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Dr. Melissa Halpern will research a gastrointestinal disorder that kills thousands of premature babies each year.

By Darci Slaten, AHSC Office of Public Affairs
April 3, 2008

A researcher at The University of Arizona College of Medicine is making progress to determine the cause of an inflammatory gastrointestinal disorder that kills thousands of premature infants each year.

Dr. Melissa Halpern, a research assistant professor at the Steele Children’s Research Center at the UA College of Medicine, recently received a five-year grant from the National Institutes of Health to investigate the mechanisms involved in the development of Necrotizing Enterocolitis, known as NEC, a painful inflammatory gastrointestinal disorder.

Each year, an estimated 9,000 premature infants are diagnosed with NEC in the United States, and 20-50 percent won’t survive. For reasons unknown, these numbers are increasing annually.

The exact cause of NEC is unknown, and no specific treatments exist for this devastating disease. In severe cases, a child’s inflamed intestines may tear or perforate, allowing bacteria to leak into the abdomen, potentially causing a life-threatening systemic infection.

Damaged intestines may require surgery to remove the infected areas. Unfortunately, many children who have surgical intervention must face lifelong digestive difficulties. New research also has shown a higher rate of learning disabilities in children who developed NEC as newborns.

Halpern and her team were the first to show that elevated levels of intestinal bile acids contribute to disease development.

Building upon its past research, her laboratory now is focused on understanding why bile acids accumulate in the intestine, causing the damage that leads to NEC.

For a variety of reasons, babies born prematurely usually are fed formula instead of breast milk. The essential fats in formula are different than those in breast milk and require more bile acids to break down the fats for digestion.

Normally, the liver produces bile acids and sends them to the intestines to do their job of breaking down the fats. Transporter systems move the bile acids into the intestinal cells to complete the digestion process.

Next, another transporter system removes the bile acids from the cells and takes them back to the liver, where the liver determines if more bile acids are needed for digestion. With NEC, however, this doesn’t happen.

Halpern and her team hypothesize that there is a malfunction with the transport system responsible for exporting the bile acids from the cells back to the liver. “Essentially, we believe that the transporter mechanisms fail to adequately remove the bile acids from the intestinal cells. Because little bile is recirculated back to the liver, the liver continues to send more bile acids to the intestine. Consequently, bile continues to accumulate, causing damage to the intestines, leading to NEC,” Halpern said.

“Our grant is exploring the reasons why the transport mechanisms are faulty,” Halpern said. “If these hypotheses are verified through our research, we may be able to use elevated levels of bile acids in premature infants’ intestines to predict which babies are at risk of developing NEC. Once identified, we can intervene before irreparable damage to the intestine occurs.”