Prevalence of duodenal ulcer-promoting gene (dupA) of Helicobacter pylori in patients with duodenal ulcer in North Indian population

BACKGROUND: The duodenal ulcer (DU)-promoting gene (dupA) of Helicobacter pylori has been identified as a novel virulent marker associated with an increased risk for DU. The presence or absence of dupA gene of H. pylori present in patients with DU and functional dyspepsia in North Indian population was studied by polymerase chain reaction (PCR) and hybridization analysis. MATERIALS AND METHODS: One hundred and sixty-six patients (96 DU and 70 functional dyspepsia) were included in this study. In addition, sequence diversity of dupA gene of H. pylori found in these patients was analyzed by sequencing the PCR products jhp0917 and jhp0918 on both strands with appropriate primers. RESULTS: PCR and hybridization analyses indicated that dupA gene was present in 37.5% (36/96) of H. pylori strains isolated from DU patients and 22.86% (16/70) of functional dyspepsia patients (p < or = .05). Of these, 35 patients with DU (97.2%) and 14 patients with functional dyspepsia (81.25%) were infected by H. pylori positive for cagA genotype. Furthermore, the presence of dupA was significantly associated with the cagA-positive genotype (p < or = .02). CONCLUSION: Results of our study have shown that significant association of dupA gene with DU in this population. The dupA gene can be considered as a novel virulent marker for DU in this population.     

Helicobacter pylori recurrence in patients with duodenal ulcer: Clinical, endoscopic, histologic, and genotypic aspects. A 10-year Brazilian series

BACKGROUND: Recurrence infection following successful eradication of Helicobacter pylori is usually low, except for countries with high prevalence of H. pylori. The aim of this study was to verify H. pylori recurrence rate in patients with duodenal ulcer after eradication and the possible relationship with environmental factors, histologic pattern of the mucosa and bacterial genotype. MATERIALS AND METHODS: One-hundred and ninety-four patients with an active duodenal ulcer and who were successfully treated for H. pylori infection from 1990 to 1999 were studied. A questionnaire was answered about their living conditions, and a 14C-urea breath test was performed. Patients with a positive breath test underwent an upper endoscopy to investigate for possible ulcer recurrence; gastric biopsy samples were than collected for rapid urease test and for histologic assessment. H. pylori vacA and cagA genotype was determined by polymerase chain reaction in those samples with positive urease test. RESULTS: H. pylori infection was detected in 11 patients (recurrence rate of 5.7%) that were not associated with the type of bacterial virulence. In 10 patients the ulcer was healed and all of them were clinically asymptomatic. In eight, histology showed an intensification of gastritis. All 11 patients had adequate housing and sanitary conditions and no other risk for H. pylori recurrence was identified. CONCLUSIONS: The recurrence rate of H. pylori in Brazil was higher than that reported in developed countries, but lower than usually reported in developing ones. Ulcer relapse rarely occurs even in long-term follow up.     

Systematic review and meta-analysis: Helicobacter pylori eradication therapy after simple closure of perforated duodenal ulcer

Background: The most common complications of peptic ulcer are bleeding and perforation. In many regions, definitive acid reduction surgery has given way to simple closure and Helicobacter pylori eradication. Aim: To perform a systematic review and meta‐analysis to ask whether this change in practice is in fact justified. Materials and Methods: A search on the Cochrane Controlled Trials Register, Medline, and Embase was made for controlled trials of duodenal ulcer perforation patients using simple closure method plus postoperative H. pylori eradication therapy versus simple closure plus antisecretory non‐eradication therapy. The long‐term results for prevention of ulcer recurrence were compared. Results: The pooled incidence of 1‐year ulcer recurrence in H. pylori eradication group was 5.2% [95% confidence interval (CI) of 0.7 and 9.7], which is significantly lower than that of the control group (35.2%) with 95% CI of 0.25 and 0.45. The pooled relative risk was 0.15 with 95% CI of 0.06 and 0.37. Conclusions: Helicobacter pylori eradication after simple closure of duodenal ulcer perforation gives better result than the operation plus antisecretory non‐eradication therapy for prevention of ulcer recurrence. All duodenal ulcer perforation patients should be tested for H. pylori infection, and eradication therapy is required in all infected patients.     

