• Logo
  • SBMUJournals

Prevalence of Cytotoxin-associated genes of Helicobacter pylori among Iranian GERD patients

Aref Shavalipour, Habib Malekpour, Hossein Dabiri, Hossein Kazemian, Homayon Zojaji, Mahboube Bahroudi




Aim: Since the impact of H. pylori and its virulence is not clear in GERD, this study aimed to evaluate the prevalence of cag A and cag E gens of H. pylori among Iranian GERD patients.

Background: Gastroesophageal reflux disease (GERD) is defined as a condition of reflux the stomach juice by low pH causes tissue damage. Helicobacter pylori may or may not influence the GERD; however, it is unclear.

Methods: This study was a case-control study performed on patients with GERD who underwent upper gastrointestinal endoscopy at Taleghani Hospital of Tehran, Iran. Prevalence of H. pylori and presence of the cag A and cag E genes in GERD and control group was investigated.

Results: H. pylori was detected in 54% and 62% of GERD and control groups respectively. Prevalence of cag A gene among GERD patients was 44.4% whereas among the control group it was 87%. Prevalence of the cag E among GERD patients and control group was 44.4% and 64% respectively. Coexistence of cag A and cag E in GERD patients was 25.7% and in the control patients it was 54.8%.  

Conclusion: We did not find correlation between H. pylori existence in GERD patients in comparison to the control group. Similar to other Asian studies, the presence of the cag A in control group was more than GERD patients significantly. The co-existence of cag A and cag E was also more in control group significantly.

Keywords: Cag A, Cag E, Helicobacter pylori, GERD, Iran.


Cag A, Cag E, Helicobacter pylori, GERD, Iran


Stadtlander CT, Waterbor JW. Molecular epidemiology, pathogenesis and prevention of gastric cancer. Carcinogenesis 1999; 20:2195–208.

Hong SJ, Kim SW. Helicobacter pylori Infection in Gastroesophageal RefluxDisease in the Asian Countries. Gastroenterol Res Pract 2015; 2015:985249.

Graham DY, Malaty HM, Evans DG, Evans DJ Jr, Klein PD, Adam E. Epidemiology of Helicobacter Pylori in an asymptomatic population the United States. Gastroenterology 1991; 100(6):1495-501.

Kazemian H, Shavalipour A, Mohebi R, Ghafurian S, Aslani A, Maleki A, et al. Estimation of the Parasitic Infection Prevalence in Children With Helicobacter pylori Infection in Ilam City (2012-2013). Arch Pediatr Infect Dis 2014; 2(3):e15294.

Tomer Y, Davies TF. Infection, thyroid disease, and autoimmunity. Endocr Rev 1993; 14:107-20.

Vaezi MF, Swoger J. Gastro-oesophageal reflux disease in the elderly. In: Granderath, FA, Pointner KT, eds. Gastro-oesophageal Reflux Disease. Springer Vienna 2006; 23– 45.

Erzin Y, Koksal V, Altun S, Dobrucali A, Aslan M, Erdamar S, et al. Prevalence of Helicobacter pylori vacA, cagA, cagE, iceA, babA2 genotypes and correlation with clinical outcome in Turkish patients with dyspepsia. Helicobacter 2006; 11(6):574-80.

Corley DA, Kubo A, Levin TR, Block G, Habel L, Rumore G, et al. Helicobacter pylori and gastroesophageal reflux disease: a case-control study. Helicobacter 2008; 13(5):352-60.

Gudlaugsdottir S, Van Dekken H, Stijnen T, Wilson JH. Prolonged use of proton pump inhibitors, CagAstatus,and the outcome of Helicobacter pylori gastritis. J Clin Gastroenterol 2002; 34(5):536-40.

Mansour-Ghanaei F, Joukar F, Atshani SM, Chagharvand S, Souti F. The epidemiology of gastroesophageal reflux disease: a survey on the prevalence and the associated factors in a random sample of the general population in the Northern part of Iran. Int J Mol Epidemiol Genet 2013; 4(3):175-182.

Dabiri H, Maleknejad P, Yamaoka Y, Feizabadi MM, Jafari F, Rezadehbashi M, et al. Distribution of Helicobacter pylori cagA, cagE, oipA and vacA in different major ethnic groups in Tehran, Iran. J Gastroenterol Hepatol 2009; 24:1380-1386.

Rokkas T, Ladas SD, Triantafyllou K, Liatsos C, Petridou E, Papatheodorou G, et al. The association between CagA status and the development of esophagitis after the eradication of Helicobacter pylori. Am J Med 2001; 110:703–707.

Take S, Mizuno M, Ishiki K, Nagahara Y, Yoshida T, Yokota K, et al. Helicobacter pylori eradication may induce de novo, but transient and mild, reflux esophagitis: prospective endoscopic evaluation. J Gastroenterol Hepatol 2009; 24:107–113.

Cremonini F, Di Caro S, Delgado-Aros S, Sepulveda A, Gasbarrini G, Gasbarrini A, et al. Meta-analysis: the relationship between Helicobacter pyloriinfection and gastrooesophageal reflux disease. Aliment Pharmacol Ther 2003; 18:279–289.

Shin WG, Kim HU, Kim SG, Kim GH, Shim KN, Kim JW, et al. Work productivity and activity impairment in gastroesophageal reflux disease in Korean full-time employees: a multicentre study. Dig Liver Dis 2012; 44(4):286-91.

Quigley EM, Hungin AP. Review article: qualityof- life issues in gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2005; 1:41-7.

Dean BB, Crawley JA, Schmitt CM, Wong J, Ofman JJ. The burden of illness of gastro-oesophageal reflux disease:impact on work productivity. Aliment Pharmacol Ther 2003; 15;17(10):1309-17.

Azuma T, Yamazaki S, Yamakawa A, Ohtani M, Muramatsu A, Suto H, Ito Yet al. Association between diversity in the Src homology 2 domain—containing tyrosine phosphatase binding site of Helicobacter pylori CagA protein and gastric atrophy and cancer. J Infect Dis 2004; 1;189(5):820-7.

Grande M, Lisi G, De Sanctis F, Grande S, Esser A, Campanelli M, et al. Does a relationship still exist between gastroesophageal reflux and Helicobacter pylori in patients with reflux symptoms?. World J Surg Oncol 2014; 12:375.

Mahdi BM. The relationship between helicobacter pylori infection and gastro-esophageal reflux disease. N Am J Med Sci 2011; 3(3):142-5.

Johnson LF, DeMeester TR. Development of the 24-hour intraesophageal pH monitoring composite scoring system. J Clin Gastroenterol 1986; 8 Suppl 1:52-8.

Smout AJPM. Endoscopy-negative acid reflux disease. Aliment Pharmacol Ther 1997; 11(S2):81- 85.

Gisbert JP, Pajares JM, Losa

DOI: https://doi.org/10.22037/ghfbb.v0i0.1062