Helicobacter pylori cagL amino acid polymorphism D58E59 pave the way toward peptic ulcer disease while N58E59 is associated with gastric cancer in north of Iran

2017 ◽  
Vol 107 ◽  
pp. 413-418 ◽  
Author(s):  
Mina Rezaee Cherati ◽  
Javad Shokri-Shirvani ◽  
Ahmad Karkhah ◽  
Ramzan Rajabnia ◽  
Hamid Reza Nouri
2005 ◽  
Vol 100 (5) ◽  
pp. 1037-1042 ◽  
Author(s):  
Susumu Take ◽  
Motowo Mizuno ◽  
Kuniharu Ishiki ◽  
Yasuhiro Nagahara ◽  
Tomowo Yoshida ◽  
...  

Ulcers ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-23 ◽  
Author(s):  
Bianca Bauer ◽  
Thomas F. Meyer

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.


Helicobacter ◽  
2001 ◽  
Vol 6 (3) ◽  
pp. 199-206 ◽  
Author(s):  
Diana M. Cittelly Pineros ◽  
Sandra C. Henao Riveros ◽  
Julian D. Martinez Marin ◽  
Oliveros Ricardo ◽  
Oscar Orozco Diaz

2011 ◽  
Vol 54 (1) ◽  
pp. 103 ◽  
Author(s):  
Mahsa Molaei ◽  
Reza Mashayekhi ◽  
Homayoun Zojaji ◽  
MohammadAmin Pourhoseingholi ◽  
Tina Shooshtarizadeh ◽  
...  

Author(s):  
Muhammad Akram Bajwa ◽  
Muhammad Idrees ◽  
Prem Kumar Maheshwari

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.


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