Distribution of vacA genotypes in Helicobacter pylori strains isolated from Brazilian adult patients with gastritis,duodenal ulcer or gastric carcinoma

This PCR-based analysis is the first molecular epidemiological study in Brazil testing Helicobacter pylori cagA and vacA distribution in adults with gastric complaints, that includes a large number of carcinoma patients. Multiple-strain infection was identified in 11/13.4% patients. vacA s1-m1 and cagA(+) genotypes were the most common in patients with a non-mixed infection. All vacA s1 strains were s1b, so subtyping s1 strains was not useful. vacA s1b-m1 and cagA(+) strains were associated with higher prevalence of peptic ulcer and gastric carcinoma than vacA s2-m2 and cagA(-) ones. In conclusion, cagA and vacA genotyping may have clinical relevance in Brazil.     

Rank order of success favors longer duration of imidazole-based therapy for Helicobacter pylori in duodenal ulcer disease: a randomized pilot study

Background. Studies on eradication therapy in developing countries have shown a success rate of 70–85%, which is suboptimal. Duration of therapy may be an important factor dictating eradication success in such regions. Aim. The study was undertaken to evaluate the effect of increasing the treatment period on eradication of Helicobacter pylori in duodenal ulcer disease. Methods. A randomized trial was carried out in which 64 consecutive H. pylori‐infected patients with duodenal ulcer disease were enrolled. The patients were randomized to one of the three trial arms. Therapy consisted of lansoprazole 30 mg twice a day (b.i.d.), amoxycillin 1 g b.i.d. and tinidazole 500 mg b.i.d. The treatment period was 1 week in group I, 2 weeks in group II and 3 weeks in group III. At inclusion, patients underwent endoscopy and the presence of H. pylori was documented by a positive urease test and C14 urea breath test. Four weeks after completion of eradication therapy, the patients were subjected to repeat endoscopy to assess ulcer healing and tests for H. pylori infection. Results. Sixty‐four patients (55 male and nine female; mean age 35.5 years) were enrolled in each group. The H. pylori eradication rate for group I (1 week of therapy) was 47.6%, that for group II (2 weeks of therapy) was 80%, and that for group III (3 weeks of therapy) was 91.3% (p = .003). The ulcer healing rates were 71.4, 80 and 95.6% in groups I, II and III, respectively (p = .09). Conclusion. The 3‐week regimen significantly improved the eradication rate as compared with the 1‐week regime. Increasing the duration of therapy significantly improved the chances of eradication of H. pylori in duodenal ulcer disease.     

cagA gene variants in Malaysian Helicobacter pylori strains isolated from patients of different ethnic groups

Helicobacter pylori infection of a distinct subtype of cagA may lead to different pathological manifestation. The aim of this study is to determine the presence of cagA gene and its variants in H. pylori infection among different ethnic groups and its effect on gastroduodenal diseases. Overall detection of cagA among the 205 clinical isolates of H. pylori was 94%. Variations in size of the 3' region of cagA gene were examined among 192 Malaysian H. pylori cagA-positive strains. Results showed that three cagA variants differing in fragment length of PCR products were detected and designated as type A (621-651bp), type B (732-735bp) and type C (525 bp). Although there was no association between any of the cagA subtypes with peptic ulcer disease (p>0.05), an association between cagA subtypes with a specific ethnic group was observed. Specific-cagA subtype A strains were predominantly isolated from Chinese compared to Malays and Indians (p<0.0005), and cagA subtype B strains were predominantly isolated from Malays and Indians compared to Chinese (p<0.05). The cagA type A strains of H. pylori is commonly found in the Chinese patients who have a higher risk of peptic ulcer disease, thus indicating that it could be used as an important clinical biomarker for a more severe infection.     

幽门螺杆菌临床分离株的随机扩增多态性DNA指纹图分析

目的:建立武汉及周边地区幽门螺杆菌(Helicobacter pylori,Hp)感染病人胃内分离的Hp的DNA指纹图谱,并进行数理统计分析,探讨Hp基因型与疾病的相互关系,为临床诊断、防治及致病机制提供理论与实践基础.方法:采取随机扩增多态性DNA指纹法(Random amplified polymorphic DNA,RAPD)对48例病人Hp基因组DNA进行PCR反应,其随机引物为:1290 5'-GTGGATGCGA-3'.反应产物经2%琼脂糖凝胶电泳,成像存盘.用统计分析软件(Statistic analysis software,SAS)对Hp DNA指纹图的相似性以及与疾病的相关性进行分析.结果:每个菌株都有其独特的DNA指纹图,显示其基因的多态性;计算机聚类分析显示:Hp DNA指纹图可分为两大类,其与宿主疾病之间有一定程度的相关性(P＜0.05).结论:(1)RAPD对 Hp DNA扩增结果是稳定、可靠的,是一种较好的分型方法.(2)幽门螺杆菌感染所致疾病可能与其基因型相关.     

