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Gastroenterology Medicine & Research

Is it really Necessary to Eradicate Helicobacter pylori?

Fernanda Machado Fonseca1*, Jacqueline Batista Sousa2, Brenda Junqueira Afonso3, Marcela Machado Fonseca4, Anderson de Almeida Amaral4 and Kennio Ferreira Paim3,5

1 Department of Biomedicine, Federal University of Piauí, Brazil

2 Institute of Natural and Biological Sciences, Federal University of Triângulo Mineiro, Brazil

3 School of Medicine, Uberaba University, Brazil

4 Santa Casa de Misericórdia Hospital, Brazil

5 Department of Clinical Pathology, Federal University of Triângulo Mineiro, Brazil

*Corresponding author: Fernanda Machado Fonseca, Department of Biomedicine, Federal University of Piauí, Campus Ministro Reis Velloso. São Sebastião Avenue, 2819, Reis Velloso, Parnaíba, Piauí, Brazil

Submission: August 24, 2018;Published: August 27, 2018

DOI: 10.31031/GMR.2018.02.000528

ISSN 2637-7632
Volume2 Issue1

Letter to Editor

Helicobacter pylori is a Gram-negative bacterium that colonizes around 50% of world population. It is frequently associated with gastrointestinal diseases such as gastritis, peptic ulcer, and in some cases, can favour the development of gastric cancer. After the host colonization, H. pylori can cause chronic infection and disease in less than 10% of symptomatic individuals after several years. Thus, the apparent colonization of H. pylori requires a long time of establishment and the continuous stimulation of the inflammatory response to produce enough histological deterioration for disease expression [1].

Several virulence factors of H. pylori have been described (i.e. cagA and vacA genes). The presence of these factors can contribute to the development of a more aggressive form of the disease, although strains not carrying these virulence factors were also recovered from stomach of infected patients. As the colonization of H. pylori can be asymptomatic for decades, most cases of the disease (i.e. peptic ulcers) occur in patients older than 40 years, and around 1% of these individuals can evolve to gastric cancer [2]. Due to its long latent period of infection, the small numbers of cases of that evolve to gastric cancer and the detection of H. pylori in the faeces of mummified humans around 3,000 years ago some authors have hypothesized that this pathogen cold be, in fact, more an ancestral commensal microorganism of humans than a true pathogen [3]. Reinforcing this hypothesis is the fact that the infection is transmitted early in life and is mainly in a family setting.

In the last years, it has been detected a decrease in the prevalence of H. pylori infection, especially in developed countries [4,5]. The improvement of sanitary conditions and changes in family size are two of many other factors that have contributed to the decrease of its transmissibility. As the prevalence H. pylori decline, other diseases have been reported more frequently, such as asthma, obesity and an increase in the susceptibility to develop diarrheal diseases [6-8]. Additionally, H. pylori have been negatively associated with gastro-oesophageal reflux disease, Barrett’s oesophagus, and adenocarcinoma of the oesophagus [9]. Thus, it seems that H. pylori interactions with human being have created double-edged sword.

The pros and cons of H. pylori infection have raised the question whether the eradication of H. pylori is really necessary from those infected and asymptomatic individuals to prevent future clinical complications. We are far to have reached a consensus between the scientific society and clinicians. However, it is important highlight that the eradication of H. pylori in some communities would be desire, like in Japan, where the population has a high risk to develop gastric cancer [10].

In fact, the eradication of H. pylori lead to peptic ulcer healing, reduces ulcer relapse rates, and prevents gastric cancer. But, the wide use of the standard triple therapy consisting of a proton pump inhibitor plus clarithromycin and amoxicillin results in declined rates of success and in resistance to clarithromycin and metronidazole also used in cases of hypersensitivity to amoxicillin [11]. Recent studies have suggested therapies containing fourthgeneration quinolones, as a high rate of H. pylori eradication were demonstrated [12,13]. Thus, additional studies regarding effective therapies for H. pylori infection are necessary and it is important to emphasize that the chosen of antimicrobial has to be done based on susceptibility test and according to geographical region.

Take all these together, it is not possible to conclude if H. pylori act as a pathogen or as an ancestral commensal of humans. Additional studies exploring its interaction with the host and the consequences of its eradication are necessary. One alternative to avoid the massive and unnecessary eradication of this microorganism in colonized and asymptomatic individuals is the early detection of gastric lesions, especially because H. pylori colonization can be important to human stomach.


  1. Li J, Perez Perez GI (2018) Helicobacter pylori the Latent human pathogen or an Ancestral Commensal Organism. Front Microbiol 9: 609.
  2. Calvet X, Ramirez Lazaro MJ, Lehours P, Mégraud F (2013) Diagnosis and epidemiology of Helicobacter pylori infection. Helicobacter 18(Suppl 1): 5-11.
  3. Allison MJ, Bergman T, Gerszten E (1999) Further studies on fecal parasites in antiquity. Am J Clin Pathol 112(5): 605-609.
  4. Sonnenberg A (2011) Time trends of mortality from gastric cancer in Europe. Dig Dis Sci 56(4): 1112-1118.
  5. Den Hollander WJ, Holster IL, Van Gilst B, Van Vuuren AJ, Jaddoe VW, et al. (2015) Intergenerational reduction in Helicobacter pylori prevalence is similar between different ethnic groups living in a Western city. Gut 64(4): 1200-1208.
  6. Rothenbacher D, Blaser MJ, Bode G, Brenner H (2000) Inverse relationship between gastric colonization of Helicobacter pylori and diarrheal illnesses in children: results of a population-based crosssectional study. J Infect Dis 182(5): 1446-1449.
  7. Holster IL, Vila AMJ, Caudri D, Den Hoed CM, Perez Perez GI, et al. (2012) The impact of Helicobacter pylori on atopic disorders in childhood. Helicobacter 17(3): 232-237.
  8. Blaser MJ (2012) The Jeremiah Metzger lecture: global warming redux: the disappearing microbiota and epidemic obesity. Trans Am Clin Climatol Assoc 123: 230-241.
  9. Rutsgi AK, El Serag HB (2014) Esophageal carcinoma. N Engl J Med 371(26): 2499-2509.
  10. Sugano K (2016) Strategies for prevention of gastric cancer: progress from mass eradication trials. Dig Dis 34(5): 500-504.
  11. Thung I, Aramin H, Vavinskaya V, Gupta S, Park JY, et al. (2016) Review article: the global emergence of Helicobacter pylori antibiotic resistance. Aliment Pharmacol Ther 43(4): 514-533.
  12. Gisbert JP, Romano M, Molina Infante J, Lucendo AJ, Medina E, et al. (2015) Two-week, high-dose proton pump inhibitor, moxifloxacin triple Helicobacter pylori therapy after failure of standard triple or nonbismuth quadruple treatments. Dig Liver Dis 47(2): 108-113.
  13. Hirata Y, Serizawa T, Shichijo S, Suzuki N, Sakitani K, et al. (2016) Efficacy of triple therapy with esomeprazole, amoxicillin, and sitafloxacin as a third-line Helicobacter pylori eradication regimen. Int J Infect Dis 51: 66- 69.

© 2018 Fernanda Machado Fonseca. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and build upon your work non-commercially.

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