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Babies Born With Heart Disease Often Harmed by Gut Bacteria

THURSDAY, Sept. 1 (HealthDay News) -- Elevated blood levels of harmful toxins from gut bacteria occur in about one in five infants and toddlers with congenital heart disease, and the risk is even higher after they have heart surgery, a new study has found.

These endotoxins -- bacterial fragments that cross into the blood from the gut -- stimulate the immune system and can impair the function of vital organs, the study authors explained.

Researchers at Imperial College London in the United Kingdom measured endotoxin levels in 40 children, aged 2 months to 46 months, who required surgery for congenital heart disease.

About 20 percent of the children had higher than normal levels of endotoxin before surgery and that increased to 27.5 percent of the children after surgery, according to the findings published online Aug. 25 in the American Journal of Respiratory and Critical Care Medicine.

The researchers also found that children with high levels of endotoxins in their blood had more signs of organ dysfunction, took longer to recover from surgery, and tended to spend more time in intensive care.

Dr. Nazima Pathan, the lead author of the study from the National Heart and Lung Institute at Imperial College London, said: "The gut usually acts as a barrier that protects the body from toxins. However, our study suggests that in some babies with congenital heart disease, the gut isn't able to do this job properly. These babies are often small and undernourished, and the heart defect can mean that the blood supply to the gut is abnormal."

And, "on top of this they have to cope with the trauma of surgery and our study suggests that all these factors can affect the protective barrier function of the gut," Pathan explained in a college news release.

The researchers said they're now investigating how to protect children with congenital heart disease from these toxins.

More information

The American Heart Association has more about congenital heart defects.

-- Robert Preidt

SOURCE: Imperial College London, news release, Aug. 26, 2011

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