Progress in vaccine development against Helicobacter pylori

Based on the very high prevalence of diseases caused by Helicobacter pylori, particularly in the developing world, and the rapid emergence of antibiotic resistance among clinical isolates, there is a strong rationale for an effective vaccine against H. pylori. In this review we describe recent promising candidate vaccines and prophylactic or therapeutic immunization strategies for use against H. pylori, as well as studies to identify immune responses that are related to protection in experimental animals. We also describe identification of different types of immune responses that may be related to protection against symptoms based on comparisons of H. pylori-infected patients with duodenal ulcers or gastric cancer and asymptomatic carriers. We conclude that there is still a strong need to clarify the main protective immune mechanisms against H. pylori as well as to identify a cocktail of strong protective antigens, or recombinant bacterial strains that express such antigens, that could be administered by a regimen that gives rise to effective immune responses in humans.     

Molecular analysis of Helicobacter pylori populations in antral biopsies from individual patients using randomly amplified polymorphic DNA (RAPD) fingerprinting

Abstract In the present study, randomly amplified polymorphic DNA (RAPD) fingerprinting has been used to analyse multiple single colony isolates of Helicobacter pylori from antral biopsies in an attempt to ascertain whether or not multiple strains are present in individual patients using single biopsy samples. The RAPD fingerprints derived from single colonies obtained from the same biopsy specimen were in all cases indistinguishable. The previously noted heterogeneity between H. pylori strains from different individuals was confirmed. RAPD fingerprinting, combined with a simple method of template preparation, was shown to be an excellent method for H. pylori strain differentiation. The results of this study indicate that the H. pylori population is homogeneous in individual patients at a single gastric site.     

Accuracy of diagnostic tests for Helicobacter pylori in patients with peptic ulcer bleeding

Background and Aims: To assess the validity of biopsy‐based tests (histology, culture, and urease test) and serology in detecting current H. pylori infection for the peptic ulcer patients who had gastric bleeding. Methods: A total of 398 peptic ulcer patients were enrolled and divided into two groups, according to the presence or absence of bleeding. The diagnosis for current H. pylori infection was verified using the gold standard combining individual H. pylori tests. Sensitivity, specificity, and positive and negative predictive values of the culture, Campylobacter‐like organism (CLO) test (urease test), histology, and serology were compared. Results: Of the total study population (N = 398), 157 (39.4%) patients were categorized into the bleeding group. The sensitivities of the culture (40.0%) and CLO (85.0%) in the bleeding group were significantly lower than culture (58.1%) and CLO (96.4%) in the nonbleeding group (p = .012 and p < .001, respectively). In the bleeding group, the sensitivity of CLO (85.0%) was significantly lower than histology (92.5%) and serology (97.4%) (p = .013 and p = .002, respectively), which was not found in the nonbleeding group. The specificity of serology in the bleeding group (56.3%) was significantly lower than that of nonbleeding group (74.2%) (p = .038). Similarly, the specificity of serology was significantly lower than the other H. pylori tests in the bleeders. Conclusions: Bleeding decreased the sensitivity of H. pylori tests in patients with peptic ulcer, especially in urease test or culture. In contrast, histology was found to be a quite reliable test, regardless of the presence of bleeding.     

Helicobacter pylori infection and perforated peptic ulcer prevalence of the infection and role of antimicrobial treatment

Although the role of Helicobacter pylori infection on noncomplicated peptic ulcer disease has been definitively established, the precise relationship between the organism and complicated ulcer has hardly been studied. The mean prevalence of H. pylori infection in patients with perforated peptic ulcer is of only about 65-70%, which contrasts with the almost 90-100% figure reported in noncomplicated ulcer disease. However, H. pylori infection rates in various studies range markedly from 0% to 100%, suggesting that differences in variables as number and type of diagnostic methods used to diagnose H. pylori infection, or frequency of nonsteroidal anti-inflammatory drug intake, may be responsible for the low prevalence reported in some studies. Recurrent ulcer disease after peptic ulcer perforation mainly occurs in patients with H. pylori infection, which suggests that the microorganism plays an important role in this complication. All patients with perforated peptic ulcer should be treated by simple closure of the perforation and with therapy aimed at healing of the ulcer and eradicating the H. pylori infection, as disappearance of the organism prevents, or at least decreases, ulcer recurrence and ulcer perforation in patients with H. pylori-associated perforated ulcers after simple closure. Therefore, H. pylori eradicating treatment should be started during the immediate postoperative period. The patients with intractable recurrent symptoms of peptic ulcer despite adequate medical treatment, but without H. pylori infection (e.g. a patient using nonsteroidal anti-inflammatory drugs), is probably the only remaining indication for elective definitive surgical treatment of peptic ulcer disease.     

