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PubMed2004

Epidemiology of Helicobacter infection in wild rodents in the Xinjiang-Uygur autonomous region of China.

Helicobacter species were detected in the feces of wild rodents captured in Qiemo and Ruoqiang in the Xinjiang-Uygur autonomous region of China by polymerase chain reaction and 16S rRNA partial sequence analysis. Forty-four wild rodents, including one Przewalski's gerbil (Brachiones przewalskii), three Northern three-toed jerboas (Dipus sagitta), one long-eared jerboa (Euchoreutes naso), 34 midday gerbils (Meriones meridianus), two short-tailed bandicoot rats (Nesokia indica) and three great gerbils (Rhombomys opimus), were examined. Epidemiological studies indicated that Helicobacter spp. were detected in all genera tested; that H. hepaticus, H. apodemus, H. canadensis, and H. winghamensis were widespread in wild rodents; and that the dominant Helicobacter species in rodents differed depending not only on the order or genus of the animal but also on the animal's habitat. H. bilis, H. pylori, H. rodentium and " H. suncus" were not detected in any animals. It appears that the wild rodents tested in this study are not a reservoir of H. pylori infection.

Animals↗
PubMed2001

Early stage gastric MALT lymphoma with high-grade component cured by Helicobacter pylori eradication.

A 68-year-old woman was diagnosed with gastric lymphoma of the mucosa-associated lymphoid tissue (MALT) type with a high-grade component. Surgical treatment was recommended because of the presence of the high-grade component, but she refused surgery. As an alternative, she received Helicobacter pylori eradication treatment, which successfully induced regression of the lymphoma. She shows no sign of recurrence endoscopically and histologically, as of 29 months after the eradication treatment. Moreover, the B-cell monoclonality and Helicobacter pylori infection demonstrated at diagnosis has disappeared. This is one of the rare cases of gastric lymphoma of the MALT type with a high-grade component cured by Helicobacter pylori eradication alone.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2003

Helicobacter pylori virulence genotypes in Portuguese children and adults with gastroduodenal pathology.

The aim of this study was to evaluate the prevalence of virulence genotypes, namely cagA, vacA and babA2, of Helicobacter pylori strains isolated from Portuguese adults and children presenting gastroduodenal pathology. One hundred thirty-six strains were studied, 82 isolated from adult patients (50 with nonulcerative gastritis and 32 with active peptic ulcer) and 58 isolated from children (54 with nonulcerative gastritis and 4 with duodenal ulcer). Genotyping of cagA, vacA and babA2 was assessed by polymerase chain reaction. Overall, Helicobacter pylori strains carrying more virulent genotypes were much more prevalent in adults than in children, particularly the type I ( vacAs1- and cagA-positive) and the triple-positive ( vacAs1-, cagA- and babA2-positive) strains ( P<0.001). A subpopulation of adults and children with nonulcerative gastritis was also studied, and differences in the prevalence of virulent genotypes were observed, either for individual genotypes ( P=0.017 for cagA, P=0.010 for vacAs1) or in combinations, i.e. the type I genotype ( P=0.005) and the triple-positive strains ( P=0.031). There was no difference between the two populations in the distribution of babA2 and m1/m2 genotypes. Considering the cohort effect in the epidemiology of Helicobacter pylori infection, these results suggest that different strains might circulate during different periods of time, or that, after infection in childhood, individual strains will undergo changes during the course of infection.

Adult↗
PubMed2003

Infection with cagA-positive and cagA-negative types of Helicobacter pylori among children and adolescents with gastrointestinal symptoms in Latvia.

In order to determine the prevalence of concomitant cagA-positive and cagA-negative Helicobacter pylori genotypes in individual subjects, a group of 56 symptomatic patients (aged 8-18 years) was studied. Among 31 patients culture-positive for Helicobacter pylori, only cagA-positive colonies were isolated from 18 patients, both cagA-positive and cagA-negative genotypes were isolated from 4 patients, and in 9 patients all of the individual colonies isolated were cagA-negative, but in seven of them a pool of colonies was positive for cagA. Thus, the presence of both cagA-positive and cagA-negative genotypes in the same individual was identified in 11 of the 31 culture-positive patients tested, and most of the patients predominantly colonized by cagA-negative strains also harbored a small amount of cagA-positive strains. Previous or current infection with cagA-positive strains of Helicobacter pylori was observed in 50 of the 56 patients studied.

