For most of the 20th century, peptic ulcers were rarely cured. The reigning theory said that ulcers resulted from psychological stress and dietary factors (such as spicy foods), and patients were routinely hospitalized, told to get bed rest, and instructed to eat a bland diet. Doctors later added excess stomach acid to the list of potential causes for peptic ulcers, and patients typically received long-term therapy with medications that reduced stomach acid or blocked its production. Even with these treatments, however, ulcers were often a recurring, life-long condition.
Yet, as far back as 1886, researchers had documented a possible association between ulcers and spiral bacteria in the lining of the human stomach. Mainstream medicine dismissed this finding, however, because it was believed that no bacteria could live in the acidic environment of the stomach. Then, almost a century later, two Australian researchers rediscovered this bacterium and radically changed -- and improved -- the way peptic ulcers are diagnosed and treated.
Meet Drs. Warren and Marshall
In 1981, Robin Warren, M.D., a pathologist at the Royal Perth Hospital in Western Australia, discovered numerous bacteria living in tissue taken during a stomach biopsy. Over time, he began to notice a pattern in stomach biopsies: The spiral bacteria that he observed always accompanied changes in the stomach lining caused by gastritis (an inflammation of the stomach lining). Generally, his colleagues dismissed his discovery.
Later that year, Barry Marshall, M.D., joined Dr. Warren in his research, and together they verified the link between the spiral bacterium -- later termed Helicobacter pylori -- and the presence of peptic ulcers. In a 1984 study published in The Lancet, Drs. Warren and Marshall found that, among 100 people undergoing endoscopy, all 13 people with duodenal (upper small intestine) ulcers and 24 of 28 people with gastric (stomach) ulcers were infected with the bacteria. Ulcers in the remaining patients were attributed to the use of nonsteroidal anti-inflammatory drugs, such as aspirin, Aleve (naproxen), and Advil (ibuprofen).
Most doctors were not convinced by the findings, and often, Drs. Warren and Marshall met with extreme skepticism and even hostility. One possible reason was that the two men had not yet proven a cause-and-effect relationship between the bacterium and peptic ulcers. Animal experiments were impossible because rats, mice, and pigs were all immune to the bacteria. So, in July 1984, Dr. Marshall decided to swallow a large number of the bacteria himself to test his ideas about H. pylori.
For five days, he noticed nothing. Then, he began to experience nausea and vomiting. Although these symptoms resolved on their own after 14 days, an endoscopy on the eighth day revealed that he had developed severe gastritis. Still, Dr. Marshall’s presentations at gastroenterology meetings did little to convince doctors who proceeded to treat ulcer patients with new acid-reducing drugs, specifically H2-blockers like Tagamet (cimetidine) and Zantac (ranitidine).
Dr. Marshall came to the University of Virginia in 1986 and continued his research on H. pylori. In 1988, Drs. Marshall and Warren and their colleagues published a report in The Lancet demonstrating the effectiveness of antibiotics in the treatment of peptic ulcers. They randomly assigned 100 people with duodenal ulcers to receive either the acid-reducing drug cimetidine or one of three antibiotic regimens that targeted H. pylori infection. In 90% of people treated with Tagame, ulcers eventually returned. But ulcers returned in only 21% of those whose H. pylori infection was eliminated with a combination of an antibiotic and bismuth (the active ingredient in Pepto-Bismol).
Though much of the medical community was slow to accept these findings, some research groups became interested in H. pylori and began their own investigations. In 1991, researchers at the Baylor College of Medicine in Houston, Texas, published a report in the Annals of Internal Medicine in which they showed that, in 105 people with duodenal ulcer, a combination of bismuth, two antibiotics, and Zantac healed ulcers better than Zantac alone. This was the first randomized study in the United States to convincingly demonstrate the effectiveness of antibiotic therapy in the treatment of ulcers.
After more evidence accumulated, the National Institutes of Health recommended in 1994 that people with peptic ulcer and H. pylori infection should receive antibiotics as a first line therapy. In 80% to 90% of people with peptic ulcers stemming from H. pylori infection (i.e., not related to other causes like nonsteroidal antiinflammatory drugs), antibiotics combined with other treatments offer a permanent cure.
Today, tests to detect the presence of H. pylori infection are relatively easy to perform. Rather than conducting an endoscopy, doctors can screen for H. pylori using a urea breath test. But not everyone needs to be tested for H. pylori infection. Estimates indicate that 30% of the U.S. population is infected with H. pylori, but, for reasons that remain unclear, only 1% of infected adults develop a peptic ulcer each year. Nonetheless, H. pylori is the cause of 90% of all duodenal ulcers and 80% of all gastric ulcers.
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