H.pylori gastric adenocarcinoma pathophysiology: Difference between revisions
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*H.pylori is considered as Type I carcinogen. Among infected individuals, 1 to 3% develop gastric adenocarcinoma.<ref name="pmid11556297">{{cite journal| author=Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S, Yamakido M et al.| title=Helicobacter pylori infection and the development of gastric cancer. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 11 | pages= 784-9 | pmid=11556297 | doi=10.1056/NEJMoa001999 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11556297 }} </ref> | *H.pylori is considered as Type I carcinogen. Among infected individuals, 1 to 3% develop gastric adenocarcinoma.<ref name="pmid11556297">{{cite journal| author=Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S, Yamakido M et al.| title=Helicobacter pylori infection and the development of gastric cancer. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 11 | pages= 784-9 | pmid=11556297 | doi=10.1056/NEJMoa001999 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11556297 }} </ref> | ||
*Patients with H.pylori infection with severe atrophic gastritis, corpus predominant gastritis, or both and Intestinal metaplasia are at increased risk for intestinal-type gastric carcinoma.<ref name="pmid11556297">{{cite journal| author=Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S, Yamakido M et al.| title=Helicobacter pylori infection and the development of gastric cancer. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 11 | pages= 784-9 | pmid=11556297 | doi=10.1056/NEJMoa001999 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11556297 }} </ref><ref name="pmid1458460">{{cite journal| author=Correa P| title=Human gastric carcinogenesis: a multistep and multifactorial process--First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. | journal=Cancer Res | year= 1992 | volume= 52 | issue= 24 | pages= 6735-40 | pmid=1458460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1458460 }} </ref> | *Patients with H.pylori infection with severe atrophic gastritis, corpus predominant gastritis, or both and Intestinal metaplasia are at increased risk for intestinal-type gastric carcinoma.<ref name="pmid11556297">{{cite journal| author=Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S, Yamakido M et al.| title=Helicobacter pylori infection and the development of gastric cancer. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 11 | pages= 784-9 | pmid=11556297 | doi=10.1056/NEJMoa001999 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11556297 }} </ref><ref name="pmid1458460">{{cite journal| author=Correa P| title=Human gastric carcinogenesis: a multistep and multifactorial process--First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. | journal=Cancer Res | year= 1992 | volume= 52 | issue= 24 | pages= 6735-40 | pmid=1458460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1458460 }} </ref> | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
*Gastric cancer is caused by H.pylori infection either by inflammatory process or by its direct effect on gastric mucosa. | |||
*H.pylori releases phospholipases, ammonia and cytotoxins directly into gastric lumen and causes epithelial degeneration.<ref name="pmid7495938">{{cite journal| author=Blaser MJ| title=The role of Helicobacter pylori in gastritis and its progression to peptic ulcer disease. | journal=Aliment Pharmacol Ther | year= 1995 | volume= 9 Suppl 1 | issue= | pages= 27-30 | pmid=7495938 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7495938 }} </ref> | |||
*Following epithelial damage, there will be persistent proliferation and regeneration of gastric epithelial cells. This increases the risk of malignant alterations of the gastric stem cells st the neck of gastric tubes.<ref name="pmid8607492">{{cite journal| author=Bechi P, Balzi M, Becciolini A, Maugeri A, Raggi CC, Amorosi A et al.| title=Helicobacter pylori and cell proliferation of the gastric mucosa: possible implications for gastric carcinogenesis. | journal=Am J Gastroenterol | year= 1996 | volume= 91 | issue= 2 | pages= 271-6 | pmid=8607492 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8607492 }} </ref> | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Pathophysiology
- Gastric cancer is the second leading cause of cancer-related deaths worldwide and H.pylori is the strongest known risk factor for gastric cancer.[1]
- H.pylori is considered as Type I carcinogen. Among infected individuals, 1 to 3% develop gastric adenocarcinoma.[1]
- Patients with H.pylori infection with severe atrophic gastritis, corpus predominant gastritis, or both and Intestinal metaplasia are at increased risk for intestinal-type gastric carcinoma.[1][2]
Pathogenesis
- Gastric cancer is caused by H.pylori infection either by inflammatory process or by its direct effect on gastric mucosa.
- H.pylori releases phospholipases, ammonia and cytotoxins directly into gastric lumen and causes epithelial degeneration.[3]
- Following epithelial damage, there will be persistent proliferation and regeneration of gastric epithelial cells. This increases the risk of malignant alterations of the gastric stem cells st the neck of gastric tubes.[4]
References
- ↑ 1.0 1.1 1.2 Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S, Yamakido M; et al. (2001). "Helicobacter pylori infection and the development of gastric cancer". N Engl J Med. 345 (11): 784–9. doi:10.1056/NEJMoa001999. PMID 11556297.
- ↑ Correa P (1992). "Human gastric carcinogenesis: a multistep and multifactorial process--First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention". Cancer Res. 52 (24): 6735–40. PMID 1458460.
- ↑ Blaser MJ (1995). "The role of Helicobacter pylori in gastritis and its progression to peptic ulcer disease". Aliment Pharmacol Ther. 9 Suppl 1: 27–30. PMID 7495938.
- ↑ Bechi P, Balzi M, Becciolini A, Maugeri A, Raggi CC, Amorosi A; et al. (1996). "Helicobacter pylori and cell proliferation of the gastric mucosa: possible implications for gastric carcinogenesis". Am J Gastroenterol. 91 (2): 271–6. PMID 8607492.