Adolescent↗
PubMed1999

Performance of native and recombinant antigens for diagnosis of Helicobacter pylori infection.

The aim of this study was to evaluate the performance of three antigenic preparations for serological diagnosis of Helicobacter pylori infection: (i) native antigens from Helicobacter pylori strain N6 or its aflagellated isogenic mutant N6flbA-, or an acellular extract (antigen AgFA) from a pool of six clinical strains; (ii) recombinant antigens consisting of CagA fused to MS2 polymerase and HspA or recombinant UreA and UreB fused to the maltose-binding protein, and (iii) the preparations provided with two commercial kits, the Cobas Core (Roche Diagnostic Systems, France) and the Pylori Stat (BioWhittaker, Belgium). All preparations were used in an enzyme immunoassay to test 92 sera from dyspeptic patients for whom the status of Helicobacter infection was established. Sensitivities were higher (90 to 100%) for the native antigens and the commercial kits than for the recombinant antigens. Specificities were higher than 90%, except with UreA + UreB (42%). The most useful antigens were those extracted from strains N6 and N6flbA-.

Adolescent↗
PubMed2005

Evaluation of the stool antigen test for Helicobacter pylori in children and adolescents.

The stool antigen test for Helicobacter pylori is a noninvasive immunoassay to diagnose active infection with Helicobacter pylori in human fecal samples. Its performance in children and teenagers has been tested in some developed countries, showing a sensitivity and specificity above 90%, however, its accuracy in developing countries and in children under 6 years is not well established. To determine the accuracy of the test for diagnosing Helicobacter pylori infection in children and teenagers, we evaluated 133 patients (4 months to 17 years old). The gold standard was a positive culture or positive histology and rapid urease test. The test was done according to the manufacturer's instructions. However, modifications were introduced for better reproducibility. Samples were analyzed twice and results are expressed as optical density (OD) determined spectrophotometrically at 450 nm. HpSA was considered positive at OD > or =0.160 and negative at OD <0.140. One hundred twenty-seven of the 133 (95.5%) patients were included. There were no infected infants. The test showed a 94.6% sensitivity (95% CI: 90.6-98.5) and a 96.5% specificity (95% CI: 93.3-99.7). At ages 2 to 6 years the specificity was 96.4% (95% CI: 85.1-99.2) and the sensitivity was 80.0% (95% CI: 64.8-89.7), at ages 6 to 10 years the sensitivity was 100.0% and the specificity 95.7%, and above 10 years the sensitivity and specificity were 100.0%. We conclude that the test is efficient in adolescents and children, however there is a need for further studies with a greater number of patients for evaluation of its accuracy in infants.

Adolescent↗
PubMed2006

Non-Helicobacter bacterial flora rarely develops in the gastric mucosal layer of children.

Non-Helicobacter bacteria can be cultured from the gastric mucosa in adults but in children, there are no studies about such microflora. The purpose of this study, therefore, was to clarify whether gastric biota develops in children. In 10 children and 10 adults or elderly (5 H. pylori-infected and 5 uninfected in each group), biopsy specimens of the gastric antrum and corpus and gastric juice were studied for bacterial examinations and the data were compared between both age groups in relation to H. pylori status and luminal pH. Bacterial genera and species were analyzed using both culture and real-time polymerase chain reaction (PCR) with the 52 genus- and species-specific primer sets. Non-Helicobacter bacteria in the mucosa were cultured from all adult patients, whereas microorganisms were cultured in only one child (p < .001). Gastric pH was lower in children (median, 1.4) than in adults (median, 2.6) (p < .005). The grade of endoscopic gastric atrophy was moderate or severe in 8 adults, but absent or mild in all 10 children. Among adults, there was a significant positive correlation between gastric pH and total bacterial counts of both the mucosa and juice. These data indicate that impaired gastric acid secretion associated with long-term H. pylori infection enables non-Helicobacter bacteria to colonize in the human stomach. Such microorganisms rarely colonize in the gastric mucosa in children regardless of H. pylori status.

