scholarly journals Recent Advances inHelicobacter pyloriInfection in Children: From the Petri Dish to the Playgound

2003 ◽  
Vol 17 (7) ◽  
pp. 448-454 ◽  
Author(s):  
Peng-Yuan Zheng ◽  
Nicola L Jones
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Petri Dish ◽  
Host Factors ◽  
Causative Role ◽  
Ulcer Disease ◽  
Recent Advances ◽  
H Pylori ◽  
Development Of Gastric Cancer

Helicobacter pyloriinfection is acquired in childhood, plays a causative role in chronic gastritis and peptic ulcer disease, and is associated with the development of gastric cancer. The present review focuses on recent advances in the scientific knowledge ofH pyloriinfection in children, including clinical sequelae, diagnosis and treatment. In addition, recent insights regarding both bacterial and host factors that mediate human diseases associated withH pyloriinfection are discussed.

The Effect of Eradicating Helicobacter Pylori on the Development of Gastric Cancer in Patients with Peptic Ulcer Disease

2005 ◽  
Vol 100 (5) ◽  
pp. 1037-1042 ◽  
Author(s):  
Susumu Take ◽  
Motowo Mizuno ◽  
Kuniharu Ishiki ◽  
Yasuhiro Nagahara ◽  
Tomowo Yoshida ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Ulcer Disease ◽  
Development Of Gastric Cancer

scholarly journals The Human Gastric Pathogen Helicobacter pylori and Its Association with Gastric Cancer and Ulcer Disease

Ulcers ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-23 ◽  
Author(s):  
Bianca Bauer ◽  
Thomas F. Meyer
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Strain Differences ◽  
Protective Effects ◽  
Ulcer Disease ◽  
Prophylactic Measures ◽  
H Pylori

With the momentous discovery in the 1980's that a bacterium, Helicobacter pylori, can cause peptic ulcer disease and gastric cancer, antibiotic therapies and prophylactic measures have been successful, only in part, in reducing the global burden of these diseases. To date, ~700,000 deaths worldwide are still attributable annually to gastric cancer alone. Here, we review H. pylori's contribution to the epidemiology and histopathology of both gastric cancer and peptic ulcer disease. Furthermore, we examine the host-pathogen relationship and H. pylori biology in context of these diseases, focusing on strain differences, virulence factors (CagA and VacA), immune activation and the challenges posed by resistance to existing therapies. We consider also the important role of host-genetic variants, for example, in inflammatory response genes, in determining infection outcome and the role of H. pylori in other pathologies—some accepted, for example, MALT lymphoma, and others more controversial, for example, idiopathic thrombocytic purpura. More recently, intriguing suggestions that H. pylori has protective effects in GERD and autoimmune diseases, such as asthma, have gained momentum. Therefore, we consider the basis for these suggestions and discuss the potential impact for future therapeutic rationales.

scholarly journals Helicobacter pylori: Basic Mechanisms to Clinical Cure

1995 ◽  
Vol 9 (2) ◽  
pp. 91-95 ◽  
Author(s):  
ABR Thomson ◽  
CN Williams
Keyword(s):  
Gastric Cancer ◽  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Clinical Cure ◽  
Eradication Therapy ◽  
Dual Therapy ◽  
Quadruple Therapy ◽  
Ulcer Disease ◽  
H Pylori

Since its rediscovery 10 years ago,Helicobacter pylorihas reshaped our thinking about the course of peptic ulcer disease. Our approach to the patient with a duodenal ulcer has become one of attempting eradication therapy at the time of first diagnosis, in the hope of curing the ulcer disease. Gastric and duodenal ulceration are only two of the manifestations of this chronic antral infection; other complications ofH pyloriinclude gastritis, gastric cancer and possible maltomas. Therapy ofH pyloriinfection is complicated and involves dual therapy with an antibiotic plus a protein pump inhibitor, such as omeprazole 20 mg bid plus amoxicillin 1 g bid for two weeks, triple or quadruple therapy with bismuth, two antibiotics and an H2-receptor antagonist. Vaccination againstH pyloriis on the far horizon.

scholarly journals Diversity of Helicobacter pylori vacA andcagA Genes and Relationship to VacA and CagA Protein Expression, Cytotoxin Production, and Associated Diseases

1998 ◽  
Vol 36 (4) ◽  
pp. 944-948 ◽  
Author(s):  
Jochen Rudi ◽  
Christof Kolb ◽  
Matthias Maiwald ◽  
Dirk Kuck ◽  
Andreas Sieg ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Signal Sequence ◽  
Peptic Ulcers ◽  
Virulence Determinants ◽  
Middle Region ◽  
Vacuolating Cytotoxin ◽  
Ulcer Disease ◽  
H Pylori

