Peptic Ulcers - Causes




Causes


Before the discovery of the bacterium Helicobacter (H.) pylori, the stomach was believed to be a sterile environment. However, in 1982, two Australian scientists identified Helicobacter pylori (H. pylori) as the main cause of stomach ulcers. This discovery showed that inflammation of the stomach and stomach ulcers result from an infection of the stomach caused by the H. pylori bacterium. This discovery was so important that the two researchers received the Nobel Price in Medicine in 2005. The bacterium appears to trigger ulcers in the following way:

  • H. pylori's corkscrew shape enables it to penetrate the mucous layer of the stomach or duodenum so that it can attach itself to the lining.
  • It survives its highly acidic environment by producing urease, an enzyme that generates ammonia and neutralizes the acid.
  • H. pylori then produces a number of toxins and factors that in certain individuals cause inflammation and damage to the lining, leading to ulcers.
  • It also alters certain immune factors that allow it to evade detection and cause persistent inflammation for a person's lifetime -- even without invading the mucous membrane.


Even if ulcers do not develop, the bacterium is now considered to be a major cause of active chronic inflammation in the stomach (gastritis) and in the upper part of the small intestine (duodenitis).

It is also strongly linked to stomach (gastric) cancer and possibly other non-intestinal problems.

Factors That Trigger Ulcers in H. pylori Carriers. It should be noted that H. pylori is found in about 25% of people who do not have peptic ulcers. The magnitude of H. pylori infection, particularly in older people, may not always predict the presence or absence of peptic ulcers. Other variables, then, need to be present to actually trigger ulcers. They may include the following:

  • Genetic Factors. Some people harbor genetic strains of H. pylori that may make the bacteria more dangerous and increase the risk for ulcers in infected individuals. The most intensively investigated genetic factor is cytotoxin-associated gene A (CagA), which has been associated with both gastric and duodenal ulcers as will as with stomach cancer. Other genetic types that may also increase bacterial severity are called vacuolating cytotoxin (vacA) and antigen-binding adhesin (BabA) genotypes. Some of these genetic factors may be more or less important for development of ulcers depending on ethnicity.
  • Immune Abnormalities. Some experts suggest that certain individuals have abnormalities in the immune response in the intestine that allow the bacteria to become injurious to the lining.
  • Lifestyle Factors. Although lifestyle factors such as chronic stress, drinking coffee, and smoking were long believed to be the primary cause of ulcers, it is now thought they only increase susceptibility to ulcers in some H. pylori carriers.

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