The University of Rochester has filed a patent on several ideas to help prevent early labor and the premature delivery of low-birth-weight babies. The discovery is an incremental step in an area of obstetrics that has seen little improvement in 20 years.
Mark Plessinger, Ph.D., assistant professor of Obstetrics and Gynecology at the University of Rochester Medical Center, discovered that certain proteins known as toll-like receptors (TLRs), located in the amniotic membranes of pregnant women, sometimes fuel a harmful inflammatory response. The inflammation, in turn, may cause the fetal membranes to rupture and lead to preterm labor.
The pending University patent protects the development of a chemical test to ascertain the effectiveness of drugs that could be used to treat women at greater risk of preterm delivery. Other claims of the patent protect the idea that once these agents are identified, a drug might be developed to block the TLRs and stop early labor.
Plessinger is showcasing the research this week in Toronto at the annual meeting of the Society for Gynecological Investigation. Although doctors today can treat women in early labor with antibiotics and other drugs designed to slow contractions, studies have demonstrated that this approach is often ineffective.
"I am optimistic that we have landed on a novel idea," Plessinger said, "although it is far from therapeutic intervention."
Premature delivery is when an infant is born before 37 weeks of pregnancy. It occurs in about 12 percent of pregnancies in the United States and is the leading cause of infant death, according to the National Vital Statistics Report for 2004. When premature babies do survive they often face many health problems.
To better understand what brings on preterm labor, Plessinger started by isolating the cells within the amniotic membranes. The membranes are balloon-like, wrapping around the fetus and the amniotic fluid in which the fetus is bathed. The cells within the membranes (both fibroblasts and epithelial) are critical to the chemical process that causes the premature rupture of the fetal membranes. This is known as when a woman's "water breaks," and once that happens it is difficult to stop the ensuing delivery.