Inflammation May Cause Premature Births
Predicting and preventing premature births are challenges that have long frustrated researchers and clinicians, as infants who are born too soon are at higher risk of death and disability than normal term newborns. A new study suggests that premature births may be caused by inflammation in the placenta or amniotic fluid, and that a certain marker may be a clue.
A premature birth is one in which the infant is delivered before 37 weeks of pregnancy. The National Institute of Child Health and Human Development notes that preterm births occur in about 12 percent of pregnancies in the United States, and that it is one of the main causes of infant deaths. Ten percent of premature infants develop a permanent disability such as cerebral palsy, blindness, or lung disease, and half of premature babies born before the 26th week of gestation are disabled, according to the Quint V. Boenker Preemie Survival Foundation.
It is very difficult to predict which women will have a premature infant, but now researchers at the Sahlgrenska Academy in Sweden have one possible clue. An examination of the amniotic fluid of 83 women who went into premature labor and of 15 women who elected a caesarean section at full term revealed that a marker associated with inflammation was much more prevalent in women who were “threatening preterm delivery and who had signs of infection in their amniotic fluid or placenta,” according to Christina Doverhag, a postgraduate student at the Department of Physiology at the Sahlgrenska Academy. This was the first time this marker, known as galectin-3, had been measured in amniotic fluid.
The research team also found a role for galectin-3 in brain damage in premature newborns or those who suffered a lack of oxygen during birth. For this they studied newborn mice and discovered that galectin-3 can exacerbate brain damage and that when they removed an enzyme called NADPH-oxidase, the brain injury and inflammation was even greater in some of the mice. From this Doverhag concluded that both galectin-3 and inflammation have a significant role in brain damage in newborn children.
This discovery is of special interest because some medications currently being developed for treatment of brain injury and stroke in adults are partly based on their ability to block NADPH-oxidase. This property appears to make them unsuitable for newborns and could also cause additional harm.
While many survivors of premature birth grow up healthy, others are not so lucky, despite the use of increasingly sophisticated medical technology. Premature births are associated with a greater risk for life-threatening infections and underdeveloped organs or organ systems, and half of all neurological disabilities in children are related to premature birth. More than 540,000 infants are born prematurely in the United States each year.
Doverhag emphasized a promising note: that lactose (milk sugar) is known to block galectin-3, and that investigators will soon be testing how it may be used to treat brain injury in newborns. More work remains to be done, however, before scientists fully understand the content of amniotic fluid and the role of the inflammation marker galectin-3 in premature births.
March of Dimes
National Institute of Child Health and Human Development
Quint V. Boenker Preemie Survival Foundation