DOI: http://dx.doi.org/10.18203/2394-6040.ijcmph20183436

The relation between Helicobacter pylori and gastroesophageal reflux disease in KSA

Faisal Alziyadi, Nouf Alshammeri, Ali Alamer, Fatimah Altarouti, Nesreen Aljehani, Khalid Asiri, Fardus Almarghalani, Easa Albalwi, Malik Almohideb, Ameen hayyan

Abstract


Estimates say that Helicobacter pylorus affects more than half of the general population over the world. Its prevalence varies significantly among different areas. Studies done in 1990 reported a prevalence of 70% of people older than 20 years who live in Saudi Arabia, and 40% of people aged 5-10 years. The first line regimen of helicobacter pylori infections in Saudi Arabia is 7 days of triple therapy. However, in areas of high antibiotic resistance, or in cases of failure of triple therapy, a ‘rescue’ quadruple therapy (that contains bismuth) is indicated. In this study we aimed to look at the prevalence of H. pylori infection and its association with gastroesphageal reflux disease in Saudi Arabia. We also tried to understand the approach for diagnoses and treatment in the Kingdom. We did a systematic search for helicobacter pylori and GERD in Saudi Arabia using PubMed search engine (http://www.ncbi.nlm.nih.gov/) and Google Scholar search engine (https://scholar.google.com). The following search terms were used: H. pylori, gastroesophageal reflux disease, prevalence of GERD in Saudi Arabia, lifestyle Saudi Arabia, gastroenterology Saudi Arabia. All studies done shows prevalence in Saudi Arabia to be relatively high (reaching 70%) and increasing. Despite being highly prevalent, no solid guidelines are present to help clinicians diagnose and treat helicobacter pylori infection properly. These, along with other causes like improper use of antibiotics have led to the emerging of new strains that are resistant to typical antibiotic treatment.


Keywords


Helicobacter pylori infection, Lifestyle Saudi Arabia, Prevalence of GERD in Saudi Arabia, Antibiotic use in Saudi Arabia

Full Text:

PDF

References


Dunn BE, Cohen H, Blaser MJ. Helicobacter pylori. Clin Microbiol Rev. 1997;10:720‑41.

Blaser MJ. Epidemiology and pathophysiology of campylobacter pylori infections. Rev Infect Dis. 1990;12(1):99‑106.

Salih BA. Helicobacter pylori infection in developing countries: The burden for how long. Saudi J Gastroenterol. 2009;15:201‑7.

Khudor MH, Strak SK, Issa AH. Isolation of CagA and VacA genes from H. pylori infected patients with various gastroduodenal lesions. Bas J Surg. 2010;16:31‑8.

Fact sheet on Helicobacter pylori and Cancer. 2013. Available at: https://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/h-pylori-fact-sheet. Accessed on 3 July 2018.

Ernst PB, Peura DA, Crowe SE. The translation of Helicobacter pylori basic research to patient care. Gastroenterology. 2006;130:188‑206.

Björkholm B, Sjolund BM, Falk PG, Berg OG, Engstrand L, Andersson DI. Mutation frequency and biological cost of antibiotic resistance in Helicobacter pylori. Proc Natl Acad Sci USA. 2001;98:14607‑12.

Falush D, Kraft C, Taylor NS, Correa P, Fox JG, Achtman M, et al. Recombination and mutation during long‑term gastric colonization by Helicobacter pylori: Estimates of clock rates, recombination size, and minimal age. Proc Natl Acad Sci USA. 2001;98:15056‑61.

Alvi A, Ansari SA, Ehtesham NZ, Rizwan M, Devi S, Sechi LA, et al. Concurrent proinflammatory and apoptotic activity of a Helicobacter pylori Protein (HP986) points to its role in chronic persistence. PLoS One 2011;6:e22530.

Rizwan M, Alvi A, Ahmed N. Novel Protein Antigen (JHP940) from the Genomic Plasticity Region of Helicobacter pylori Induces tumor necrosis factor alpha and interleukin‑8 secretion by human macrophages. J Bacteriol. 2008;190:1146‑51.

Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev. 2006;19:449‑90.

Axon AT. Are all helicobacter equal? Mechanisms of gastroduodenal pathology and their clinical implications. Gut 1999;45(1):11‑4.

Jenks PJ, Megraud F, Labigne A. Clinical outcome after infection with Helicobacter pylori does not appear to be reliably predicted by the presence of any of the genes of the cag pathogenicity island. Gut. 1998;43:752‑8.

Van der Ende A, Rauws EA, Feller M, Mulder CJ, Tytgat GN, Dankert J. Heterogeneous Helicobacter pylori isolates from members of a family with a history of peptic ulcer disease. Gastroenterol. 1996;111:638‑47.

Buta N, Tanih NF, Ndip RN. Increasing trend of metronidazole resistance in the treatment of Helicobacter pylori infection: A global challenge. Afr J Biotechnol. 2010;9:1115‑21.

Megraud F. H. pylori antibiotic resistance: Prevalence, importance, and advances in testing. Gut. 2004;53:1374‑84.

