine active and four with a history of ulcer) or gastritis (43) were included in an open, randomized, controlled trial. H. pylori infection was initially detected by CLO-test and histology on antral and corpus biopsies. H.?pylori-positive patients were randomized to receive L plus clarithromycin (C) 250 mg b.d. plus tinidazole (T) 500 mg b.d. (LCT) or RBC plus C 250 mg b.d. and T 500 mg b.d. for 7 days (RbcCT). L or RBC were administered for a further 3 weeks in patients with active peptic ulcers. A second endoscopy was performed at least 6 weeks after the end of therapy for the assessment of H. pylori infection by CLO-test and histology. Eradication was assumed if all the tests were negative for H. pylori.

Results:

Forty-eight patients in the LCT group and 45 in the RbcCT group were assessed for H. pylori eradication. The eradication rates, according to intention-to-treat (ITT) and per protocol (PP) analyses were, respectively, 76.8% and 89.5% for the LCT group, and 73.2% and 91.1% for the RbcCT group. No statistically significant difference in eradication rates was found between the two groups by Mantel–Haenszel test. All peptic ulcers were healed. In patients in whom H. pylori had been eradicated, the severity of gastritis was significantly reduced. Side-effects were rare. One patient in the LCT group and two in the RbcCT group were withdrawn because of adverse events.

Conclusion:

Short-term triple therapy with either lansoprazole or RBC is equally effective and well tolerated.

     

One-week use of ranitidine bismuth citrate, amoxycillin and clarithromycin for the treatment of Helicobacter pylori-related duodenal ulcer

Background:

Proton pump inhibitors have been widely used in combination with amoxycillin, clarithromycin or metronidazole for the treatment of Helicobacter pylori infection.

Aim:

To study the effects of 1-week ranitidine bismuth citrate (RBC)-based triple therapy in the treatment of H. pylori-related duodenal ulcers.

Method:

Patients with duodenal ulcers and H. pylori infection were prospectively randomized to receive either RBC with amoxycillin and clarithromycin for 1 week (RAC), or omeprazole with amoxycillin and clarithromycin for 1 week (OAC). No additional ulcer healing drug was used after the 1-week medication. Patients were assessed for H. pylori eradication, ulcer healing and side-effects after receiving the therapies.

Results:

One hundred consecutive patients were recruited to this study, with 50 patients randomized to each treatment group. In the intention-to-treat analysis, duodenal ulcers were completely healed in 45 (90%) patients in the RAC group and 43 (89.6%) in the OAC group (P = 1.0). H. pylori eradication was confirmed in 47 (94%) in the RAC group and 42 (87.5%) in the OAC group (P = 0.31). There was no significant difference in the severity of side-effects experienced by the two treatment groups.

Conclusion:

One-week RBC-based triple therapy is an effective treatment for H. pylori-related duodenal ulcers. The therapeutic effects are comparable to a 1-week course of proton pump inhibitor-based triple therapy.

     

Omeprazole or ranitidine bismuth citrate triple therapy to treat Helicobacter pylori infection: a randomized, controlled trial in Vietnamese patients with duodenal ulcer

Aim:

To evaluate the effectiveness of triple therapy containing either omeprazole or ranitidine bismuth citrate (RBC) to treat H. pylori infection in Vietnamese duodenal ulcer patients.

Methods:

Patients infected with H. pylori were randomized to receive either omeprazole (20 mg b.d.), clarithromycin (500 mg b.d.) and amoxycillin (1 g b.d.) for 10 days (OAC), or RBC (400 mg b.d.), clarithromycin (500 mg b.d.) and amoxycillin (1 g b.d.) for 10 days (RAC). H. pylori eradication and ulcer healing was established by a follow‐up oesophagogastroduodenoscopy (EGD) at least 4 weeks after therapy. Side‐effects and compliance were assessed.

Results:

One hundred and four out of 108 (96%) patients with a duodenal ulcer were infected with H. pylori. Eighty per cent of infected patients had detectable CagA IgG antibodies. Fifty‐seven patients received OAC and 47 received RAC. OAC eradicated H. pylori in 91 and 86% of patients by per protocol (PP) and intention‐to‐treat (ITT) analysis, respectively. PP and ITT eradication rates for RAC were 96 and 91%. Ulcer healing at the follow‐up EGD was 89% with OAC and 100% with RAC. Side‐effects were minor. No patient failed to complete the protocol due to side‐effects.

Conclusion:

Triple therapy with either omeprazole or RBC is highly effective in eradicating H. pylori and healing duodenal ulcer in Vietnamese patients.

