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  • 1. Aims and Scope

    Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE

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    Yong Chan Lee Professor of Medicine
    Director, Gastrointestinal Research Laboratory
    Veterans Affairs Medical Center, Univ. California San Francisco
    San Francisco, USA

    Deputy Editor

    Deputy Editor
    Jong Pil Im Seoul National University College of Medicine, Seoul, Korea
    Robert S. Bresalier University of Texas M. D. Anderson Cancer Center, Houston, USA
    Steven H. Itzkowitz Mount Sinai Medical Center, NY, USA
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    All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
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Is It Rationale to Apply Strict Colonoscopic Surveillance in Patients with Helicobacter pylori Associated Chronic Atrophic Gastritis?

Ji Hyun Kim

Department of Internal Medicine, Inje University College of Medicine, Busan, Korea

Correspondence to: Ji Hyun Kim, Department of Internal Medicine, Inje University Busan Paik Hospital, Inje University College of Medicine, 75 Bokji-ro, Busanjin-gu, Busan 47392, Korea, Tel: +82-51-890-6930, Fax: +82-51-892-0273, E-mail: zep2000@inje.ac.kr

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gut Liver 2016;10(6):867-868. https://doi.org/10.5009/gnl16445

Published online November 15, 2016, Published date November 15, 2016

Copyright © Gut and Liver.

Colonic carcinogenesis is believed to be multifactorial process. In addition to hereditary and genetic factors, environmental factors such as Westernized dietary practice, smoking and alcohol consumption had also been contributed to increase the risk of colorectal cancer.1

There has been growing interest in the relationship between infectious agents and colonic carcinogenesis. Especially, Helicobacter pylori, which is ubiquitous pathogen inducing chronic inflammation and eventually leading to development of chronic gastritis, peptic ulcer and even gastric cancer. There is also conflicting evidence on the relevance of chronic H. pylori infection as a risk factor for colorectal neoplasia.2,3

Several pathophysiologic mechanisms had been also suggested for this correlation between colorectal neoplasm and H. pylori infection. Increased serum gastrin caused by persistent H. pylori infection, which is estimated to have trophic effect on colonic mucosa, could contribute to colorectal carcinogenesis,4 although this hypothesis was disputed by other reports showing discordant results.5 The facts that measurement of nonamidated gastrin which seems to act as more important carcinogen of colorectal carcinoma is not available, and autocrine secretion of gastrin by colorectal cancer cells themselves may explain these inconsistent results.

Intestinal dysbiosis induced by H. pylori-related chronic atrophic gastritis resulting in hypochlorhydria was supposed to be another contributory to the colorectal carcinogenesis.6,7

Although H. pylori is known as not to invade colonic mucosa, study reporting fecal shedding of viable H. pylori suggested the it may move through colonic lumen and locally activate colonic carcinogenesis. Study reporting higher detection rate of H. pylori in neoplastic lesion than normal mucosa also supported this hypothesis,8 although exact pathophysiologic mechanism of H. pylori induced local activation of carcinogenesis should be evaluated.

Enhanced systemic inflammatory response caused by H. pylori, especially by Cag A-positive H. pylori infection, also had assumed to play a causative role in colorectal carcinogenesis.4

Although the insufficient evidence for a definitive causal relationship, it appears that H. pylori related gastritis is associated with an increased, although modest, risk of colorectal adenoma and cancer.

Lee et al.9 tried retrospective cross-sectional study to evaluate the correlation between H. pylori, atrophic gastritis and colorectal neoplasm using a single center health check program. Authors analyzed 6,351 subjects who underwent screening colonoscopy and H. pylori infection was confirmed with serology testing IgG antibody. This study showed H. pylori infection was a significantly associated with overall colorectal neoplasm. In addition, presence of atrophic gastritis, which was known as a precancerous environment, enhanced this correlation, especially advanced colorectal neoplasm, even after adjusting the confounding factors such as age, gender, family history of colorectal cancer, body mass index, metabolic syndrome, smoking and alcohol consumption (odds ratio [OR], 1.40; 95% confidence interval [CI], 1.03 to 1.91). Further subgroup analysis showed H. pylori seropositivity state which was not accompanied with atrophic gastritis was revealed not to be associated with colorectal neoplasm. Although atrophic gastritis was defined based on the endoscopy which retained indispensable bias originating from interobserver difference, those results is meaningful data for explaining the relationship between chronic inflammatory processing mediated by H. pylori infection and colorectal carcinogenesis, especially proximal colon cancer. This result was somewhat concordant with previously reported case-control study reporting association of prevalence of H. pylori infection and higher histopathologic severity or advanced type of colonic neoplasms.10