Adolescent↗
PubMed2003

Helicobacter and gastric cancer disease mechanisms: host response and disease susceptibility.

Helicobacter infection is the single most common cause of gastric cancer worldwide. Although infection prevention and eradication of established infection offer the potential for cure, these strategies are neither feasible nor practical for widespread implementation. Patients most at risk need to be identified and targeted for treatment. For disease to occur, bacterial, environmental, and nutritional factors require a genetically susceptible host. Consequently, it is important to understand how the organism interacts with the host to cause disease. Only through an understanding of what places a patient at risk can we hope to identify susceptible patients early enough in disease to have an impact on their outcome. The immune response is the single most important determinant of disease. Single nucleotide polymorphisms within the promoter region of several critical proinflammatory genes dramatically increase the risk of Helicobacter-associated gastric cancer. Additionally, environmental and dietary factors may modulate the immune response or directly influence key apoptotic and proliferative signaling cascades to alter disease presentation. Lastly, concurrent disease states may have a dramatic impact on the host response to Helicobacter infection and influence disease. An understanding of the immune signaling pathways responsible for disease and the ways in which environmental risk factors influence these pathways will allow identification of populations that are most at risk and targeted prevention and treatment strategies.

Animals↗
PubMed1995

Helicobacter pylori as a risk factor for cancer.

In 1985, gastric cancer was the second most common cause of cancer death in the world. The rapid decline in gastric cancer rates over the last few decades has been attributed to a decline in the prevalence of environmental risk factors for gastric cancer and/or an increase in the prevalence of protective factors. One such risk factor could be the bacterium Helicobacter pylori. Epidemiological studies have shown that areas with high gastric cancer rates often have a correspondingly high prevalence of H. pylori and prospective studies have shown that subjects with serological evidence of H. pylori infection were significantly more likely to go on to develop gastric cancer than those who did not. Helicobacter pylori itself does not appear to be either genotoxic or mutagenic. Infection is, however, associated with increased cell turnover, a chronic immune response accompanied by increased levels of reactive oxygen metabolites and a reduction in gastric levels of ascorbic acid, all conditions that could favour the development of cancer. Nonetheless, the majority of those who are infected with H. pylori do not go on to develop gastric cancer and other factors, such as the strain of the infecting organism or consumption of dietary antioxidants including vitamin C, could also affect the risk of cancer. Finally, it has been estimated that more than one third, and possibly as many as 90% of gastric cancers might be attributable to infection with H. pylori. Prevention and treatment of infection are, therefore, possible approaches to reducing gastric cancer rates. It is, however, unclear what, if any, effect eradication of the infection would have on an individual's risk of gastric cancer and, to date, anti-Helicobacter therapy has only been shown to be of potential benefit in the treatment of low grade gastric MALT lymphomas.

Chronic Disease↗
PubMed1996

Ex-vivo treatment of gastric Helicobacter infection by photodynamic therapy.

Attempts to develop PDT for eradication of Helicobacter infection have only been successful in vitro. We have investigated the effect of topical sensitization (except ALA) of Helicobacter mustelae on explanted ferret gastric mucosa using one of five sensitizers (methylene blue (MB), toluidine blue O (TBO), phthalocyanine, haematoporphyrin derivative and 5-aminolavulinic acid), followed by irradiation with an appropriately tuned copper vapour pumped dye laser. A 90% reduction in counts of bacteria sensitized with 0.75 mg TBO kg-1 were seen after irradiation with 200 J cm-2. Concentrations of MB of 0.75 mg kg-1 and 7.5 mg kg-1 were not toxic to H. mustelae, but the further addition of 20 J cm-2 laser light reduced colony counts by more than 99%. MB at a concentration of 75 mg kg-1 exhibited significant dark toxicity towards H. mustelae, but further addition of 20 J cm-2 laser light resulted in near eradication of all colonies. The remaining three compounds were ineffective. Finally, we studied the microscopic fluorescence distribution of MB (7.5 mg kg-1) on ferret gastric mucosa after topical administration. Fluorescence was greatest in the superficial mucosal layer, upon which lies the bacteria. However, from experiments on rats, the energy required to kill the sensitized bacteria was insufficient to damage the underlying mucosa. We conclude that Helicobacter can be killed on host mucosal epithelium following topical administration of MB and subsequent exposure to laser light.