     

Effect of MDR1 C3435T polymorphism on cure rates of Helicobacter pylori infection by triple therapy with lansoprazole, amoxicillin and clarithromycin in relation to CYP 2C19 genotypes and 23S rRNA genotypes of H. pylori

Summary

Background

Polymorphism in MDR1 is associated with variation in the plasma level of a proton pump inhibitor.

Aim

To investigate whether MDR1 polymorphism is associated with eradication rates of Helicobacter pylori by a triple therapy with lansoprazole, amoxicillin and clarithromycin in relation to CYP2C19 genotype status and bacterial susceptibility to clarithromycin.

Methods

A total of 313 patients infected with H. pylori completed the treatment with lansoprazole 30 mg b.d., clarithromycin 200 mg b.d. and amoxicillin 750 mg b.d. for 1 week. MDR1 C3435T polymorphism and CYP2C19 genotypes of patients and sensitivity of H. pylori to clarithromycin were determined.

Results

Logistic regression analysis revealed that the MDR1 polymorphism as well as CYP2C19 genotypes of patients and clarithromycin‐resistance of H. pylori were significantly associated with successful eradication. Eradication rates for H. pylori were 82% (83/101: 95% CI = 73–89), 81% (112/139: CI = 73–87), and 67% (44/73: CI = 48–72) in patients with the MDR1 3435 C/C, C/T and T/T genotype, respectively (P = 0.001).

Conclusions

Polymorphism of MDR1 is one of the determinants of successful eradication of H. pylori by the triple therapy with lansoprazole, amoxicillin and clarithromycin, together with CYP2C19 genotype and bacterial susceptibility to clarithromycin.

     

Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during and after 12 months of treatment with ranitidine and lansoprazole in patients with duodenal ulcer disease

Background:

Several studies have shown that acid-suppressing treatment leads to aggravation of Helicobacter pylori gastritis in the corpus. It remains unclear whether this augmentation of the inflammation reverts to baseline after termination of treatment.

Methods:

In 114 H. pylori-infected duodenal ulcer patients we investigated the gastritis parameters in antral and corpus mucosa before treatment, after 6 and 12 months of therapy, and 6 months after termination of treatment with 15 mg lansoprazole or 150 mg ranitidine/day.

Results:

Lansoprazole and ranitidine led to a significant aggravation of gastritis in the corpus after 6 and 12 months of treatment. However, while there was no change in gastritis in the antrum with ranitidine, treatment with lansoprazole led to partial elimination of H. pylori with improvement of the inflammation in this part of the stomach. Following termination of therapy, the observed changes reverted to baseline. No increase in intestinal metaplasia and/or atrophy in the antrum or corpus was observed.

Conclusion:

Both substances are associated with an aggravation of H. pylori gastritis in the corpus. However, only lansoprazole leads to a partial elimination of H. pylori with improvement of the inflammation in the antrum. The changes provoked by acid-suppressing treatment revert to baseline after termination of therapy.

     

Two-week course of pantoprazole combined with 1 week of amoxycillin and clarithromycin is effective in Helicobacter pylori eradication and duodenal ulcer healing

Background:

Experience with proton pump inhibitor-based triple therapy is predominantly with omeprazole-containing regimens.

Aim:

To investigate the efficacy of a pantoprazole-based regimen, with either a 1 or 2-week course of antibiotic co-therapy, in eradicating H. pylori, healing duodenal ulcers and to assess the antibiotic sensitivity profiles of isolated H. pylori strains.

Methods:

A single-blind, multicentre, parallel group comparison of patients with endoscopically proven, H.?pylori associated, active duodenal ulceration. All patients received pantoprazole, 40 mg b.d. for 2 weeks. Patients were randomized to receive either 1 or 2 weeks of therapy with amoxycillin, 1 g b.d. and clarithromycin 500 mg b.d. Patients were endoscoped at entry, at 14 days and a minimum of 4 weeks after cessation of all therapy. H. pylori status was determined by urease reaction, histological assessment and culture from antral and body biopsies. Antibiotic sensitivity was determined using the agar dilution technique.

Results:

Sixty-seven patients were randomized. One week co-therapy (n = 33): eradication efficacy, ITT = 79% (95% CI: 61–91%); ulcer healing efficacy (at 6-week visit) = 88% (95% CI: 72–97%). Two-week co-therapy (n = 34): eradication efficacy, ITT = 91% (95% CI: 76–98%; ulcer healing efficacy = 88% (95% CI: 73–97%). Both regimens were well tolerated and no primary antibiotic resistance was noted.

Conclusion:

Pantoprazole-based triple therapy, with either 1 or 2 weeks of co-therapy with amoxycillin and clarithromycin, is effective in eradicating H. pylori and healing duodenal ulceration.