Efficacy and safety of faropenem in eradication therapy of Helicobacter pylori

Aims: While triple therapy with a proton pump inhibitor, amoxicillin, and clarithromycin is the standard therapy for Helicobacter pylori eradication, it is ineffective against clarithromycin‐resistant strains. To seek a better regimen for eradication therapy, we assessed the sensitivity of clinical strains seen in Japan to faropenem and then evaluated the efficacy and safety of eradication therapy containing this antibiotic. Methods: Minimum inhibitory concentrations (MICs) of faropenem were determined in 78 Japanese clinical H. pylori isolates using the agar dilution method. H. pylori‐positive patients were consecutively assigned to a 7‐day eradication therapy protocol with LAF (lansoprazole 60 mg/day, amoxicillin 2000 mg/day, and faropenem 600 mg/day), and then to a 14‐day protocol. The outcomes of the therapies were assessed by ¹³C‐urea breath tests. Results: All 78 strains showed MICs of faropenem that were equal to or less than 0.2 µg/mL. The eradication rates according to intention‐to‐treat analyses were 46.5% with the 7‐day therapy (n = 43) and 62.5% with the 14‐day therapy (n = 32). No special measures were required to treat the adverse events observed in approximately one‐third of the patients. Conclusions: Faropenem was found to have good antimicrobial action against H. pylori in vitro. The 14‐day LAF therapy successfully eradicated H. pylori in about two‐thirds of the patients although the incidence of adverse events was high.     

Eradication of Helicobacter pylori does not reduce the incidence of gastroduodenal ulcers in patients on long-term NSAID treatment: double-blind, randomized, placebo-controlled trial

BACKGROUND: Helicobacter pylori and nonsteroidal antiinflammatory drugs (NSAIDs) are the major causes of gastroduodenal ulcers. Studies on the benefit of eradication of H. pylori in NSAID users yielded conflicting results. OBJECTIVE: To investigate whether H. pylori eradication in patients on long-term NSAIDs reduces the incidence of gastroduodenal ulcers. METHODS: Patients on long-term NSAID treatment and who are H. pylori positive on serologic testing, were randomly assigned to either H. pylori eradication (omeprazole, amoxicillin, and clarithromycin) or placebo. Primary endpoint was the presence of endoscopic gastric or duodenal ulcers 3 months after randomization. RESULTS: One hundred sixty-five (48%) of a total of 347 patients were on gastroprotective medication. At endoscopy, gastroduodenal ulcers were diagnosed in 6 (4%) and 8 (5%) patients in the eradication and placebo group, respectively (p = .65). During follow-up of 12 months, no symptomatic ulcers or ulcer complications developed. No significant differences were found in the development of gastroduodenal erosions, dyspepsia, or in quality of life. CONCLUSION: H. pylori eradication therapy in patients on long-term NSAID treatment had no beneficial effect on the occurrence of ulcers, erosions, or dyspepsia. Ulcer rates in both study arms are remarkably low, in both patients with and without gastroprotective therapy.     

Effect of Helicobacter pylori infection on gastric acid secretion and meal-stimulated serum gastrin in children