The vacuolating cytotoxin and the cytotoxin-associated protein, encoded by vacA and cagA, respectively, are important virulence determinants of Helicobacter pylori. Sixty-five H. pylori strains were isolated from dyspeptic patients (19 with peptic ulcer disease, 43 with chronic gastritis, and 3 with gastric cancer) and studied for differences in thevacA and cagA genes and their relationship to VacA and CagA expression, cytotoxin activity, and the clinical outcome of infection. By PCR, fifty-four (83.1%) of 65 strains had thevacA signal sequence genotype s1 and only 10 (15.4%) had the type s2. After primer modification, the vacAmiddle-region types m1 and m2 were detected in 24 (36.9%) and 41 (63.1%) strains, respectively. The combinations s1-m2 (31 [47.7%]) and s1-m1 (23 [35.4%]) occurred more frequently than s2-m2 (10 [15.4%]) (P = 0.01). No strain with the combination s2-m1 was found. All 19 patients with peptic ulcers harbored type s1 strains, in contrast to 32 (74.4%) of 43 patients with gastritis (P = 0.02). The vacA genotype s1 was associated with the presence of cagA (P < 0.0001), VacA expression (P < 0.0001), and cytotoxin activity (P = 0.003). The cagA gene was detectable in 48 (73.8%) of 65 isolates and present in 16 (84.2%) of 19 ulcer patients and 29 (67.4%) of 43 patients with gastritis (P = 0.17). The vacA genotypes of GermanH. pylori isolates are identical to those previously reported. H. pylori strains of vacA type s1 are associated with the occurrence of peptic ulceration and the presence ofcagA, cytotoxin activity, and VacA expression.

scholarly journals Association of dupA, iceA, homB Genes of Helicobacter pylori with Gastritis, Peptic Ulcer Disease and Gastric Cancer

2020 ◽  
pp. 1-6
Author(s):  
Muhammad Akram Bajwa ◽  
Muhammad Idrees ◽  
Prem Kumar Maheshwari
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Analytical Study ◽  
Pcr Primers ◽  
Cross Sectional ◽  
Ulcer Disease ◽  
Gastric Biopsies ◽  
H Pylori

Objective: To determine the association of dupA, iceA, homB genes of Helicobacter pylori with gastro-duodenal diseases such as gastritis, peptic ulcer disease PUD and gastric cancer. Materials and Methods: This cross-sectional analytical study was conducted at Gastroenterology Department, Shaikh Zayed Hospital Lahore. Patients with gastro-duodenal diseases and positive H. pylori were included. Gastric biopsies were taken from fundus, body and antrum. H. pylori DNA were removed utilizing Gentra DNA extraction Kit (Life Technologies, USA) as per the technique and Qualitative PCR for the recognition of H. Pylori DNA. The PCR primers sets were designed for the specific detection of dupA, iceA and homB genes of H. pylori. All the data was recorded in proforma and analyzed by SPSS version 20. Results: Mean age of the cases was 41.22+8.04 years. Males were more affected 118(60.2%). HomB was the most common 76(38.8%) followed by dupA and iceA 28.6% and 24.5% respectively. Peptic ulcer disease and gastritis were higher among patients having dup A and iceA positive strains as compared to homB gene patients, while gastric cancer was significantly higher among HomB gene infected patients, p-values were quite significant. Conclusion: It was concluded that homB gene was most frequent in H. pylori infected population. Peptic ulcer disease and gastritis are markedly associated with dupA and iceA genes, while homB gene infected patients are at high risk of gastric cancer.

Cost-Effectiveness of Population Screening for Helicobacter Pylori in Preventing Gastric Cancer and Peptic Ulcer Disease, Using Simulation

2003 ◽  
Vol 10 (3) ◽  
pp. 148-156 ◽  
Author(s):  
P Roderick ◽  
R Davies ◽  
J Raftery ◽  
D Crabbe ◽  
R Pearce ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Population Screening ◽  
Sensitivity Analyses ◽  
Ulcer Disease ◽  
H Pylori ◽  
The Cost

Objectives: To evaluate the cost-effectiveness of population screening for Helicobacter pylori in preventing gastric cancer and peptic ulcer disease in England and Wales. Methods: A discrete event simulation model used parameter estimates, derived from peer-reviewed literature, routine data and statistical modelling. Population screening was compared with no screening but with opportunistic eradication in patients presenting with dyspepsia. Costs included screening, eradication and costs averted to provide costs per life years saved (cost/LYSj for preventing gastric cancer and peptic ulcer disease. Sensitivity analyses were undertaken. Results: The cost/LYS from screening at age 40 years was £5860 at discount rates of 6%. The outcomes were sensitive to H. pylori prevalence, the degree of opportunistic eradication, the discount rate, the efficacy of eradication on gastric cancer risk, the risk of complicated peptic ulcer disease and gastric cancer associated with H. pylori infection, and the duration of follow-up. In sensitivity analyses, the cost/LYS rarely exceeded £20000 over an 80-year follow-up, but did for shorter periods. Conclusions: H. pylori screening may be cost-effective in the long term. However, before screening can be recommended further evidence is needed to resolve some of the uncertainties, particularly over the efficacy of eradication on risk of gastric cancer, the risk associated with complicated peptic ulcers, and the effect of more widespread opportunistic testing of patients with dyspepsia.