     

Lansoprazole triple therapy for Helicobacter pylori—is 5 days enough?

Background:

Seven-day proton pump inhibitor triple therapy is currently the treatment of choice for Helicobacter pylori infection. It is unclear whether triple therapy for less than 7 days might preserve efficacy while at the same time improving patient acceptability and compliance.

Aim:

To evaluate the Helicobactericidal efficacy, ulcer healing capacity and patient acceptability of a 5-day lansoprazole-based triple therapy regimen.

Methods:

Sixty-nine consecutive patients with H. pylori-positive peptic ulcer received lansoprazole 30 mg twice daily in combination with metronidazole 400 mg twice daily and clarithromycin 250 mg twice daily for 5 days. Ulcer healing medication was not continued after the 5-day regimen. H. pylori status was assessed before and at least 4 weeks after therapy by rapid urease test and histology. Adverse events and compliance were assessed by direct questioning.

Results:

All 69 patients attended for repeat endoscopy and 63 were H. pylori-negative after therapy giving a cure rate of 91% (95% Cl: 85–98%). Of the 59 patients with active ulcers, 58 were healed at repeat endoscopy giving an ulcer healing rate of 98% (95% Cl: 92–100%). All patients fully complied with therapy and mild adverse events, mainly gastrointestinal, were reported by 11 patients (16%).

Conclusions:

Five-day lansoprazole triple therapy is an effective regimen for H. pylori infection which combines a high cure rate and ulcer healing efficacy with the advantages of excellent patient acceptability and compliance.

     

Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during 12 months of treatment with omeprazole and lansoprazole in patients with gastro-oesophageal reflux disease

Background:

Several studies have shown that treatment with omeprazole leads to aggravation of Helicobacter pylori gastritis in the corpus. Whether this also applies to lansoprazole, and whether, in comparison with omeprazole, there are differences in therapy-induced gastritis parameter changes remains unclear.

Methods:

In 111 patients infected with H. pylori and with gastro-oesophageal reflux disease we investigated the gastritis parameters in antral and corpus mucosa before and after 2, 6 and 12 months of treatment with 15 or 30 mg lansoprazole or 20 mg omeprazole/day.

Results:

In all groups the different treatments had a similar effect: in both regions of the stomach, suppression or partial elimination of H. pylori was seen. However, improvement in the inflammation was observed only in the antrum, while in the corpus most gastritis parameters worsened significantly. There was no increase in intestinal metaplasia or atrophy.

Conclusion:

In common with omeprazole, lansoprazole aggravates the gastritis parameters in the corpus but improves them in the antrum. Treatment with proton pump inhibitors does not result in any increase in the incidence of atrophy/intestinal metaplasia. However, as gastritis predominating in the corpus seems to be associated with an elevated carcinogenic risk, consideration should be given to prophylactic H. pylori eradication therapy before initiating proton pump inhibitor treatment.

     

Randomized comparison of 1-hour topical method vs. amoxycillin plus omeprazole for eradication of Helicobacter pylori in duodenal ulcer patients

Background:

A novel 1-h topical method eradicated Helicobacter pylori in 96% of dyspeptic patients. The eradication rate of amoxycillin/omeprazole therapy varies from 0 to 93%.

Aim:

To compare both methods in patients with endoscopically proven duodenal ulcer.

Methods:

Eighty patients (59 males, 21 females; median age 43 years) were randomized into two therapeutic groups. The first group (group A) was treated with a 6-week course of ranitidine 300 mg/day, then omeprazole 20 mg b.d. with pronase 36 000 units/day for 2 days, followed by 1-h topical therapy with a solution of bismuth, metronidazole, amoxycillin and pronase. The second group (group B) consisted of patients treated with omeprazole 20 mg b.d. and amoxycillin 2 g/day for 2 weeks, followed by a 4-week course of ranitidine 300 mg/day. Eradication of H.?pylori was assessed by urease test, histology, a polymerase chain reaction and a ¹³C-urea breath test, all of which were performed 4 weeks after discontinuation of the antibacterial treatment.

Results:

Eradication rates in groups A and B were 2.5% and 35% in an intention-to-treat analysis, respectively. Side-effects were encountered in 40.5% and 12.5% of subjects in groups A and B, respectively. Treatment tolerance was rated as poor by 54% of patients in group A and 2.5% of patients in group B.

Conclusions:

Both treatment regimens, the 1-h topical method and amoxycillin with omeprazole, have low eradication rates in patients with duodenal ulcer. In addition, the topical treatment is characterized by a high rate of side-effects and poor tolerance. Based on the results of our study, neither method can be recommended for eradication of H. pylori in patients with duodenal ulcer.

