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Scientists ID 2 New Genes for Bowel Disease in Kids

September 5 (HealthDay News) -- Variations of two new genes appear to increase the risk of developing inflammatory bowel disease in childhood, researchers say.

Inflammatory bowel disease (IBD) is a painful, chronic inflammation of the gastrointestinal tract. It affects about 2 million children and adults in the United States.

IBD that begins in childhood is usually more severe than that in adulthood.

A new study in the Aug. 31 online edition of Nature Genetics looked at DNA samples from 1,000 people who had childhood-onset IBD. To search for gene variations related to IBD, the researchers compared these DNA samples to those from 4,250 healthy people.

In addition to finding the gene variations that have been found in the past, the researchers found two new gene variants associated with childhood-onset IBD.

And future research may find that these new variants are also related to IBD that appears in adulthood.

"Although the gene variants we found may have a stronger signal in pediatric IBD than in adult-onset IBD, we do not believe them to be limited to varieties of the disease that begin in childhood," study co-first author Robert N. Baldassano, director of the Center for Pediatric Inflammatory Bowel Disease at The Children's Hospital in Philadelphia, said in a hospital news release.

The researchers proposed that their findings could lead to improvements in the treatment of IBD.

Current treatments of IBD include anti-TNF (tumor necrosis factor) medications such as infliximab, adalimumab and certolizumab. One of the new genes is already known to participate in the biological pathway of TNF.

"As we better understand the complex gene interactions in IBD, we may be able to diagnose patients by their genetic profile to predict who will better respond to anti-TNF drugs," study leader Hakon Hakonarson, director of the Center for Applied Genomics at The Children's Hospital, said in the news release.


SOURCE: The Children's Hospital of Philadelphia, news release, Aug. 31, 2008

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