When it comes to the relationship between H. pylori infection and location of colorectal neoplasms, studies provided conflicting results. Animal model-based experimental study reported that mitogenic effect of gastrin is prominent in left colon. On the other hand, aberrant DNA methylation resulting from overproduction of bile acids by bacterial overgrowth has known to be associated with proximal colon neoplasms. A population-based case control study conducted in Japan reported proximal adenoma risk increased as the degree of H. pylori-related gastritis increased, showing maximal increase in chronic atrophic gastritis group.2 Lee et al.9 also reported increased prevalence of proximal colon neoplasms in stepwise manner according to the H. pylori seropositivity and presence of atrophic gastritis, showing highest OR (1.29; 95% CI, 1.10 to 1.51) in H. pylori (+)/atrophic gastritis (+) group. Author’s also suggested that methylation change in proximal colon caused by atrophic gastritis induced colonic bacterial overgrowth may be the reason for the results.

Possibly, based on these results, we can consider strict colonoscopic surveillance in H. pylori infected subjects, especially in subjects accompanied with atrophic gastritis, gastric adenoma and gastric cancer. In addition, effect of eradication therapy on the risk of advanced colorectal neoplasms will be problem for future study.

No potential conflict of interest relevant to this article was reported.

  1. Le Marchand, L, Wilkens, LR, Kolonel, LN, Hankin, JH, and Lyu, LC (1997). Associations of sedentary lifestyle, obesity, smoking, alcohol use, and diabetes with the risk of colorectal cancer. Cancer Res. 57, 4787-4794.
    Pubmed
  2. Inoue, I, Mukoubayashi, C, and Yoshimura, N (2011). Elevated risk of colorectal adenoma with Helicobacter pylori-related chronic gastritis: a population-based case-control study. Int J Cancer. 129, 2704-2711.
    Pubmed CrossRef
  3. Chen, XZ, Sch?ttker, B, and Castro, FA (2016). Association of helicobacter pylori infection and chronic atrophic gastritis with risk of colonic, pancreatic and gastric cancer: a ten-year follow-up of the ESTHER cohort study. Oncotarget. 7, 17182-17193.
    Pubmed KoreaMed
  4. Hartwich, A, Konturek, SJ, and Pierzchalski, P (2001). Helicobacter pylori infection, gastrin, cyclooxygenase-2, and apoptosis in colorectal cancer. Int J Colorectal Dis. 16, 202-210.
    Pubmed CrossRef
  5. Selgrad, M, Bornschein, J, and Kandulski, A (2014). Helicobacter pylori but not gastrin is associated with the development of colonic neoplasms. Int J Cancer. 135, 1127-1131.
    Pubmed CrossRef
  6. Wang, X, Allen, TD, May, RJ, Lightfoot, S, Houchen, CW, and Huycke, MM (2008). Enterococcus faecalis induces aneuploidy and tetraploidy in colonic epithelial cells through a bystander effect. Cancer Res. 68, 9909-9917.
    Pubmed KoreaMed CrossRef
  7. Toprak, NU, Yagci, A, and Gulluoglu, BM (2006). A possible role of Bacteroides fragilis enterotoxin in the aetiology of colorectal cancer. Clin Microbiol Infect. 12, 782-786.
    Pubmed CrossRef
  8. Soylu, A, Ozkara, S, and Alis, H (2008). Immunohistochemical testing for Helicobacter pylori existence in neoplasms of the colon. BMC Gastroenterol. 8, 35.
    Pubmed KoreaMed CrossRef
  9. Lee, JY, Park, HW, and Choi, JY (2016). Helicobacter pylori infection with atrophic gastritis is an independent risk factor for advanced colonic neoplasm. Gut Liver. 10, 902-909.
    Pubmed CrossRef
  10. Sonnenberg, A, and Genta, RM (2013). Helicobacter pylori is a risk factor for colonic neoplasms. Am J Gastroenterol. 108, 208-215.
    CrossRef

Article

Editorial

Gut and Liver 2016; 10(6): 867-868

Published online November 15, 2016 https://doi.org/10.5009/gnl16445

Copyright © Gut and Liver.

