Case still out on bacterium’s link to gastritis

In 1984, an obscure Australian doctor named Barry Marshall drank a broth laced with the bacterium H. pylori and then waited for the results. They were not long in coming. Within two weeks Marshall was exhibiting all the classic symptoms of gastritis, the first step toward ulcers and perhaps stomach cancer. He took this drastic step to convince his skeptical colleagues that most stomach ulcers were caused not by the traditional scapegoats – smoking, alcohol, poor diet and stress – but by a common bacterium that has inhabited the human race for millions of years.

Garry Hamilton, writing in the Aug. 11 issue of New Scientist, related Marshall’s account of experimenting on himself and the startling conclusion. He noted it was a dramatic way of proving a point.

As a junior premedical student writing in the April 1994 issue of the University of Maine’s Preventive Medicine Update, Monika Duvare recalled Marshall’s work on the origin of ulcers and stomach cancer.

Two years before experimenting on himself, Duvare wrote about how Marshall and his colleague, J. Robin Warren, had isolated the H. pylori bacterium while studying a biopsy taken from an ulcer patient’s stomach. Subsequent tests with 100 ulcer patients showed that 87 percent of them harbored H. pylori in their stomachs. Realizing that H. pylori was susceptible to antibiotics, Marshall treated one group of patients with antibiotics while a similar group received the standard treatment of antacids and diet. The ulcers healed in 92 percent of those receiving antibiotics as compared to 61 percent of those on standard treatment. Despite the results, the medical community remained highly skeptical.

Over the years, supporting research began to sway medical researchers in favor of Marshall’s theory, and in 1994 the National Institute of Health issued a statement endorsing the idea that H. pylori was the causative agent in ulcer disease. NIH’s report in the July 6, 1994, issue of the Journal of the American Medical Society states that, while the connection between H. pylori and ulcers has not been proven, the link is strong enough that ulcer patients infected with the bacterium should be treated with antibiotics.

Two British doctors, Anthony Axon and David Forman, made the case even stronger in the May 17, 1997, issue of the British Medical Journal stating that H. pylori is the “main cause of human gastritis, the major cause of peptic ulcers, and a risk factor for gastric cancer.” They claim that 75 percent of the 7,500 deaths from gastric cancer in England and Wales each year are directly attributable to H. pylori infection. Indeed, the World Health Organization labeled H. pylori a “category 1 carcinogen,” a title reserved for the most dangerous cancer-causing agents, in 1994.

But not everyone is convinced that H. pylori is as bad as it is painted and some go so far as to warn that its eradication in ulcer patients may be counterproductive. Hamilton points out that while fully half of the world’s population harbors H. pylori, only a small fraction ever develop gastritis. He cites the example of a clinic in Maitland, Fla., where only 30 percent of the ulcer patients carry H. pylori, a level barely higher than the general population.

More surprising is the fact that eradicating an H. pylori infection may prove harmful to the patient, says Charles Marwick in the Aug. 23, 2000, issue of JAMA. Speaking on behalf of the National Foundation for Infectious Diseases, Dr. Martin Blaser said that if you have an H. pylori infection, “It’s bad news for your lower stomach, but if you don’t have one, it’s bad news for your esophagus.”

Blaser is quoted as saying that, “Persons infected with H. pylori are nine times more likely to develop gastric cancer than those without it.” But then he goes on to say that eliminating H. pylori increases the risk of a particularly virulent cancer called esophageal adenocarcinoma. The numbers tend to verify this statement as gastric cancer was in a steady decline during the 20th century while esophageal cancer is rising at a rate of 11 percent a year in the United States.

Blaser attributes this fact to the disappearance of H. pylori and says it can be explained by the fact that there are two separate strains of H. pylori. The more virulent of the two, cagA-positive H. pylori, poses a far greater risk of causing ulcers and stomach cancer than does its cagA-negative counterpart. At the same time, a study of more than 700 patients with esophageal diseases found that only about 15 percent harbored H. pylori. This dropped to less than 6 percent for patients with a condition known as Barrett’s esophagus, a frequent precursor to cancer. Somehow, says Blaser, the presence of cagA-positive strains of H. pylori increases the risk for gastric diseases while lowering that for esophageal disease.

Finally some researchers believe that H. pylori is an accomplice, but not the root cause for gastric ulcers and cancer. Dr. Susan Levenstein, writing in the January 2000 issue of Psychosomatic Medicine, maintains that psychological stress is the primary cause for ulcers and the role of H. pylori is that of a “co-factor” heightening the risk for gastric disease. She points to the large numbers of H. pylori-infected people who never develop gastric problems as proof of her contention. She ends her article with a statement with which few doctors who treat gastric illnesses would disagree.

Gastric problems are complicated by smoking, alcohol, diet, anti-inflammatory drugs, mental state, and quite likely H. pylori all playing a role. This makes treatment as individual as the lifestyle and symptoms of every patient who comes through the doctor’s door.

Clair Wood taught physics and chemistry for more than a decade at Eastern Maine Technical College in Bangor.