H.pylori gastric adenocarcinoma pathophysiology

For more information on gastric adenocarcinoma click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S [2]

Overview

Gastric cancer is the second leading cause of cancer-related deaths worldwide and H. pylori is the strongest known risk factor for gastric cancer. H. pylori is considered as type I carcinogen. Among infected individuals, 1 to 3% develop gastric adenocarcinoma.

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]
- Distal adenocarcinoma is the most common gastric adenocarcinoma which is caused by H. pylori.

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 (metaplastic changes) of the gastric stem cells at the neck of gastric tubes.^[4]
The nitric oxide (NO) and reactive oxygen metabolites are released by [[neutrophils] during the inflammatory process, which contribute to the DNA damage of epithelial cells.
The above process along with deficiency of ascorbic acid(vitamin C) , vitamin E and calcium leads to epithelial cell DNA damage.^[5]
Diet containing high amount of salt, nitrates or nitrosamines also contribute to the DNA damage leading to gastric cancer.^[6]^[7]
Patients with duodenal ulcer have predominant antral gastritis where as gastric cancer patients have severe gastritis predominantly in the corpus of the stomach.^[8]
Severe gastritis in corpus leads to decreased acid production resulting in suppression of a defense mechanism against atypical cell production (atypical cells are very sensitive to gastric acid) leading to persistence and progression of atypical cells.

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.
↑ Jarosz M, Dzieniszewski J, Dabrowska-Ufniarz E, Wartanowicz M, Ziemlanski S, Reed PI (1998). “Effects of high dose vitamin C treatment on Helicobacter pylori infection and total vitamin C concentration in gastric juice”. Eur J Cancer Prev. 7 (6): 449–54. PMID 9926292.
↑ Tsugane S, Sasazuki S (2007). “Diet and the risk of gastric cancer: review of epidemiological evidence”. Gastric Cancer. 10 (2): 75–83. doi:10.1007/s10120-007-0420-0. PMID 17577615.
↑ Jakszyn P, Gonzalez CA (2006). “Nitrosamine and related food intake and gastric and oesophageal cancer risk: a systematic review of the epidemiological evidence”. World J Gastroenterol. 12 (27): 4296–303. PMC 4087738. PMID 16865769.
↑ Stolte M, Bethke B (1990). “Elimination of Helicobacter pylori under treatment with omeprazole”. Z Gastroenterol. 28 (6): 271–4. PMID 2238754.

[pmid11556297-1] 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.

[pmid1458460-2] 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.

[pmid7495938-3] 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.

[pmid8607492-4] 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.

[pmid9926292-5] Jarosz M, Dzieniszewski J, Dabrowska-Ufniarz E, Wartanowicz M, Ziemlanski S, Reed PI (1998). “Effects of high dose vitamin C treatment on Helicobacter pylori infection and total vitamin C concentration in gastric juice”. Eur J Cancer Prev. 7 (6): 449–54. PMID 9926292.

[pmid17577615-6] Tsugane S, Sasazuki S (2007). “Diet and the risk of gastric cancer: review of epidemiological evidence”. Gastric Cancer. 10 (2): 75–83. doi:10.1007/s10120-007-0420-0. PMID 17577615.

[pmid16865769-7] Jakszyn P, Gonzalez CA (2006). “Nitrosamine and related food intake and gastric and oesophageal cancer risk: a systematic review of the epidemiological evidence”. World J Gastroenterol. 12 (27): 4296–303. PMC 4087738. PMID 16865769.

[pmid2238754-8] Stolte M, Bethke B (1990). “Elimination of Helicobacter pylori under treatment with omeprazole”. Z Gastroenterol. 28 (6): 271–4. PMID 2238754.

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