Is It Rationale to Apply Strict Colonoscopic Surveillance in Patients with Helicobacter pylori Associated Chronic Atrophic Gastritis?

Ji Hyun Kim

Department of Internal Medicine, Inje University College of Medicine, Busan, Korea

Correspondence to: Ji Hyun Kim, Department of Internal Medicine, Inje University Busan Paik Hospital, Inje University College of Medicine, 75 Bokji-ro, Busanjin-gu, Busan 47392, Korea, Tel: +82-51-890-6930, Fax: +82-51-892-0273, E-mail: zep2000@inje.ac.kr

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

BODY

Colonic carcinogenesis is believed to be multifactorial process. In addition to hereditary and genetic factors, environmental factors such as Westernized dietary practice, smoking and alcohol consumption had also been contributed to increase the risk of colorectal cancer.1

There has been growing interest in the relationship between infectious agents and colonic carcinogenesis. Especially, Helicobacter pylori, which is ubiquitous pathogen inducing chronic inflammation and eventually leading to development of chronic gastritis, peptic ulcer and even gastric cancer. There is also conflicting evidence on the relevance of chronic H. pylori infection as a risk factor for colorectal neoplasia.2,3

Several pathophysiologic mechanisms had been also suggested for this correlation between colorectal neoplasm and H. pylori infection. Increased serum gastrin caused by persistent H. pylori infection, which is estimated to have trophic effect on colonic mucosa, could contribute to colorectal carcinogenesis,4 although this hypothesis was disputed by other reports showing discordant results.5 The facts that measurement of nonamidated gastrin which seems to act as more important carcinogen of colorectal carcinoma is not available, and autocrine secretion of gastrin by colorectal cancer cells themselves may explain these inconsistent results.

Intestinal dysbiosis induced by H. pylori-related chronic atrophic gastritis resulting in hypochlorhydria was supposed to be another contributory to the colorectal carcinogenesis.6,7

Although H. pylori is known as not to invade colonic mucosa, study reporting fecal shedding of viable H. pylori suggested the it may move through colonic lumen and locally activate colonic carcinogenesis. Study reporting higher detection rate of H. pylori in neoplastic lesion than normal mucosa also supported this hypothesis,8 although exact pathophysiologic mechanism of H. pylori induced local activation of carcinogenesis should be evaluated.

Enhanced systemic inflammatory response caused by H. pylori, especially by Cag A-positive H. pylori infection, also had assumed to play a causative role in colorectal carcinogenesis.4

Although the insufficient evidence for a definitive causal relationship, it appears that H. pylori related gastritis is associated with an increased, although modest, risk of colorectal adenoma and cancer.

Lee et al.9 tried retrospective cross-sectional study to evaluate the correlation between H. pylori, atrophic gastritis and colorectal neoplasm using a single center health check program. Authors analyzed 6,351 subjects who underwent screening colonoscopy and H. pylori infection was confirmed with serology testing IgG antibody. This study showed H. pylori infection was a significantly associated with overall colorectal neoplasm. In addition, presence of atrophic gastritis, which was known as a precancerous environment, enhanced this correlation, especially advanced colorectal neoplasm, even after adjusting the confounding factors such as age, gender, family history of colorectal cancer, body mass index, metabolic syndrome, smoking and alcohol consumption (odds ratio [OR], 1.40; 95% confidence interval [CI], 1.03 to 1.91). Further subgroup analysis showed H. pylori seropositivity state which was not accompanied with atrophic gastritis was revealed not to be associated with colorectal neoplasm. Although atrophic gastritis was defined based on the endoscopy which retained indispensable bias originating from interobserver difference, those results is meaningful data for explaining the relationship between chronic inflammatory processing mediated by H. pylori infection and colorectal carcinogenesis, especially proximal colon cancer. This result was somewhat concordant with previously reported case-control study reporting association of prevalence of H. pylori infection and higher histopathologic severity or advanced type of colonic neoplasms.10

