Helicobacter (HELICOBACTER)

Publications in this journal

• Article: Endoscopic and and histopathologic characteristics of H. pylori infection in a Canadian Arctic hamlet. W1.8

  K J Goodman, J Cheung, J Huntington, R Munday, R N Fedorak, S J Zanten
  Helicobacter 01/2009; 14:314.
• Article: Demographics of Helicobacter pylori infection in a Canadian Arctic Hamlet. P03.06

  K J Goodman, R Munday, J Huntington, B Archie, G Gordon, S J Zanten
  Helicobacter 01/2009; 14:314.
• Article: Neonatal co-infection with helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10(-/-) mice.

  Laura P Hale, Dinushi Perera, Marcia R Gottfried, Lillian Maggio-Price, Sudha Srinivasan, Douglas Marchuk
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  ABSTRACT: Inflammatory bowel disease (IBD) is hypothesized to represent an aberrant immune response against enteric bacteria that occurs in a genetically susceptible host. Humans and mice with IBD are at markedly increased risk for colonic neoplasia. However, the long lead time required before development of inflammation-associated colon neoplasia in commonly used murine models of IBD slows the development of effective chemopreventative therapies. Neonatal coinfection with Helicobacter typhlonius and Helicobacter rodentium was used to trigger the onset of IBD in mice deficient in the immunoregulatory cytokine interleukin (IL)-10. The severity of colon inflammation and incidence of neoplasia was determined histologically. IL-10(-/-) mice demonstrated early onset, severe colon inflammation following neonatal infection with H. typhlonius and H. rodentium. The incidence of inflammation-associated colon neoplasia was approximately 95% at a mean age of 21 +/- 2 weeks. Mutation of endoglin, an accessory receptor for TGF-beta, did not affect the severity of IBD or the incidence of neoplasia in this model. The rapid onset of severe colon inflammation and multiple neoplastic lesions in the colons of IL-10(-/-) mice neonatally coinfected with H. typhlonius and H. rodentium makes this model well-suited for investigating the mechanisms involved in inflammation-associated colon cancer as well as its chemoprevention.
  Helicobacter 01/2008; 12(6):598-604.
• Article: Efficacy and safety of faropenem in eradication therapy of Helicobacter pylori.

  Keiji Ogura, Yuzo Mitsuno, Shin Maeda, Yoshihiro Hirata, Ayako Yanai, Wataru Shibata, Tomoya Ohmae, Haruhiko Yoshida, Takao Kawabe, Masao Omata
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  ABSTRACT: 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. 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 (13)C-urea breath tests. All 78 strains showed MICs of faropenem that were equal to or less than 0.2 microg/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. 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.
  Helicobacter 01/2008; 12(6):618-22.
• Article: The effect of the cag pathogenicity island on binding of Helicobacter pylori to gastric epithelial cells and the subsequent induction of apoptosis.

  Yutaka Minohara, David K Boyd, Hal K Hawkins, Peter B Ernst, Janak Patel, Sheila E Crowe
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  ABSTRACT: Helicobacter pylori infection leads to gastritis, peptic ulcer, and gastric cancer, in part due to epithelial damage following bacteria binding to the epithelium. Infection with cag pathogenicity island (PAI) bearing strains of H. pylori is associated with increased gastric inflammation and a higher incidence of gastroduodenal diseases. It is now known that various effector molecules are injected into host epithelial cells via a type IV secretion apparatus, resulting in cytoskeletal changes and chemokine secretion. Whether binding of bacteria and subsequent apoptosis of gastric epithelial cells are altered by cag PAI status was examined in this study. AGS, Kato III, and N87 human gastric epithelial cell lines were incubated with cag PAI-positive or cag PAI-negative strains of H. pylori in the presence or absence of clarithromycin. Binding was evaluated by flow cytometry and scanning electron microscopy. Apoptosis was assessed by detection of DNA degradation and ELISA detection of exposed histone residues. cag PAI-negative strains bound to gastric epithelial cells to the same extent as cag PAI-positive strains. Both cag PAI-positive and cag PAI-negative strains induced apoptosis. However, cag PAI-positive strains induced higher levels of DNA degradation. Incubation with clarithromycin inactivated H. pylori but did not affect binding. However, pretreatment with clarithromycin decreased infection-induced apoptosis. cag PAI status did not affect binding of bacteria to gastric epithelial cells but cag PAI-positive H. pylori induced apoptosis more rapidly than cag PAI-negative mutant strains, suggesting that H. pylori binding and subsequent apoptosis are differentially regulated with regard to bacterial properties.
  Helicobacter 01/2008; 12(6):583-90.
• Article: A pilot study evaluating sequential administration of a PPI-amoxicillin followed by a PPI-metronidazole-tetracycline in Turkey.

