HELICOBACTER
In 1983, a pair of Australian microbiologists
suggested that gastritis and peptic ulcers were infectious diseases,
contradicting long-held beliefs concerning their epidemiology, pathogenesis,
and treatment. In the same year, the 10th edition of Harrison’s Principlesof Internal Medicine described peptic ulcers
as due to an unfavorable balance betweengastric acid – pepsin secretion and
gastric or duodenal mucosal resistance. Underlying causes cited included
genetic and lifestyle (smoking) as well as psychological factors (anxiety,
stress). Treatment with bismuth salts, antacids, and inhibitors of acid
secretion gave relief but not cure. Relapsing patients (50 to 80%) were
subjected to surgical treat-ments (vagotomy, partial gastrectomy), which had
their own set of complications (reflux, afferent loop syndrome, dumping
syndrome). All of this was logical and supported by clinical observations and
research studies. It was simply incorrect. The bacteria now called Helicobacter had been observed but
dismissed because they were so common and its urease was once considered a
secretory product of the stomach itself. The paper by Warren and Marshall (see
Additional Reading) stimulated the reversal, which has led to cures using
antimicrobics and new ideas linking Helicobacter
infection to cancer. This experience has also left us with a sense that we can
never be smug about what we “know” in medicine.
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