When it comes to the relationship between H. pylori infection and location of colorectal neoplasms, studies provided conflicting results. Animal model-based experimental study reported that mitogenic effect of gastrin is prominent in left colon. On the other hand, aberrant DNA methylation resulting from overproduction of bile acids by bacterial overgrowth has known to be associated with proximal colon neoplasms. A population-based case control study conducted in Japan reported proximal adenoma risk increased as the degree of H. pylori-related gastritis increased, showing maximal increase in chronic atrophic gastritis group.2 Lee et al.9 also reported increased prevalence of proximal colon neoplasms in stepwise manner according to the H. pylori seropositivity and presence of atrophic gastritis, showing highest OR (1.29; 95% CI, 1.10 to 1.51) in H. pylori (+)/atrophic gastritis (+) group. Author’s also suggested that methylation change in proximal colon caused by atrophic gastritis induced colonic bacterial overgrowth may be the reason for the results.

Possibly, based on these results, we can consider strict colonoscopic surveillance in H. pylori infected subjects, especially in subjects accompanied with atrophic gastritis, gastric adenoma and gastric cancer. In addition, effect of eradication therapy on the risk of advanced colorectal neoplasms will be problem for future study.

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

References

  1. Le Marchand, L, Wilkens, LR, Kolonel, LN, Hankin, JH, and Lyu, LC (1997). Associations of sedentary lifestyle, obesity, smoking, alcohol use, and diabetes with the risk of colorectal cancer. Cancer Res. 57, 4787-4794.
    Pubmed
  2. Inoue, I, Mukoubayashi, C, and Yoshimura, N (2011). Elevated risk of colorectal adenoma with Helicobacter pylori-related chronic gastritis: a population-based case-control study. Int J Cancer. 129, 2704-2711.
    Pubmed CrossRef
  3. Chen, XZ, Sch?ttker, B, and Castro, FA (2016). Association of helicobacter pylori infection and chronic atrophic gastritis with risk of colonic, pancreatic and gastric cancer: a ten-year follow-up of the ESTHER cohort study. Oncotarget. 7, 17182-17193.
    Pubmed KoreaMed
  4. Hartwich, A, Konturek, SJ, and Pierzchalski, P (2001). Helicobacter pylori infection, gastrin, cyclooxygenase-2, and apoptosis in colorectal cancer. Int J Colorectal Dis. 16, 202-210.
    Pubmed CrossRef
  5. Selgrad, M, Bornschein, J, and Kandulski, A (2014). Helicobacter pylori but not gastrin is associated with the development of colonic neoplasms. Int J Cancer. 135, 1127-1131.
    Pubmed CrossRef
  6. Wang, X, Allen, TD, May, RJ, Lightfoot, S, Houchen, CW, and Huycke, MM (2008). Enterococcus faecalis induces aneuploidy and tetraploidy in colonic epithelial cells through a bystander effect. Cancer Res. 68, 9909-9917.
    Pubmed KoreaMed CrossRef
  7. Toprak, NU, Yagci, A, and Gulluoglu, BM (2006). A possible role of Bacteroides fragilis enterotoxin in the aetiology of colorectal cancer. Clin Microbiol Infect. 12, 782-786.
    Pubmed CrossRef
  8. Soylu, A, Ozkara, S, and Alis, H (2008). Immunohistochemical testing for Helicobacter pylori existence in neoplasms of the colon. BMC Gastroenterol. 8, 35.
    Pubmed KoreaMed CrossRef
  9. Lee, JY, Park, HW, and Choi, JY (2016). Helicobacter pylori infection with atrophic gastritis is an independent risk factor for advanced colonic neoplasm. Gut Liver. 10, 902-909.
    Pubmed CrossRef
  10. Sonnenberg, A, and Genta, RM (2013). Helicobacter pylori is a risk factor for colonic neoplasms. Am J Gastroenterol. 108, 208-215.
    CrossRef
Gut and Liver

Vol.18 No.1
January, 2024

pISSN 1976-2283
eISSN 2005-1212

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