  Orhan Sezgin, Engin Altintaş, Erdinç Nayir, Enver Uçbilek
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  ABSTRACT: There is no effective regimen for the eradication of Helicobacter pylori in our country. It may be due to the increasing prevalence of resistance to antibiotics used for the treatment of H. pylori. Recently, a study from Turkey has revealed that a new treatment scheme consisting of sequential administration of pantoprazole plus amoxicillin for 7 days followed by pantoprazole plus metronidazole, and tetracycline for the remaining 7 days was effective in the first-line treatment of H. pylori. Therefore, we aimed to confirm efficacy of a new therapy scheme in the first-line H. pylori eradication. This is a prospective, open label, single center, pilot study and included 32 patients infected with H. pylori diagnosed by both histologic examinations, rapid urease test and (13)C-urea breath test (UBT). The patients received a 14-day sequential regimen (pantoprazole 40 mg b.d. plus amoxicillin 1000 mg b.d. for 7 days and pantoprazole 40 mg b.d., metronidazole 500 mg b.d. and tetracycline 500 mg q.d. for the remaining 7 days). Eradication was assessed with (13)C-UBT 4 weeks after completion of the therapy. Intention-to-treat and per-protocol eradication rates were determined. At intention-to-treat analysis, the eradication rate was 50% (16/32). For the per protocol analysis, the eradication rate was 57% (16/28). There were no significant adverse effects and treatment compliance was good. A new therapy consisting of sequentially administered drugs for 14 days yielded unacceptably low eradication rates. This scheme was not efficient for H. pylori eradication in our region. Further investigations are needed to determine the effectiveness of this scheme in other regions of Turkey.
  Helicobacter 01/2008; 12(6):629-32.
• Article: Efficacy of Lansap combination therapy for eradication of H. pylori.

  Akihito Nagahara, Hiroto Miwa, Mariko Hojo, Takashi Yoshizawa, Masato Kawabe, Taro Osada, Akihiko Kurosawa, Toshifumi Ohkusa, Sumio Watanabe
  Helicobacter 01/2008; 12(6):643-4.
• Article: Failure of sequential therapy to eradicate Helicobacter pylori in previously treated subjects.

  Suhair Shehada, Isaac Srugo, Ron Shaoul
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  ABSTRACT: Recently, studies in adults and subsequently in children have demonstrated a very high success rate for sequential therapy as a primary therapy when compared to traditional therapy regimens. METHODs: We report our experience with a sequential therapy regimen for the eradication of Helicobacter pylori in five infected children and a young adult, whose conventional therapy regimens had been unsuccessful. Five patients failed the sequential therapy. All of them experienced between two and four failures of traditional therapy prior to the sequential treatment protocol. The only patient who succeeded on the sequential therapy had just one previous failure. All of our patients who had failed sequential therapy achieved eradication of the bacteria with quadruple therapy. In view of our disappointing results, sequential therapy is unsuccessful as a therapy for children and young adults who have failed previous treatment regimens. At the present time, quadruple therapy is indicated for this group. Well-designed placebo-controlled trials are indicated to further characterize this group of patients.
  Helicobacter 01/2008; 12(6):645-7.
• Article: Rabeprazole- versus esomeprazole-based eradication regimens for H. pylori infection.

  I-Chen Wu, Deng-Chyang Wu, Ping-I Hsu, Chien-Yu Lu, Fang-Jung Yu, Tsang-En Wang, Wen-Hsiung Chang, Jyh-Jon Chen, Fu-Chen Kuo, Jeng-Yih Wu, Wen-Ming Wang, Ming-Jong Bair
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  ABSTRACT: Different kinds of proton pump inhibitor-based triple therapies could result in different Helicobacter pylori eradication rates. The aims of this study were to compare the efficacy and safety of rabeprazole- and esomeprazole-based triple therapy in primary treatment of H. pylori infection in Taiwan. From June 2005 to March 2007, 420 H. pylori-infected patients were randomly assigned to receive a 7-day eradication therapy with either esomeprazole 40 mg daily (EAC group, n = 209) or rabeprazole 20 mg b.i.d. (RAC group, n = 211) in combination with amoxicillin 1 g b.i.d. and clarithromycin 500 mg b.i.d.. Follow-up endoscopy with biopsy was done 12-16 weeks after completion of eradication therapy. Those who refused endoscopic exams underwent (13)C-urea breath test to assess the treatment response. Intention-to-treat analysis revealed that the eradication rate was 89.4% in the EAC group and 90.5% in RAC groups (p-value = .72). All of the subjects returned for assessment of compliance (100% in EAC group vs. 99.5% in RAC group, p-value = .32) and adverse events (3.83% in EAC group vs. 6.16% in RAC group, p-value = .27). Sixty (28.7%) and 37 (17.6%) patients in EAC and RAC group, respectively, refused endoscopy and underwent a (13)C-urea breath test to determine the treatment effect. In conclusion, rabeprazole- and esomeprazole-based primary therapies for H. pylori infection are comparable in efficacy and safety.
  Helicobacter 01/2008; 12(6):633-7.
• Article: Phenylphosphonate transport by Helicobacter pylori.

