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Cause of Gastritis and Ulcer Treatment : Infection Connection, Diagnosis
(Page 2 of 3) Discovering the Infection Connection In 1982, two young Australian physicians, Barry J. Marshall and J. Robin Warren, isolated bacteria from patients with ulcers or gastritis (stomach inflammation). In a paper published in the medical journal Lancet in early 1983, they proposed that a spiral- shaped bacterium, later named Helicobacter pylori, causes gastritis and possibly ulcers. But few physicians accepted their work, so entrenched was the idea that ulcers stem from stress. So Marshall and Warren took drastic measures to prove their point — they swallowed some of the bacteria. And their digestive tracts soon became inflamed. But most of the medical community felt this was not sufficient proof to definitively implicate the bacteria in causing ulcers. A medical dictionary published in 1986, for example, lists the causes of ulcers in order of importance as high acid, irritation, decreased blood supply to the digestive tract, decreased mucus, and last, with a question mark, infection. | ||||||||||||||||
"We had treated ulcers with anti-secretory compounds for so many years, it was hard to accept that a germ, a bacterium, would produce a disease like that. It took a while. Even academicians were not convinced. Gradually other people found the same thing," says Gallo-Torres. The accumulating evidence became the basis of the February 1994 consensus development conference, which concluded: "Ulcer patients with Helicobacter pylori infection require treatment with anti-microbial agents in addition to anti-secretory drugs." In a nutshell, the evidence for the link between bacteria and ulcers is that: All patients examined who are infected with the bacteria have evidence at the tissue level of gastritis (inflammation), but most are asymptomatic. Clearing up the infection cures the gastric inflammation. Giving the bacteria to laboratory animals (and Warren and Marshall) causes gastritis. However, even though nearly all people who are infected develop gastritis, not all develop ulcers. This suggests that other factors — such as heredity, diet, stress, and other environmental influences — may be important for the development of peptic ulcers. According to the consensus development report, "the strongest evidence for the pathogenic role of H. pylori in peptic ulcer disease is the marked decrease in recurrence rate of ulcers following the eradication of infection." How common are bacterial ulcers? The consensus report estimates that "almost all" duodenal ulcers are attributable to H. pylori, as are about 80 percent of gastric ulcers, making the microbes a very major cause. A very small percentage of ulcer sufferers develop ulcers from using aspirin or a nonsteroidal anti- inflammatory drug (NSAID) such as Voltaren (diclofenac), Feldene (piroxicam), or Ansaid (flurbiprofen). Ibuprofen, also an NSAID, is less likely to cause gastric inflammation. Diagnosis For ulcer patients, diagnosis and treatment are changing. Several different tests detect H. pylori. "You can biopsy [take tissue samples of] gastric and duodenal mucosa, then culture bacteria and identify them. But this approach is not very sensitive because it depends upon where you biopsy," says Gallo-Torres. To sample stomach or intestinal tissue, a physician snakes a lighted tube called an endoscope down through the throat. Less invasive techniques are available, too. Blood tests can detect IgG antibodies to H. pylori in a person's blood, representing the immune system's response to the microbe. These tests are cleared for marketing by FDA. Other diagnostic tests in development, but not yet evaluated by FDA, are based on the ability of H. pylori to break down urea, human metabolic waste, with an enzyme called urease, which humans do not produce. Elevated levels of breakdown products of urea, detected in a person's breath after drinking chemically labeled urea, indicate H. pylori infection.
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