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Researchers Identify Possible Causative Mutation for Crohn's Disease: Crohn's & Colitis Foundation Annual Conference to Present Emerging Research
Date:11/24/2009

The molecular cause of inflammatory bowel disease is largely unknown, but research will be presented at the upcoming 2009 Advances in Inflammatory Bowel Diseases, the Crohn’s & Colitis Foundation’s Clinical & Research Conference, December 3-6 in Hollywood, Florida, that may identify a causative mutation for Crohn’s disease.

New York, NY (Vocus) November 24, 2009 -- The molecular cause of inflammatory bowel disease is largely unknown, but research will be presented at the upcoming 2009 Advances in Inflammatory Bowel Diseases, the Crohn’s & Colitis Foundation’s Clinical & Research Conference, December 3-6 in Hollywood, Florida, that may identify a causative mutation for Crohn’s disease. Evidence suggests that pathogenic mechanisms of Crohn’s disease may change with time, and the research abstract to be presented at the conference describes recessive mutations in the IL-10 receptor alpha and beta that may be causative for Crohn’s disease. The abstract was submitted by Dr. Bodo Grimbacher of the Department of Immunology and Molecular Pathology, Royal Free Hospital and University College London, and has recently been published in the New England Journal of Medicine (www.nejm.org, 11/4/09).

“This is very important and extremely exciting information, “says conference co-chair Richard P. MacDermott, MD of Albany Medical College. “Although just a first step in identifying the process that causes Crohn’s disease, eventually this may mean that successful treatment of patients may be possible using high local concentrations of interleukin-10.”

A record number of scientific abstracts have been submitted to the 2009 Advances in Inflammatory Bowel Diseases, outlining a broad scope of research projects. In addition to the I
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Researchers Identify Possible Causative Mutation for Crohn's Disease: Crohn's & Colitis Foundation Annual Conference to Present Emerging Research
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