Aminolevulinic Acid↗
PubMed2006

Eradication of Helicobacter pylori with triple therapy: an epidemiologic analysis of trends in Turkey over 10 years.

BACKGROUND: There is increasing concern about the efficacy of current regimens for the eradication of Helicobacter pylori. OBJECTIVES: This study examined rates of H. pylori eradication with a commonly used triple-therapy regimen consisting of a proton pump inhibitor (PPI), clarithromycin, and amoxicillin in trials performed in Turkey from 1996 to 2005. It also investigated the relationship between eradication rates and the duration of treatment (7, 10, or 14 days), choice of PPI, and indication for treatment (dyspepsia or peptic ulcer). METHODS: This was a retrospective epidemiologic analysis. Articles concerning H. pylori eradication in Turkey that were published in peer-reviewed national and international journals were identified through searches of MEDLINE using the terms Helicobacter, eradication, and Turkey, and of the Turkish Medical Index using the terms Helicobacter and eradication. Abstracts from the Turkish Gastroenterology Congress from 1996 through 2005 were searched manually. Open-label trials, controlled trials, treatment arms, and case series that included a triple-therapy regimen consisting of standard doses of any PPI (omeprazole 20 mg BID, lansoprazole 30 mg BID, pantoprazole 40 mg BID, or esomeprazole 40 mg BID) with clarithromycin 500 mg BID and amoxicillin 1 g BID for 7 to 14 days were selected for analysis. Trials including patients who had undergone a previous attempt at eradication of H. pylori were excluded. RESULTS: Of 138 trials or treatment arms identified, 94 met the criteria for inclusion (3637 subjects). The pooled eradication rate was 68.8% (95% CI, 67.3-70.3). A marked decrease in eradication was noted after 2000. Pooled eradication rates each year from 1996 through 2005 were 79.4%, 83.7%, 81.8%, 81.8%, 75.1%, 61.3%, 65.6%, 65.1%, 55.3%, and 61.1%, respectively. Eradication rates were not affected by the duration of treatment, choice of PPI, or indication for treatment. CONCLUSIONS: Rates of H. pylori eradication with the triple-therapy regimen decreased in Turkey over the 10-year period studied. In an era of increasing clarithromycin use, the effectiveness of this regimen for H. pylori eradication appears to require reassessment.

Amoxicillin↗
PubMed2005

HpSA fecoprevalence in patients suspected to have Helicobacter pylori infection in Istanbul, Turkey.

OBJECTIVE: This study aims to investigate the Helicobacter pylori antigen in the stool samples of patients suspected to have H. pylori infection. It also aims to determine the fecoprevalence in different age groups and to look for the relationship between the clinical symptoms seen in patients and the existence of H. pylori. Current information in Turkey is insufficient. METHODS: The Helicobacter pylori antigen was investigated in the stool samples of 445 patients of whom 148 were in the 2-15 year age group, 96 in the 16-30 year age group, 85 in the 31-40 year age group and 116 in the 41-48 year age group. The main clinical complaints of the patients (stomach pain, heart burn, indigestion, gas, nausea, vomiting, diarrhea, abdominal pain) were recorded. RESULTS: The Helicobacter pylori antigen was found in 36.6% (163/445) of the patients and in the statistical evaluation made for different age groups, a significant linear relationship was found between age and infection (chi2=14.77, p=0.002). CONCLUSION: It was found that stomach pain was seen at a higher rate in patients with H. pylori antigen compared to those without it. The difference was highly statistically significant (chi2=117.70, p<0.001, OR=20.36, 95% CI=10.56-39.27).