Background. Comparative studies of gastric acid secretion in children related to Helicobacter pylori infection are lacking. The purpose of this study was to compare acid secretion and meal‐stimulated gastrin in relation to H. pylori infection among pediatric patients. Materials and Methods. Thirty‐six children aged 10–17 years (17 with H. pylori infection) undergoing diagnostic endoscopy participated in the study. Diagnoses included gastritis only (n = 23), duodenal ulcer (n = 5) and normal histology (n = 8). Gastric acid output was studied using the endoscopic gastric secretion test before and 2–3 months after H. pylori eradication. Meal‐stimulated serum gastrin response was assessed before and 12 months after eradication. Results. H. pylori gastritis was typically antrum‐predominant. Acid secretion was greater in H. pylori‐positive patients with duodenal ulcer than in gastritis‐only patients or controls [mean ± standard error (SE): 6.56 ± 1.4, 3.11 ± 0.4 and 2.65 ± 0.2 mEq/10 minutes, respectively; p < .001]. Stimulated acid secretion was higher in H. pylori‐positive boys than girls (5.0 ± 0.8 vs. 2.51 ± 0.4 mEq/10 minutes, respectively; p < .05). Stimulated acid secretion pre‐ and post‐H. pylori eradication was similar (5.47 ± 0.8 vs. 4.67 ± 0.9 mEq/10 minutes, respectively; p = .21). Increased basal and meal‐stimulated gastrin release reversed following H. pylori eradication (e.g. basal from 134 to 46 pg/ml, p < .001 and peak from 544 to 133 pg/ml, p < .05). Conclusions. H. pylori infection in children is associated with a marked but reversible increase in meal‐stimulated serum gastrin release. Gastric acid hypersecretion in duodenal ulcer remains after H. pylori eradication, suggesting that the host factor plays a critical role in outcome of the infection.     

Genetic polymorphisms of NOD1 and IL-8, but not polymorphisms of TLR4 genes, are associated with Helicobacter pylori-induced duodenal ulcer and gastritis

BACKGROUND: Intracellular pathogen receptor NOD1 is involved in the epithelial cell sensing Helicobacter pylori, which results in a considerable interleukin (IL)-8 production. The aim of this study was to evaluate the relationship between NOD1 and IL-8 genetic polymorphisms and the development of H. pylori-induced gastritis and duodenal ulcer (DU), as compared with TLR4 polymorphisms. MATERIALS AND METHODS: Eighty-five patients with DU and 135 patients with gastritis were enrolled in the study. Seventy-five serologically H. pylori-positive subjects without gastric or duodenal symptoms served as controls. The G796A (E266K) NOD1 polymorphism was determined by restriction fragment length polymorphism, and the -251 IL-8 polymorphism by amplification refractory mutation system method. The TLR4 (ASP/299/Gly and Thr/399/Ile) gene polymorphisms were examined by melting point analysis. RESULTS: AA homozygote mutant variants of NOD1 were detected in 20% of the H. pylori-positive patients with DU versus 7% of H. pylori-positive patients with gastritis and versus 6% of the H. pylori-positive healthy controls. The IL-8 heterozygote mutant variant was detected with a significantly higher frequency among the DU patients and those with gastritis than among the H. pylori-positive controls. However, no significant correlation concerning the frequency of the TLR4 gene polymorphism could be revealed between any group of patients and the controls. CONCLUSION: E266K CARD4/NOD1, but not the TLR4 gene polymorphism increases the risk of peptic ulceration in H. pylori-positive patients. The -251 IL-8 polymorphism was significantly associated with either gastritis or DU in H. pylori-infected subjects. Host factors including intracellular pathogen receptors and IL-8 production play an important role in H. pylori-induced gastric mucosal damage.     

Eradication of Helicobacter pylori by 7-day triple-therapy regimens combining pantoprazole with clarithromycin, metronidazole, or amoxicillin in patients with peptic ulcer disease: results of two double-blind, randomized studies

Aim. To compare the short‐term (7‐day) safety and efficacy of two triple‐therapy regimens using pantoprazole with those of two dual‐therapy regimens (one with pantoprazole and one without), for Helicobacter pylori eradication in patients with peptic ulcer disease. Methods. H. pylori infection was identified by rapid urease (CLOtest), and confirmed by histology and culture. Patients were enrolled into one of two randomized, double‐blind, multicenter, parallel‐group studies. In study A, patients received oral pantoprazole 40 mg, clarithromycin 500 mg, and metronidazole 500 mg (PCM); pantoprazole, clarithromycin and amoxicillin 1000 mg (PCA); or pantoprazole and clarithromycin (PC). In study B, patients received PCM, PCA, PC, or clarithromycin and metronidazole without pantoprazole (CM). Treatments were given twice daily for 7 days. H. pylori status after therapy was assessed by histology and culture at 4 weeks after completing the course of study treatment. Modified intent‐to‐treat (MITT; each study: n = 424, n = 512) and per‐protocol (PP; each study: n = 371, n = 454) populations were analyzed. The MITT population comprised all patients whose positive H. pylori status was confirmed by culture and histology; the PP population comprised patients who also complied with ≥ 85% of study medication doses. Results. A total of 1016 patients were enrolled. Cure rates among patients with clarithromycin‐susceptible H. pylori strains were 82 and 86% for PCM, and 72 and 71% for PCA, in studies A and B, respectively. Cure rates among patients with metronidazole‐susceptible H. pylori strains were 82 and 87% for PCM, and 71 and 69% for PCA, in studies A and B, respectively. The combined eradication rates observed with the PCM regimen were superior to those of all other regimens tested. Side‐effects were infrequent and mild. Conclusions. PCM had the highest overall eradication rate in these two studies examining 7‐day treatment regimens. All regimens were safe and well tolerated.     

