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ShareAug. 9, 2010 — McMaster University researchers have identified a specific chemical that may trigger remission in patients with the debilitating disease of ulcerative colitis.
The team from the Farncombe Family Digestive Health Research Institute has found that people in long-term remission of ulcerative colitis have elevated levels of the same chemical, prostaglandin D2, which they previously found to be important in promoting healing and maintaining remission of the condition in laboratory rats.
"The levels of prostaglandin D2 were only elevated in those patients in long-term remission, and that suggests it is a key factor in preventing new episodes of ulcerative colitis," said John Wallace, director of the Institute and a professor of medicine for the Michael G. DeGroote School of Medicine.
Ulcerative colitis impacts 100,000 Canadians and millions worldwide, but has an unknown cause and limited treatment options. Most people are never cured, and often require surgical removal of the colon.
The discovery may lead to a new treatment for inflammatory bowel disease which would promote production of prostaglandin D2, Wallace said. "It is entirely possible our findings could extend to Crohn's disease as well."
The study by Wallace and post doctoral student Linda Vong with colleagues from the University of Calgary is being published in the journal Proceedings of the National Academy of Sciences (PNAS) on June 14. Funding for the research was provided by the Canadian Institutes for Health Research and the Crohn's and Colitis Foundation of Canada.
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The above story is reprinted from materials provided by McMaster University, via EurekAlert!, a service of AAAS.
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Journal Reference:
- Linda Vong, Jose G. P. Ferraz, Remo Panaccione, Paul L. Beck, John L. Wallace. A pro-resolution mediator, prostaglandin D2, is specifically up-regulated in individuals in long-term remission from ulcerative colitis. Proceedings of the National Academy of Sciences, 2010; DOI: 10.1073/pnas.1004982107
Note: If no author is given, the source is cited instead.
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