Submitted: 30 Oct 2014
Revised: 26 Nov 2014
Accepted: 02 Dec 2014
First published online: 06 Oct 2016
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Int J Enteric Pathog. 2015;3(2): e25022.
doi: 10.17795/ijep25022
  Abstract View: 1269
  PDF Download: 744

Research Article

Helicobacter Pylori and CagA: Relationships With Esophageal and Gastroduodenal Disorders in Iranian Patients

Omid Teymournejad 1,2, Leili Shokoohizadeh 3 * , Ashraf Mohabati Mobarez 3, Mohsen Amini 4

1 Department of Microbiology, School of Medicine, Babol University of Medical Sciences, Babol, IR Iran
2 Department of Bacteriology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, IR Iran
3 Department of Laboratory Medical Science, Faculty of Paramedicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, IR Iran
4 Baqiyatallah Research Center for Gastroenterology and Liver Disease, Baqiyatallah University of Medical Sciences, Tehran, IR Iran
*Corresponding author: Leili Shokoohizadeh, Department of Laboratory Medical Science, Faculty of Paramedicine, Ahvaz Jundishapur University of Medical Sciences, P. O. Box: 61357-15794, Ahvaz, IR Iran. Tel: +98-6113738319, +98-6113738317, Fax: +98-6113738330, Email: shokoohizadeh_l@ajums.ac.ir

Abstract

Background: The severity of Helicobacter pylori infection is associated with virulence factors of the bacteria and host immune response. H. pylori has several virulence factors which a number of them are essential to emerge clinical outcomes. Cytotoxin-associated gene A (CagA) is the most important H. pylori virulence factor.

Objectives: The aim of our study was to assess a significant relationship between presence of cagA and severity of clinical manifestation in esophageal and gastroduodenal disorders.

Patients and Methods: A total of 240 gastric biopsies were collected between March 2012 and August 2013 from Tehran's hospitals. Three sets of biopsy specimens were obtained from the antrum and rapid urease tests, histological examination, Polymerase Chain Reaction (PCR) assay were performed on the biopsy specimens.

Results: One hundred and eight (45%) of biopsy specimens were positive with rapid urease test and ureC gene PCR. Moreover, thirty eight (35.1%) of positive specimens had cagA gene. The rate of gastric and duodenum inflammation was more in patients who carried CagA positive H. pylori strains. Whereas less inflammation and sever lesions in esophagus were found in CagA negative H. pylori strains.

Conclusions: Our study demonstrates a strong relationship between CagA and esophageal and gastroduodenal disorders. The number of CagA negative H. pylori was larger than CagA positive in esophagus lesion grade A, C, and D. Therefore, cagA may have a protective effect on some esophageal diseases. In addition, the number of CagA positives was larger than CagA negative H. pylori in gastric antrum and duodenum ulcer. Thus, CagA play a role to emerge peptic and duodenal ulcers.

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