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Peptic Ulcers

Tuesday, April 21, 2009

Description

An in-depth report on the causes, diagnosis, treatment, and prevention of stomach and GI ulcers.

Alternative Names

Duodenal Ulcers; Gastric Ulcers; H. Pylori; Nonsteroidal Anti-inflammatory Drugs, or NSAIDs

Causes

Before the discovery of the bacterium Helicobacter (H.) pylori, the stomach was believed to be a sterile environment. Now, H. pylori is known to be a major cause of peptic ulcers. The bacteria 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 (e.g., chronic stress, coffee-drinking, smoking) were long believed to be the primary cause of ulcers, it is now thought they only increase susceptibility to them in some H. pylori carriers.

When H. pylori was first identified as the major cause of peptic ulcers, it was found in 90% of people with duodenal ulcers and in about 80% of people with gastric ulcers. As more people are being tested and treated for the bacteria, however, the rate of H. pylori associated ulcers has declined. For example, a 2001 study suggested that about half of ulcers are not caused by H. pylori. Instead, they tend to be due to regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), which include aspirin and other common pain relievers. Genetic factors, or, rarely, Crohn's disease or Zollinger-Ellison syndrome also cause ulcers.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) is the second most common cause of ulcers and the rate of NSAID-caused ulcers is increasing. About 20 million people take prescription NSAIDs regularly, and over 25 billion tablets of over-the-counter brands are sold each year in America. The most common NSAIDs are aspirin, ibuprofen (Advil), and naproxen (Aleve, Naprosyn), although many others are available.

Their damaging effects appears to rest primarily on actions that block an enzyme called cyclooxygenase (COX), which is involved in the production of prostaglandins. The COX enzyme has two forms:

  • COX-2 causes intestinal contractions and inflammation. When NSAIDs block this enzyme, they help reduce pain and inflammation. This is their primary benefit.
  • COX-1 also protects the stomach by its release of prostaglandins that protect the mucous layer, maintain normal bicarbonate levels, and keep blood flowing in the intestinal tract. When NSAIDs block COX-2, they expose the mucous lining to attack.

Standard NSAIDs block both COX-1 and COX-2. Even if an NSAID is injected intravenously, the drug will still inhibit prostaglandins in the stomach and duodenum. NSAIDs are mild acids and can cause some injury by direct exposure to the lining of the stomach. Their primary damaging effects, however, are from their actions against COX-1. Studies suggest the following risks:

  • An analysis of controlled trials reported that about 1% of patients taking aspirin over a 28 month period will experience gastrointestinal bleeding. A significant risk existed even at low doses or with the use of modified-release formulations.
  • Of further concern was a 1998 study indicating that taking NSAIDs for only six months posed a risk for symptomatic ulcers that was greater than 1%.

The risk for bleeding is continuous for as long as a patient is on these drugs and may even persist for about a year after taking them. Taking short courses of NSAIDs for temporary pain relief should not cause major problems because the stomach has time to recover and repair any damage that has occurred.

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