scholarly journals Helicobacter pyloriAnti-CagA Antibodies: Prevalence in Symptomatic and Asymptomatic Subjects in Turkey

2002 ◽  
Vol 16 (8) ◽  
pp. 527-532 ◽  
Author(s):  
M Fatih Abasiyanik ◽  
Ersan Sander ◽  
Barik A Salih
Keyword(s):  
Gastric Cancer ◽  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Chronic Gastritis ◽  
Molecular Weights ◽  
Cancer Antigens ◽  
Gastroduodenal Disease ◽  
H Pylori ◽  
Asymptomatic Subjects

BACKGROUND: Several reports have shown the prevalence of anti-CagA antibodies to be associated with the development of peptic ulcer diseases, while others have indicated that there is no such association.AIM: To examine the prevalence of antibodies to CagA and otherHelicobacter pyloriantigens in symptomatic and asymptomatic subjects in Turkey.SUBJECTS AND METHODS: Sixty-six symptomatic subjects, 16 to 74 years of age, were examined forH pyloriby biopsy-based tests and ELISA. One hundred nineteen asymptomatic subjects, 20 to 65 years of age, were also tested serologically for the presence ofH pylori. Samples from both groups that were found to be positive forH pyloriby ELISA were then tested by immunoblotting.RESULTS: Fifty-four (82%) symptomatic subjects and 76 (64%) asymptomatic subjects were found to beH pylori-positive by ELISA. Samples from 30 symptomatic subjects who were found to beH pylori-positive by ELISA were analyzed by immunoblotting. Antibodies to CagA (116 kDa) antigen were detected in immunoblots of 11 of 14 (79%) with chronic gastritis, 12 of 13 (92%) with duodenal ulcer and three of three (100%) with gastric cancer. Antigens of the following molecular weights were also detected in these 30 subjects: 89 kDa (VacA) in 21 (70%), 37 kDa in 21 (70%), 35 kDa in 19 (63%), 30 kDa in 27 (90%) and 19.5 kDa in 19 (63%). Immunoblots of 40 ELISA-positive asymptomatic subjects showed that 33 (83%) had antibodies to CagA antigen, 26 (65%) to VacA antigen, 30 (75%) to a 37 kDa antigen, 30 (75%) to a 35 kDa antigen, 39 (98%) to a 30 kDa antigen and 36 (90%) to a 19.5 kDa antigen.CONCLUSIONS: Antibodies to CagA antigen were prevalent in both groups, regardless of the presence of gastroduodenal disease.

scholarly journals Identification of Markers for Helicobacter pylori Strains Isolated from Children with Peptic Ulcer Disease by Suppressive Subtractive Hybridization

2006 ◽  
Vol 74 (7) ◽  
pp. 4064-4074 ◽  
Author(s):  
Mónica Oleastro ◽  
Lurdes Monteiro ◽  
Philippe Lehours ◽  
Francis Mégraud ◽  
Armelle Ménard
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Subtractive Hybridization ◽  
Suppressive Subtractive Hybridization ◽  
Ulcer Disease ◽  
Lipopolysaccharide Biosynthesis ◽  
The Difference ◽  
H Pylori

ABSTRACT Peptic ulcer disease (PUD) occurs after a long-term Helicobacter pylori infection. However, the disease can develop earlier, and rare cases have been observed in children, suggesting that these H. pylori strains may be more virulent. We used suppressive subtractive hybridization for comparative genomics between H. pylori strains isolated from a 5-year-old child with duodenal ulcer and from a sex- and age-matched child with gastritis only. The prevalence of the 30 tester-specific subtracted sequences was determined on a collection of H. pylori strains from children (15 ulcers and 30 gastritis) and from adults (46 ulcers and 44 gastritis). Two of these sequences, jhp0562 (80.0% versus 33.3%, P = 0.008) and jhp0870 (80.0% versus 36.7%, P = 0.015), were highly associated with PUD in children and a third sequence, jhp0828, was less associated (40.0% versus 10.0%, P = 0.048). Among adult strains, none of the 30 sequences was associated with PUD. However, both jhp0562 and jhp0870 were less prevalent in adenocarcinoma strains than in PUD strains from children and adults, the difference being statistically significant for jhp0870. In conclusion, two H. pylori genes were identified as being strongly associated with PUD in children, and their putative roles as an outer membrane protein for jhp0870 and in lipopolysaccharide biosynthesis for jhp0562, suggest that they may be novel virulence factors of H. pylori.

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