J. Robin Warren (2015) - The Discovery of Helicobacter

J. Robin Warren (2015)

The Discovery of Helicobacter

J. Robin Warren (2015)

The Discovery of Helicobacter

Abstract

Before the 1970s, well fixed specimens of gastric mucosa were rare. Then the flexible endoscope was introduced. This enabled gastroenterologists to take numerous well-fixed small biopsies from the stomach. Gastric histology and pathology were clearly demonstrated by Whitehead in 1972, including a feature he termed ‘active’ gastritis. This description involved only the superficial gastric epithelium, with polymorph infiltration and epithelial cell distortion.
In June 1979 I was examining a gastric biopsy showing chronic inflammation and active change. A thin blue line on the surface showed numerous small curved bacilli. These were clearly visible with a Warthin Starry silver stain. They also appeared to grow on the surface of the foveolar epithelial cells.
Over the next two years I collected numerous similar cases. The changes were often much milder or more focal than the original biopsy, but the main features were usually similar, with chronic gastritis and usually some of the active change. These features could show considerable variation, from near normal to severe.
In 1981 I met Barry Marshall and we completed a clinico-pathological study of 100 outpatients referred for gastroscopy. There was little relation between the infection and the patients’ symptoms. Peptic ulcers, particularly duodenal ulcers, were very closely related to the infection. We cultured Helicobacter pylori.
In 1986, with Marshall et al, I studied the effect of eradication of H pylori on the recurrence of duodenal ulcer. I graded the gastritis (0 – 36) using the features seen with active gastritis. The range was 15 – 35 before treatment. After eradication of H pylori, this changed to 5 – 20 within 2 weeks. This provides powerful evidence that H pylori causes the active change.
Duodenal ulcer usually occurs in the duodenal cap. Gastric mucosa normally extends through the pylorus. In this study, the proximal border of all ulcers was either definite gastric mucosa, or scarred and consistent with a gastric origin. This suggests duodenal ulcer is either actually a distal pyloric ulcer or gastro-duodenal. It may well arise in the damaged, inflamed and infected mucosa in the position of maximum stress – the lip of the pyloric sphincter.

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