Scientists may have figured out what causes the intestines of premature infants to become infected, a major cause of death in babies born before 36 weeks.
The condition, called necrotizing enterocolitis (NEC), is fatal about 30 percent of the time. A new study links it to a disruption in mitochondrial metabolism, which generates the energy needed for cells in the body to work properly.
“Early detection of NEC would give doctors a chance to head off the disease before it’s too late.”
“At this time we think the discovery that mitochondrial metabolism is a hallmark of mature intestinal development may provide a new way to screen and diagnose NEC before children are born, or at the time of their birth,” says Michael Verzi, assistant professor in genetics at Rutgers University-New Brunswick and the study’s lead author. “Early detection of NEC would give doctors a chance to head off the disease before it’s too late.”
Babies with the disease—which results in a swollen belly, fever, and constipation usually within two weeks of birth—are treated with intravenous fluids, antibiotics, or surgery. While research indicates it’s much less common in babies who are fed breast milk, even infants treated successfully for NEC can have problems absorbing nutrients as they develop.
The new study, published in the journal Development, suggests a genetic deficiency might stop this critical process from occurring in the fetus near the end of gestation, when the intestines should become fully developed. Although more research is needed to determine the exact cause, scientists say one possibility for the deficiency may be linked to a mother’s exposure to environmental toxins during pregnancy, which inhibit the process from taking place.
“Without this metabolic process, the intestine cannot fully mature,” Verzi says. “If children are born before their intestine is fully developed, it can lead to severe inflammation that leads to tissue death.”
Verzi and his team examined data from premature infants who died as a result of the disease and conducted studies on mice in which the gene needed to regulate the mitochondrial function was inactivated in the developing intestine. When the mitochondrial metabolism was blocked, the intestine was not able to mature, he says.
“This shift in metabolism during intestinal development has never been recognized as crucial for intestinal growth to take place,” Verzi says. “We think that the deficiencies in this important mitochondrial function serve not only as a cause for NEC but also could become a marker to help identify babies at risk.”
Source: Rutgers University
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