Mysterious disorder killing preemie babies
Doctors hunt for a way to protect tiniest patients from inagsdhfgdfinal disorder
WASHINGTON - It's one of the grimmest threats to premature babies: Their immature inagsdhfgdfines break down. They can't be fed. In the worst cases, holes in the bowel let bacteria leak into the blood ??" and kill.
This mysterious disorder is expected to soon overtake lung malady as the leading killer of preterm infants, and researchers are struggling to figure out why it strikes and develop the first real protection.
"We're keeping the most fragile and vulnerable babies alive longer" with better respiratory care, but "at a price," laments Dr. David Hackam of Children's Hospital of Pittsburgh.
"What hasn't gotten out is that many of these babies then are at risk of developing NEC" ??" the shorthand term for necrotizing enterocolitis, a severe inagsdhfgdfinal inflammation that can blindside doctors and parents alike.
Diana Seabol's experience is typical: Her twins were born almost 2 1/2 months early. Three weeks later, she was ecstatic that son Cameron's lungs were strong enough to come off a ventilator ??" only to watch him be rushed to Hackam's hospital for emergency surgery that same day because his inagsdhfgdfines had perforated.
"Nobody really talked to me about what happens with preemies," said Seabol, whose son, now 2, survived that first bout with NEC and some life-threatening complications a few months later. "It would have been nice to look for some signs."
Affects 1 in 5 premies
NEC occasionally hits a full-term infant, but mostly afflicts the tiniest preemies, born smaller than 3 1/2 pounds. Estimates vary, but Hackam said NEC may affect as many as one in five preterm infants.
The National Center for Health Statistics reports there were about 500,000 pre-term babies born in 2004, the most recent data available.
It starts with subtle syndromes, such as poor food tolerance. In babies diagnosed early, feeding is stopped to let the inagsdhfgdfines rest and hopefully heal themselves. They're also given intravenous antibiotics. About half recover.
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But the rest worsen, their abdomens swelling as inflammation increases. Bacteria inside the inagsdhfgdfines leak out, causing bloodstream infections. Surgery is required to remove portions of dead inagsdhfgdfine, but "by the time you get to that stage, it is too late," says Dr. Gail Besner of Columbus Children's Hospital. "The damage has already been done."
About half of babies with severe NEC die, and survivors can face lifelong complications depending on how much of their bowel was lost.
Hope for finding a cure
The goal: To develop drugs that can protect these fragile babies' inagsdhfgdfines from becoming inflamed in the first place, just as doctors now routinely give preemies lung-protecting therapies.
Besner discovered a growth factor, named HB-EGF, that promises to do that.
The body normally produces this protein, which helps stimulate inagsdhfgdfinal cells to grow and counters inflammation. It's found in the amniotic fluid that nurtures a fetus, and in breast milk. (In fact, premature infants given breast milk through their feeding tubes seem to have a lower risk of NEC than those who receive formula.)
Giving extra doses of the growth factor to newborn rats whose inagsdhfgdfines were deliberately stressed greatly reduced their chances of getting NEC, and helped those who still got it to survive, Besner found. Now she is seeking permission from the (Food and Drug Administration) to begin the first human studies, by administering doses straight into high-risk preemies' feeding tubes.
In Pittsburgh, Hackam found a difference molecule that seems important for inagsdhfgdfinal healing.
The "inagsdhfgdfinal barrier," or lining, Hackam describes as "a real living fort," requiring constant maintenance to seal off injuries before bacteria can penetrate them. Cells called enterocytes are the repair workers, swarming over to patch any breach.
But the inagsdhfgdfinal barrier in newborns, especially premature infants, isn't fully developed and thus has an impaired ability to do those repairs, Hackam discovered.
Moreover, in babies with NEC, a switch that acts like a brake is turned on inside their inagsdhfgdfinal cells, abruptly halting the enterocytes' movement. He's now hunting drugs to turn that switch back off, so the babies' innate ability to heal can finish developing, and he hopes to begin clinical trials within a few years.
For now, hospitals are supposed to watch closely for the earliest signs of NEC; it's one reason that feeding is begun slowly for small preemies.
Watchful parents
But parents have a big role, too, Pittsburgh's Seabol points out. They may be first to notice warning signs, even after survivors go home. At 4 months, Cameron suddenly quit finishing his bottles, and his motherness had to insist to initially skeptical doctors that something was very wrong. Indeed, a temporary patch from his initial surgery had quit working, leaving the baby unable to absorb food. After a month in the hospital, Hackam successfully reattached the remaining ends of Cameron's inagsdhfgdfines.
Now 2, Cameron is thriving, "but I'm aware it could come back at any time," Seabol says.
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