Robin Warren was born in 1937, in Adelaide, South Australia. He graduated MB, BS from the University of Adelaide in 1961. After training at the Royal Melbourne Hospital, he was admitted to the Royal College of Pathologists of Australasia in 1967. He has been a senior pathologist at the Royal Perth Hospital in Western Australia, becoming emeritus consultant pathologist in 1998. Robin was the guest of honour at the Sixth International Workshop on Campylobacter, Helicobacter and Related Organisms in 1991 and guest speaker at the centenary meeting of the German Society of Pathology in May 1997. He received the Distinguished Fellows Award of the Royal College of Pathologists of Australasia in 1995; the Inaugural Award of the First Western Pacific Helicobacter Congress in February 1996; the medal of the University of Hiroshima in September 1996; the University of Adelaide Alumni Association Distinguished Alumni Award in October 1996; and was granted the honorary degree of Doctor of Medicine by The University of Western Australia in September 1997. Jointly with Dr Barry Marshall, he received: the Warren Alpert Foundation Prize in 1994; the Australian Medical Association Award in 1995; the Paul Ehrlich and Ludwig Darmstaedter Award in March 1997; the Faulding Florey Medal in September 1998; inclusion in the Cavalcade of Australian Scientists of the 20th Century; and the 2005 Nobel Prize for Physiology or Medicine.

Helicobacter, active gastritis and duodenal ulcers
by Professor Robin Warren

With the introduction of the flexible endoscope in the 1970s, well-fixed biopsies of gastric mucosa became available. Biopsies were described in 1972 by Whitehead, who reported ‘active’ change, with superficial inflammation and damage. I first saw Helicobacter pylori in 1979, in a biopsy with severe active gastritis.

Studies in 1986 showed the effect of eradication of H. pylori on the recurrence of duodenal ulcer. The gastritis was graded 0 – 36 using the features seen with active gastritis. The range was 15 – 35 before treatment, and changed to 15 – 20 within 2 weeks of eradication of H. pylori. The antibacterial therapy was only related if it was successful, providing evidence that H. pylori caused the active change.

Duodenal ulcer usually occurs in the duodenal cap, and the gastric mucosa normally extends to the cap. Studies show the proximal border of ulcers is either definite gastric mucosa, or scarred and consistent with a gastric origin, suggesting duodenal ulcers are either pyloric or gastro-duodenal in origin. Ulcers arise in the damaged, inflamed and infected mucosa in the position of maximum stress – the lip of the pyloric sphincter.

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