Adolescent↗
PubMed2005

Short-term zinc supplementation attenuates Helicobacter felis-induced gastritis in the mouse.

BACKGROUND: Mucosal damage by H. pylori infection is mainly caused by neutrophils producing large quantities of reactive oxygen species (ROS). Metallothionein (MT) an intracellular, low-molecular, cysteine-rich protein, which is inducible by dietary zinc (Zn), has been implicated in sequestering ROS. This study examines the effects of Zn supplementation on Helicobacter colonisation and associated gastritis and the relationship with gastric MT levels. METHODS: C57Bl/6 mice were inoculated with either 10(8) H. pylori or H. felis and were infected for 4 weeks or 6 and 12 weeks, respectively. Mice infected with H. pylori (4 weeks) or H. felis (6 weeks) were treated with either Zn acetate (ZnA; 1 mg/ml), or Zn sulphate (ZnSO4; 5 mg/ml) for 2 weeks with 0.1 ml oro-gastric gavage twice daily. H. pylori load and H. felis colonisation density were determined by culture and microscopy, respectively. MT levels and H. felis-induced gastritis were also determined. RESULTS: Zn treatment showed no significant difference in Helicobacter load and gastric MT, however, ZnSO4 treatment showed a significant (p<0.05) increased in gastric MT in H. felis infected mice. Both Zn-treated groups showed a significant (p<0.05) difference in gastritis score in the antrum of the stomach within the basal and submucosal compartments compared to H. felis-infected controls. CONCLUSIONS: We found that H. felis-induced gastritis can be attenuated by short-term treatment of Zn. This observation suggests that Zn alone may be effective for the suppression of gastric mucosal inflammation induced by Helicobacter.

Administration, Oral↗
PubMed2005

Helicobacter pylori infection in children: prevalence, diagnosis and treatment outcome.

The clinical significance of Helicobacter pylori infection in children remains largely unknown. The rate of acquisition at different ages has not been ascertained using reliable tests on gastric biopsies. We determined prospectively the prevalence of H. pylori infection in children and its association with gastroduodenal disease. We evaluated 240 children undergoing upper gastrointestinal endoscopy for H. pylori infection by rapid urease test, culture, ureA PCR and histopathology. Group I constituted 58 children with upper abdominal pain (UAP) and group II (controls) of 182 children without UAP who underwent diagnostic or therapeutic endoscopy for other reasons. Helicobacter pylori-positive children with UAP received anti-H. pylori therapy. Helicobacter pylori infection was significantly higher in children with UAP than controls (53.4% vs. 28%; P<0.001) and overall prevalence increased with age. On follow-up endoscopy, H. pylori had been eradicated from 82% of children with UAP; it was eradicated from the remaining 18% after a second regimen. Treated H. pylori-positive children with UAP remained symptom-free for a median of 25 months. Control children remained chronically H. pylori infected. Chronic inflammation was present in all infected children, and active inflammation in 48.8%. The study shows H. pylori infection increases with age and is strongly linked to UAP in children.

Abdominal Pain↗
PubMed2004

Immunisation against Helicobacter felis infection protects against the development of gastric MALT Lymphoma.

UNLABELLED: The formation of mucosa-associated lymphoid tissue (MALT) in response to Helicobacter pylori infection is closely associated with the development of primary gastric MALT lymphoma. AIM: To examine whether immunisation against Helicobacter felis can protect against development of MALT lymphoma. RESULTS: The majority of control infected mice demonstrated MALT formation (13/15) and five developed lymphoma. Fifteen immunised mice were protected against bacterial challenge, of which only five had evidence of MALT formation and none developed lymphoma. Interestingly, of the four mice in which immunisation failed, all developed MALT and two of these had lymphoma. CONCLUSION: Effective immunisation against Helicobacter infection can protect against gastric MALT lymphoma. To our knowledge this is the first demonstration of vaccination protecting against a bacteria-induced malignancy.