幽门螺杆菌感染的分子机制

幽门螺杆菌(Helicobacterpylori)是居留于人胃上皮组织并引起胃炎、消化性胃溃疡和胃癌的病原菌。近年来,随着幽门螺杆菌全基因组序列的报道和功能基因的研究深入,对幽门螺杆菌的感染的分子、免疫等机制逐渐阐明。现对幽门螺杆菌基因组特点和幽门螺杆菌黏附、毒性因子等对人体感染的分子机制等方面的研究进展做一综述。     

High relative content of lysophospholipids of Helicobacter pylori mediates increased risk for ulcer disease

Helicobacter pylori phospholipase A (OMPLA) degrades bacterial membrane phospholipids to lysophospholipids. High levels of lysophospholipids are associated with higher hemolytic activity, increased release of urease and vacA and better adherence to epithelial cells in vitro. The phospholipase A gene (pldA) displays phase variation due to a slippage in a homopolymeric tract. The aim of this study was to determine if the relative amount of lysophospholipids in the cell wall is associated with ulcer disease, and to further investigate the significance of pldA phase variation. H. pylori isolates of 40 patients were examined. The relative lysophospholipid content of each isolate was determined and the pldA gene was sequenced. The study indicated that H. pylori can regulate its OMPLA activity by phase variation in the pldA gene or by protein level regulation among phase variants in the pldA 'ON' status. We found a significant difference between the relative amount of lysophospholipids of the ulcer group and the non-ulcer group (p=0.022). When the lysophospholipid/phospholipid ratios were compared with outcome, the OR for ulcer disease was 9.0 (95% CI 1.6-49.4; p=0.014). Isolates with a high OMPLA activity are significantly associated with patients with ulcer disease.     

Nonbismuth quadruple (concomitant) therapy: empirical and tailored efficacy versus standard triple therapy for clarithromycin-susceptible Helicobacter pylori and versus sequential therapy for clarithromycin-resistant strains

Background:  Using quadruple clarithromycin‐containing regimens for Helicobacter pylori eradication is controversial with high rates of macrolide resistance. Aim:  To evaluate antibiotic resistance rates and the efficacy of empirical and tailored nonbismuth quadruple (concomitant) therapy in a setting with cure rates <80% for triple and sequential therapies. Methods:  209 consecutive naive H. pylori‐positive patients without susceptibility testing were empirically treated with 10‐day concomitant therapy (proton pump inhibitors (PPI), amoxicillin 1 g, clarithromycin 500 mg, and metronidazole 500 mg; all drugs b.i.d.). Simultaneously, 89 patients with positive H. pylori culture were randomized to receive triple versus concomitant therapy for clarithromycin‐susceptible H. pylori, and sequential versus concomitant therapy for clarithromycin‐resistant strains. Eradication was confirmed with ¹³C‐urea breath test or histology 8 weeks after completion of treatment. Results:  Per‐protocol (PP) and intention‐to‐treat eradication rates after empirical concomitant therapy without susceptibility testing were 89% (95%CI:84–93%) and 87% (83–92%). Antibiotic resistance rates were: clarithromycin, 20%; metronidazole, 34%; and both clarithromycin and metronidazole, 10%. Regarding clarithromycin‐susceptible H. pylori, concomitant therapy was significantly better than triple therapy by per protocol [92% (82–100%) vs 74% (58–91%), p = 0.05] and by intention to treat [92% (82–100%) vs 70% (57–90%), p = 0.02]. As for antibiotic‐resistant strains, eradication rates for concomitant and sequential therapies were 100% (5/5) vs 75% (3/4), for clarithromycin‐resistant/metronidazole‐susceptible strains and 75% (3/4) vs 60% (3/5) for dual‐resistant strains. Conclusions:  Empirical 10‐day concomitant therapy achieves good eradication rates, close to 90%, in settings with multiresistant H. pylori strains. Tailored concomitant therapy is significantly superior to triple therapy for clarithromycin‐susceptible H. pylori and at least as effective as sequential therapy for resistant strains.