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Ulcers, stress, and the discovery of Helicobacter pylori

幽门螺杆菌 压力(语言学) 医学 胃肠病学 哲学 语言学
作者
Christopher Crenner
出处
期刊:The Lancet [Elsevier]
卷期号:403 (10444): 2586-2587
标识
DOI:10.1016/s0140-6736(24)01206-6
摘要

In 2005 Australian clinician Barry Marshall and pathologist J Robin Warren were awarded the Nobel Prize in Physiology or Medicine for their discovery of the bacterium Helicobacter pylori and its harmful effects on the stomach. They had published their initial findings in The Lancet, on June 16, 1984, and backed them up with a famous self-experiment. Convinced that this new organism was pathological, Marshall swallowed a mouthful of culture medium teeming with the bacteria. He soon developed unpleasant abdominal symptoms, which proved to be gastritis. Cultures taken from his stomach then grew the same bacteria. Marshall had walked himself through Robert Koch's famous steps for proving infectious causation. The discovery of H pylori changed the understanding of gastric disease, with far-reaching effects on the treatment and perception of duodenal ulcers. By the time of the 2005 Nobel Prize, duodenal ulcers had shed much of their long association with the pressures of modern life and occupational stress, and no longer posed the mortal threat they once did. We rarely blame our boss for our ulcers now, and rarely call a surgeon to treat them. 40 years after the discovery of Helicobacter pylori: towards elimination of H pylori for gastric cancer preventionThe discovery of Helicobacter pylori 40 years ago revolutionised the prevention and treatment of gastritis, peptic ulcers, and gastric cancer, earning Barry Marshall and Robin Warren the Nobel Prize in Physiology or Medicine in 2005.1 This breakthrough transformed peptic ulcer disease from a chronic condition to one curable with antibiotics, as shown by reduced recurrence rates and a substantial decline in ulcer incidence and hospitalisations in various countries.2–4 Randomised trials have shown that eradicating H pylori reduces the risk of gastric cancer, particularly when done before precancerous lesions develop, and also lowers the risk of metachronous gastric cancer after curative endoscopic resection of early gastric cancer. Full-Text PDF
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