Robin Warren (born 1937), a pathologist from Perth, Australia, observed small curved bacteria colonizing the lower part of the stomach (antrum) in about 50% of patients from which biopsies had been taken. He made the crucial observation that signs of inflammation were always present in the gastric mucosa close to where the bacteria were seen.
Barry Marshall (born 1951), a young clinical fellow, became interested in Warren’s findings and together they initiated a study of biopsies from 100 patients. After several attempts, Marshall succeeded in cultivating a hitherto unknown bacterial species (later denoted Helicobacter pylori) from several of these biopsies.
Together they found that the organism was present in almost all patients with gastric inflammation, duodenal ulcer or gastric ulcer. Based on these results, they proposed that Helicobacter pylori is involved in the aetiology of these diseases.
Even though peptic ulcers could be healed by inhibiting gastric acid production, they frequently relapsed, since bacteria and chronic inflammation of the stomach remained.
In treatment studies, Marshall and Warren as well as others showed that patients could be cured from their peptic ulcer disease only when the bacteria were eradicated from the stomach.
Thanks to the pioneering discovery by Marshall and Warren, peptic ulcer disease is no longer a chronic, frequently disabling condition, but a disease that can be cured by a short regimen of antibiotics and acid secretion inhibitors.
Nobel Prize in Physiology or Medicine 2005 went to Barry Marshall and Robin Warren, who with tenacity and a prepared mind challenged prevailing dogmas.
By using technologies generally available (fibre endoscopy, silver staining of histological sections and culture techniques for microaerophilic bacteria), they made an irrefutable case that the bacterium Helicobacter pylori is causing disease. By culturing the bacteria they made them amenable to scientific study.
In 1982, when this bacterium was discovered by Marshall and Warren, stress and lifestyle were considered the major causes of peptic ulcer disease. It is now firmly established that Helicobacter pylori causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers. The link between Helicobacter pylori infection and subsequent gastritis and peptic ulcer disease has been established through studies of human volunteers, antibiotic treatment studies and epidemiological studies.
Helicobacter pylori is a spiral-shaped Gram-negative bacterium that colonizes the stomach in about 50% of all humans. In countries with high socio-economic standards infection is considerably less common than in developing countries where virtually everyone may be infected.
Infection is typically contracted in early childhood, frequently by transmission from mother to child, and the bacteria may remain in the stomach for the rest of the person’s life. This chronic infection is initiated in the lower part of the stomach (antrum).
As first reported by Robin Warren, the presence of Helicobacter pylori is always associated with an inflammation of the underlying gastric mucosa as evidenced by an infiltration of inflammatory cells.
This research made the remarkable and unexpected discovery that inflammation in the stomach (gastritis) as well as ulceration of the stomach or duodenum (peptic ulcer disease) is the result of an infection of the stomach caused by the bacterium Helicobacter pylori.
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