  Justin L Ford, Paul A Gugger, S Bruce Wild, George L Mendz
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  ABSTRACT: Helicobacter pylori can utilize phenylphosphonate as a sole source of phosphorus, and it is able to transport the phosphonate N-phosphonoacetyl-L-aspartate. However, H. pylori does not have any genes homologous to those of the known pathways for phosphonate degradation in bacteria, indicating that it must have novel pathways for the transport and metabolism of phosphonates. Phenylphosphonate transport by H. pylori was studied in strains LC20, J99 and N6 by the centrifugation through oil method using [(14)C]-labeled phenylphosphonate. The Michaelis constants of transport K(t) and V(max) for phenylphosphonate showed similar kinetics in the three strains. The Arrhenius plot for phenylphosphonate transport rates at permeant concentrations of 50 micromol/L was linear over the temperature range 10-40 degrees C with an activation energy of 3.5 kJ/mol, and a breakpoint between 5 and 10 degrees C. Transport rates increased with monovalent cation size. The effects of various inhibitors were investigated: iodoacetamide, amiloride, valinomycin, and nigericin reduced the rate of phenylphosphonate transport; sodium azide and sodium cyanide increased the transport rate; and monensin had no effect. The kinetics and properties of H. pylori phenylphosphonate transport were characterized, and the data suggested a carrier-mediated transport mechanism.
  Helicobacter 01/2008; 12(6):609-15.
• Article: Persisting chronic gastritis and elevated Helicobacter pylori antibodies after successful eradication therapy.

  Lea Veijola, Aino Oksanen, Auli Linnala, Pentti Sipponen, Hilpi Rautelin
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  ABSTRACT: The persistence of chronic inflammation in gastric mucosa and elevated Helicobacter pylori antibodies after successful eradication therapy are common findings in clinical practice. We studied their possible association with each other and disappearance in long-term follow up, as well as their possible connection with gastric atrophy. The study population consisted of 108 dyspeptic patients with successful eradication therapy median 6.4 years earlier. The patients underwent gastroscopy, and biopsies from antrum and corpus were evaluated by an experienced pathologist. Serum samples collected from 77 patients were studied for H. pylori antibodies, parietal cell antibodies, as well as for pepsinogen I, pepsinogen II, and gastrin-17 levels. The prevalence of chronic gastric inflammation and elevated H. pylori antibodies after successful eradication therapy decreased by time, but still after 5 years, 17 of 51 (33%) subjects had elevated H. pylori antibodies and 14 of 68 (21%) had a mild inactive chronic inflammation in gastric mucosa. In patients with and without chronic inflammation in gastric mucosa, elevated H. pylori antibodies were detected in three of 10 (30%) and 14 of 41 (34%), elevated parietal cell antibodies in one of 10 (10%) and six of 41 (15%), low pepsinogen I in one of 10 (10%) and none of 41, and elevated gastrin-17 in three of 10 (30%) and six of 41 (15%), respectively. More than 5 years after successful H. pylori eradication therapy, mild persistent chronic inflammation may occur in gastric mucosa in up to one-fifth and elevated H. pylori antibodies even in one-third of patients, although these two are independent phenomena.
  Helicobacter 01/2008; 12(6):605-8.
• Article: In vitro proinflammatory properties of Helicobacter pylori strains causing low-grade gastric MALT lymphoma.

  Barbara Ferreira-Chagas, Gwenaëlle Lasne, Sandrine Dupouy, Anne Gallois, Andrea Morgner, Armelle Ménard, Francis Mégraud, Philippe Lehours
  Helicobacter 01/2008; 12(6):616-7.
• Article: Double-dose, new-generation proton pump inhibitors do not improve Helicobacter pylori eradication rate.