Animals↗
PubMed2002

Helicobacter bilis infection accelerates and H. hepaticus infection delays the development of colitis in multiple drug resistance-deficient (mdr1a-/-) mice.

mdr1a-deficient mice lack P-glycoprotein and spontaneously develop colitis with age. Helicobacter spp. are gram-negative organisms that have been associated with colitis in certain mouse strains, but Helicobacter spp. have been excluded as contributing to the spontaneous colitis that develops in mdr1a-/- mice. We wished to determine whether infection with either H. bilis or H. hepaticus would accelerate the development of inflammatory bowel disease (IBD) in mdr1a-/- mice. We found that H. bilis infection induced diarrhea, weight loss, and IBD in mdr1a-/- mice within 6 to 17 weeks post-inoculation and before the expected onset of spontaneous IBD. Histopathology of H. bilis-induced IBD included crypt hyperplasia, inflammatory cell infiltrates, crypt abscesses, and obliteration of normal gut architecture. Reverse transcription-polymerase chain reaction and Taqman analysis from colonic tissue showed increased transcripts for interferon-gamma and interleukin-10 from H. bilis-infected colitic mdr1a-/- mice. Additionally, mesenteric lymph nodes had increased cellularity with expansion of CD4+ and CD8+ T cells and B cells and increased proliferation to soluble H. bilis antigens with elaboration of interferon-gamma, tumor necrosis factor-alpha and interleukin-10. In contrast, H. hepaticus infection of mdr1a-/- mice did not accelerate disease but rather delayed the onset of spontaneous colitis which was milder in severity. mdr1a-/- mice infected with Helicobacter spp. may provide a useful tool to explore the pathogenesis of microbial-induced IBD in a model with a presumed epithelial cell "barrier" defect.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2003

Helicobacter pylori is associated with modified lipid profile: impact on Lipoprotein(a).

OBJECTIVES: Helicobacter pylori is a controversial risk factor for atherosclerosis. We investigated whether the bacterium persistent inflammation or the expression of the cytotoxin-associated gene A (CagA) may affect serum lipids as well as Lipoprotein(a). DESIGN AND METHODS: Two hundred-eleven healthy volunteers were evaluated for lipids and Lipoprotein(a). Helicobacter pylori was characterized by Urea Breath Test and IgG-anti-CagA. apo(a) Kringle-IV polymorphism was genotyped. RESULTS: Prevalence of the infection was 72%; 43% of subjects expressed CagA reactivity. Infected subjects showed increased levels of cholesterol, LDL-cholesterol, and cholesterol/HDL-cholesterol atherogenic index. Association with the Helicobacter pylori CagA(-) strains persisted after the adjustment for covariates. Significant difference between infected and uninfected subjects was found in Lipoprotein(a) levels. This difference did not arise from the Kringle-IV genotype. CONCLUSIONS: The infection per se significantly modified serum lipid and Lipoprotein(a) concentrations. CagA does not seem to be a reliable marker of pathogenicity for the atherogenic complications of H. pylori infection.

Adult↗
PubMed1997

Murine CD4 T-cell response to Helicobacter infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load.

BACKGROUND & AIMS: Previous findings suggest that TH1 cellular immune responses contribute to Helicobacter-associated gastritis. To further investigate this issue, interleukin 4 gene targeted mice were infected with Helicobacter felis, and a series of adoptive transfer experiments was performed to evaluate the role of both TH1 and TH2 cells. METHODS: Antigen-specific spleen cells from immunized/challenged or nonimmunized/infected mice or CD4+ T-cell lines were transferred adoptively into naive recipients before live bacterial challenge. RESULTS: Transfer of cells from both groups of donors as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients. No effect on bacterial load was observed in recipients of bulk spleen cells from infected mice or recipients of TH1 cell lines. In contrast, when either a TH2 cell line or bulk cells from immunized challenged mice were transferred adoptively, recipients showed a dramatic reduction in bacterial load. Increased numbers of bacteria were also noted in interleukin 4-deficient mice. CONCLUSIONS: These data suggest a differential contribution of TH1 and TH2 cell-mediated immune responses in Helicobacter infection: one associated with the pathogenesis of disease (TH1 phenotype) and the other associated with protection from or control of infection (TH2 phenotype).

Adoptive Transfer↗