     

There are some benefits for eradicating Helicobacter pylori in patients with non-ulcer dyspepsia

Background

: The relationship between Helicobacter pylori infection and non‐ulcer dyspepsia is not established.

Aim

: To determine whether eradication of H. pylori might be of benefit in non‐ulcer dyspepsia patients.

Methods

: We randomly assigned 129 H. pylori infected patients with severe epigastric pain, without gastro‐oesophageal reflux symptoms, to receive twice daily treatment with 300 mg of ranitidine, 1000 mg of amoxicillin, and 500 mg of clarithromycin for 7 days and 124 such patients to receive identical‐appearing placebos.

Results

: Treatment was successful (decrease of symptoms at 12 months) in 62% of patients in the active‐treatment group and in 60% of the placebo group (N.S.). At 12 months, the rate of eradication of H. pylori was 69% in the active‐treatment group and 18% in the placebo group (P < 0.001). Complete relief of symptoms occurred significantly more frequently in patients on the active treatment (43%) than in placebo‐treated patients (31%, P=0.048). Within the active‐treatment group, therapeutic success was significantly more frequent in the non‐infected patients (84% vs. 64%, P=0.04).

Conclusions

: Although eradicating H. pylori is not likely to relieve symptoms in the majority of patients with non‐ulcer dyspepsia, a small proportion of H. pylori‐infected patients may benefit from eradication treatment.

     

Helicobacter pylori-positive peptic ulcer patients do not adapt to aspirin

Background:

Recent studies indicate that eradication of Helicobacter pylori might prevent peptic ulcer formation in patients treated with non-steroidal anti-inflammatory drugs (NSAIDs). On the other hand, gastric adaptation after repeated exposures to aspirin (ASA) is well documented but the influence of H. pylori on this process remains to be elucidated.

Aim:

To compare gastric damage and adaptation following repeated exposures to ASA in a group of patients with H. pylori infection, before and after eradication of the bacterium, and in H. pylori-negative controls.

Methods:

Eight healthy volunteers without H. pylori infection and eight patients with duodenal ulcer (DU) history and H. pylori infection before and after H. pylori eradication were given ASA 2 g/day for a period of 14 days. Mucosal damage was evaluated by endoscopy and histology of biopsy samples. Gastric microbleeding, DNA synthesis in the gastric mucosa and mucosal expression, as well as luminal content of transforming growth factor-α (TGFα) were determined on days 0, 3, 7 and 14 of the ASA course.

Results:

In all patients aspirin-induced gastric damage reached a maximum on day 3. In H. pylori-positive patients, this damage was maintained at a similar level up to day 14, whereas in H. pylori-negative controls and H. pylori-eradicated patients this damage significantly lessened on day 14 and was accompanied by elevated DNA synthesis as well as increased mucosal expression and luminal release of TGFα.

Conclusions:

H. pylori-positive DU patients do not adapt to continued administration of ASA but eradication of the bacterium restores adaptation. This phenomenon deserves further clinical evaluation.

     

Pantoprazole-based 10-day triple therapy is effective in Helicobacter pylori eradication

Aim:

To investigate the efficacy of a short course of pantoprazole-based triple therapy in Helicobater pylori eradication in a single-centre pilot study.

Methods:

Patients with active or healed duodenal ulcer or with gastric erosions or gastritis, all of whom were H. pylori-positive, received 10 days of twice-daily open treatment with pantoprazole 40 mg, plus clarithromycin 250 mg and tinidazole 500 mg. H. pylori was assessed at entry and 28–35 days after the end of treatment by rapid urease test (at entry only), culture and antimicrobial sensitivity, histology and ¹³ C urea breath test. The criterion for eradication was a negative result in all three tests.

Results:

Seventy patients were treated, of whom four were excluded from analysis due to major deviations from the study protocol. Eradication of H. pylori was achieved in 57/66 patients (per protocol analysis 86% (95% CI: 78–95%)) and was higher in patients with organisms sensitive to nitroimidazole before treatment (sensitive: 47/53 (89%), insensitive: 10/13 (77%)). There was marked reduction in acute gastritis throughout the stomach while chronic gastritis decreased only in the corpus. Healing was achieved in all 24 patients with active duodenal ulcer. Treatment was complied with; only one patient missed one of the 20 doses. Adverse events were of mild or moderate intensity and did not require withdrawal from treatment.

Conclusion:

A short course of pantoprazole-based triple therapy is well tolerated and effective in eradicating H. pylori.