  Hyo Sun Choi, Dong Il Park, Sang Jun Hwang, Jung Sik Park, Hong Joo Kim, Yong Kyun Cho, Chong Il Sohn, Woo Kyu Jeon, Byung Ik Kim
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  ABSTRACT: Up to present, omeprazole plus two antibiotics are used for Helicobacter pylori eradication therapy . Few studies have compared double-dose new-generation, proton pump inhibitors (PPI) with omeprazole. Therefore, we conducted a randomized, prospective study to evaluate differences in H. pylori eradication rates by PPI type. Between January 2006 and December 2006, 576 consecutive patients with proven H. pylori infection were enrolled prospectively. Four different PPIs [omeprazole 20 mg b.i.d. (old generation), or pantoprazole 40 mg b.i.d., rabeprazole 20 mg b.i.d., or esomeprazole 40 mg b.i.d. (new generation)] were added to clarithromycin (500 mg b.i.d.) and amoxicillin (1 g b.i.d.) for 1 week. By intention-to-treat analysis, no difference was found between the eradication rates of these four PPIs: 64.9% (omeprazole, n = 148), 69.3% (pantoprazole, n = 140), 69.3% (rabeprazole, n = 140), and 72.9% (esomoprazole, n = 148). When eradication rates were analyzed according to whether patients had an ulcer or not on a per-protocol basis, no difference was found between the eradication rates of the four PPIs. However, side-effects were more common in the esomeprazole-based triple therapy group than in the other groups (p < .05). No convincing evidence was obtained that double-dose new-generation PPIs have better H. pylori eradication rates and tolerability than omeprazole.
  Helicobacter 12/2007; 12(6):638-42.
• Article: Evolution of Helicobacter pylori research as observed through the workshops of the European Helicobacter Study Group.

  Francis Mégraud
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  ABSTRACT: The European Helicobacter Study Group established a yearly workshop that has been held from 1988 to 2007. The analysis of the data from these workshops shows that 7246 abstracts were presented originating from 76 different countries. The distribution according to specific years follows a Gauss-type curve with a peak in the mid-1990s. The presenters were mainly from Europe, but an increasing number coming from non-European countries was observed throughout the years. The evolution of the topics selected also evolved but was relatively stable these last 10 years. Some landmarks have been highlighted. These data constitute an important source of information with regard to the evolution of Helicobacter pylori research over these 20 years.
  Helicobacter 12/2007; 12 Suppl 2:1-5.
• Article: Helicobacter pylori gastritis, the unifying concept for gastric diseases.

  Brian J Egan, Kate Holmes, Humphrey J O'Connor, Colm A O'Morain
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  ABSTRACT: Helicobacter pylori infection causes a broad spectrum of clinical diseases and the clinical manifestations of the infection depend on host, environmental, and bacterial factors. These factors have an impact on the pattern and severity of gastritis and ultimately determine the clinical outcome of H. pylori infection. Better staging of gastritis may help to identify patients at risk of gastric cancer. In this article we will examine the complex interaction between host, environmental, and bacterial factors in the pathogenesis of H. pylori infection.
  Helicobacter 12/2007; 12 Suppl 2:39-44.
• Article: Evolution of Helicobacter pylori therapy from a meta-analytical perspective.

  Javier P Gisbert, Ramón Pajares, José María Pajares
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  ABSTRACT: Even before the discovery of Helicobacter pylori as their cause, chronic gastritis and peptic ulcer disease were empirically treated with anti-infectious agents. However, it was not until that finding that an antibiotic approach began to be used systematically. The main aim of this article is to review the evolution of H. pylori therapy from a meta-analytical perspective. Initially, antibiotic monotherapy had a minor efficacy on H. pylori. Dual therapy including either bismuth compounds or proton-pump inhibitors (PPI) and one antibiotic also resulted in insufficient cure rates. Bismuth-based triple therapy (the first used) and PPI-based triple therapies (combined with two antibiotics, including amoxicillin, nitroimidazole, or clarithromycin) have been the most widely recommended. PPI-based regimens are superior to H2-antagonist-based ones. The influence of the type of PPI, the dose and the duration of the treatment will be discussed. Among the factors influencing the efficacy of therapy, resistance to clarithromycin and metronidazole are the most important risk factors for eradication failure. Several rescue therapies can be used. Bismuth-based quadruple therapy is effective, but the complexity of the regimen and the associated adverse effects limit the compliance. PPI-based triple therapy with amoxicillin and levofloxacin is at least equally effective and better tolerated.
  Helicobacter 12/2007; 12 Suppl 2:50-8.
• Article: Prevalence of duodenal ulcer-promoting gene (dupA) of Helicobacter pylori in patients with duodenal ulcer in North Indian population.