Chey WD, Wong BC:Practice Parameters Committee of the American College of Gastroenterology. Guideline on the Management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808‑25.

De Francesco V, Ierardi E, Hassan C, Zullo A. Helicobacter pylori therapy: Present and Future. World J Gastrointest Pharmacol Ther. 2012;3:68‑73.

O’connor A, Taneike I, Nami A, Fitzgerald N, Murphy P, Ryan B, et al. Helicobacter pylori resistance to metronidazole and clarithromycin in Ireland. Eur J Gastroenterol Hepatol. 2010;22:1123‑7.

Wu W, Yang Y, Sun G. Recent insights into antibiotic resistance in Helicobacter pylori eradication. Gastroenterol Res Pract. 2012;2012:723183.

De Francesco V, Giorgio F, Hassan C, Manes G, Vannella L, Panella C, et al. Worldwide H. pylori Antibiotic Resistance: A Systematic Review. J Gastrointestin Liver Dis. 2010;19:409‑14.

Megraud F. Antibiotic resistance in Helicobacter pylori infection. Br Med Bull. 1998;54:207‑16.

Taneike I, Nami A, O`Connor A, Fitzgerald N, Murphy P, Qasim A, et al. Analysis of drug resistance and virulence‑factor genotype of Irish H pylori strains:Is there any relationship between resistance to metronidazole and cagA status? Aliment Pharmacol Ther. 2009;30:784‑90.

Al Moagel MA, Evans DG, Abdulghani ME, Adam E, Evans DJ Jr, Malaty HM, et al. Prevalence of Helicobacter pylori (formerly Campylobacter) Infection in Saudi Arabia, and comparison of those with and without upper gastrointestinal symptoms. Am J Gastroenterol. 1990;85:944‑8.

Marie MA. Patterns of H. pylori Resistance to metronidazole, clarithormycin and Amoxicillin in Saudi Arabia. J Bacteriol Virol. 2008;38:173‑8.

Khan MA, Ghazi OH. Helicobacter pylori infection in asymptomatic subjects in Makkah. J Pak Med Assoc. 2007;57:114‑6.

Available at: http://www.saudiembassy.net/about/ country‑information/. Accessed on 3 July 2018.

Marie MA. Seroprevalence of Helicobacter pylori infection in large series of patients in an urban area of Saudi Arabia. Korean J Gastroenterol. 2008;52:226‑9.

Momenah AM, Asghar AH. Prevalence and antibiotic resistance among Helicobacter pylori clinical isolates from main Hospitals in the Western Region of Saudi Arabia. Pak J Med Sci. 2008;24:100‑3.

Lee SY. Current progress toward eradicating Helicobacter pylori in East Asian countries: differences in the 2013 revised guidelines between China, Japan, and South Korea. World J Gastroenterol. 2013;20:1493-502.

Kandulski A, Malfertheiner P. Helicobacter pylori and gastroesophageal reflux disease. Curr Opin Gastroenterol. 2014;30:402‐7.

Bor S, Kitapcioglu G, Kasap E. Prevalence of gastroesophageal reflux disease in a country with a high occurrence of Helicobacter pylori. World J Gastroenterol. 2017;23:525‐32.

Dore MP, Pes GM, Bassotti G, Farina MA, Marras G, Graham DY. Risk factors for erosive and non-erosive gastroesophageal reflux disease and barrett’s esophagus in Nothern Sardinia. Scand J Gastroenterol. 2016;51:1281‐7.

Sonnenberg A, Turner KO, Spechler SJ, Genta RM. The influence of Helicobacter pylori on the ethnic distribution of barrett’s metaplasia. Aliment Pharmacol Ther. 2017;45:283‐90.

Tomasello G, Giordano F, Mazzola M, Jurjus R, Jurjus A, Damiani P, et al. Helicobacter pylori and barretts esophagus: a protective factor or a real cause? J Biol Regul Homeost Agents. 2017;31:9‐15.

Vakil N. Rationale for a Helicobacter pylori Test and Treatment Strategy in Gastroesophageal Reflux Disease. Gastroenterol Clin N Am. 2015;28:971–85.

Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection-the maastricht V/florence consensus report. Gut. 2017;66:6‐30.

Yang HB, Sheu BS, Wang ST, Cheng HC, Chang WL, Chen WY. H. pylori eradication prevents the progression of gastric intestinal metaplasia in reflux esophagitis patients using long-term esomeprazole. Am J Gastroenterol. 2009;104(7):1642–9.

Lundell L, Miettinen P, Myrvold HE, Pedersen SA, Thor K, Andersson A, et al. Lack of effect of acid suppression therapy on gastric atrophy. Nordic GERD Study Group. Gastroenterology. 1999;117(2):319–26.

Fiocca R, Mastracci L, Attwood SE, Ell C, Galmiche JP, Hatlebakk J, et al. LOTUS Trial Collaborators. Gastric exocrine and endocrine cell morphology under prolonged acid inhibition therapy:results of a 5-year follow-up in the LOTUS trial. Aliment Pharmacol Ther. 2012;36(10):959–71.