Helicobacter pylori (formerly known as Campylobacter pylori or pyloridis) is a gram-negative bacterium usually found in the stomach and duodenum. H.pylori infection may cause gastritis and gastric ulcers and is linked to stomach cancer (namely, non-cardia gastric cancer), non-Hodgkin Lymphoma and bowel cancer and, respectively, H.pylori was recognized as a type I carcinogen. Approximately 50% of the world’s population is infected with these bacteria, although not all of them experience the symptoms of the disease and only 1-3% of them develop cancer at some point. H.pylori eradication therapy may reduce the risk of developing cancer by 40%.
Role of H.pylori in the development of cancer
It is considered that H.pylori infection increases the risk of developing gastric cancer 3 to 6 times. However, H.pylori is not the only factor associated with an increased risk of gastric cancer. Consumption of smoked food and high salt containing diet with low content of vitamins and calcium were linked to the development of gastric cancer as well. The high concentration of nitrates in the tap water may play an important role in cancerogenesis.
The bacteria thrive within the mucous membrane of the stomach and the duodenum thanks to their ability to live in the environment with low oxygen concentrations and their high urease production – this substance neutralizes stomach acid and protects the bacteria. H.pylori induces the infiltration of the mucosa by plasma cells and neutrophils, namely, causing chronic inflammation, decreased mucus production and changes of the epithelial cells which form the stomach inner lining. Ammonia, phospolipases, and cytotoxins produced by H.pylori are probably responsible for the epithelial damage observed in type B (H.pylori-associated) gastritis. Damaged cells start to proliferate and once they start to multiply uncontrollably cancer may develop.
It should be noted that only certain strains of H.pylori are thought to be involved in the cancerogenesis. Nowadays CagA (cytotoxin-associated gene A) protein producing H.pylori is associated with the increased risk of intestinal-type gastric cancer. Another potential mechanism by which CagA-positive H. pylori may lead to cancer development is the inactivation of tumor suppressor proteins which are the body’s natural defence against cancer.
In the meantime, H.pylori infection is also associated with the reduced risk of esophageal cancer, although the reason for this fact remains unknown.
Gastric cancer symptoms
H.pylori infection is associated with the increased risk of adenocarcinoma of the distal part of the stomach. Gastric lymphomas occur less often.
The symptoms suggestive of stomach cancer are the following:
- Stomach pain;
- Blood in the stool;
- Constipation or diarrhea;
- Disgust for meat;
- Loss of appetite;
- Loss of weight;
- Weakness, general malaise;
- Enlarged lymph nodes;
Chronic superficial gastritis in the future lead to the atrophy of the mucosa, provoke metaplasia (reversible transformation of one cell type to another) and dysplasia (irreversible transformation of cells into the immature cells type) of the epithelial cells and the development of an intestinal-type adenocarcinoma.
Gastric mucosa-associated lymphoid tissue (MALT) lymphoma
Gastric MALT lymphoma is considered a type of non-Hodgkin lymphoma induced by the persisting H. pylori infection. This tumor occurs when B lymphocytes start to multiply slowly in the mucous membrane (inner lining) of the stomach. Gastric MALT lymphoma is extremely rare, although almost all of the individuals who suffer from this type of lymphoma are infected with H.pylori. In healthy individuals there is no lymphoid tissue in the epithelial layer of the stomach, however, H.pylori infection induces its occurrence.