  H S Jayasinghe Arachchi, Vijay Kalra, Banwari Lal, Vikram Bhatia, C S Baba, S Chakravarthy, S Rohatgi, Priyangshu M Sarma, V Mishra, Bimal Das, Vineet Ahuja
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  ABSTRACT: 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. 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. 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). 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 12/2007; 12(6):591-7.
• Article: Helicobacter pylori as a vaccine delivery system.

  Barry Marshall, Tobias Schoep
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  ABSTRACT: For more than 10 years a vaccine against Helicobacter pylori has been the elusive goal of many investigators. The need for a vaccine was highlighted when eradication attempts in developing countries were foiled by reinfection rates of 15-30% per annum. In addition, physicians in developed countries were concerned that attempts at total eradication of H. pylori would result in widespread macrolide resistance in both H. pylori and other important pathogens. Although attempts to produce vaccines against H. pylori have failed in their ultimate goal, considerable knowledge has been developed on the pathogenesis and immunology of Helicobacter infections. In this article we describe an alternative use for this new knowledge, i.e. a plan to use live Helicobacter species to deliver vaccines against other organisms. Because of its intimate attachment to the gastric mucosa and long-term residence there, H. pylori might succeed as an antigen delivery system, a goal which has eluded most other strategies of nonparenteral vaccination.
  Helicobacter 12/2007; 12 Suppl 2:75-9.
• Article: Second-line treatment for Helicobacter pylori infection: 10-day moxifloxacin-based triple therapy versus 2-week quadruple therapy.

  Jung Mook Kang, Nayoung Kim, Dong Ho Lee, Young Soo Park, Yu Rim Kim, Joo Sung Kim, Hyun Chae Jung, In Sung Song
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  ABSTRACT: The aim of this study was to test the efficacy of 10-day moxifloxacin-based triple therapy versus 2-week quadruple therapy for the second-line treatment of Helicobacter pylori infection. One hundred and ninety-two patients who had failed previous H. pylori eradication on standard triple therapy were randomized to one of two regimens: 1, moxifloxacin (400 mg q.d.), amoxicillin (1000 mg b.i.d.), and esomeprazole (20 mg b.i.d.) for 10 days (the 10MEA group), or 2, esomeprazole (20 mg b.i.d.), tripotassium dicitrate bismuthate (300 mg q.i.d.), metronidazole (500 mg t.i.d.), and tetracycline 500 mg (q.i.d.) for 14 days (the 14EBMT group). The eradication rates, drug compliances, and side-effect rates of these two regimens were compared. Eradication rates by intention-to-treat and per-protocol analyses in the 10MEA and 14EMBT groups were 71.9% and 82.6%, and 71.7% and 90.5% (p = .973 and .321), respectively. The 10MEA group was significantly superior to the 14EMBT group in terms of side-effect rates (12.2% vs. 39.6%, p = .001), and discontinuation rates due to side-effects were lower in the 10MEA group than in the 14EMBT group (0.7% vs. 13.2%, p < .001). Moreover, compliance was higher in the 10MEA group (94.2% (131/139)) than in the 14EBMT group (83.0% (44/53)) (p = .014). The 10-day moxifloxacin-based triple therapy was found to have a high eradication rate with few side-effects and good drug compliance. These findings suggest that this regimen is a safe and effective second-line treatment option for H. pylori infection in Korea.
  Helicobacter 12/2007; 12(6):623-8.
• Article: Epidemiology of premalignant gastric lesions: implications for the development of screening and surveillance strategies.

  Annemarie C de Vries, Ernst J Kuipers
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  ABSTRACT: Gastric cancer is one of the most common cancers worldwide; however, gastric cancer incidence varies greatly between different geographic areas. As gastric cancer is usually diagnosed at an advanced stage, the disease causes considerable morbidity and mortality. To detect gastric carcinomas at an early and curable stage, screening and surveillance seem necessary. Premalignant gastric lesions are well known risk factors for the development of intestinal type gastric adenocarcinomas. In a multistep cascade, chronic Helicobacter pylori-induced gastritis progresses through premalignant stages of atrophic gastritis, intestinal metaplasia and dysplasia, to eventually gastric cancer. Therefore, this cascade may provide a basis for early detection and treatment of gastric cancer. Epidemiology of gastric cancer and premalignant gastric lesions should guide the development of screening and surveillance strategies, as distinct approaches are required in countries with low and high gastric cancer incidences.
  Helicobacter 12/2007; 12 Suppl 2:22-31.