Dr. Sudhansu K. Dey, director of Reproductive Sciences at Cincinnati Children's Hospital Medical Center, and colleagues have reported the first successful prevention of preterm birth caused by a combination of genetic factors and environmental stress leading to inflammation in the Aug. 27, 2013, issue of the Journal of Clinical Investigation.
The researcher used a mouse model and identified the same chemical compounds in human females that lead to early birth and a much higher death in children than children who are carried to full term.
Two factors were found to produce a higher propensity to preterm birth. A genetic defect in the TP53 gene was found to initiate the production of prostaglandins that trigger uterine contractions. Inflammation increased the potential for preterm birth.
The researchers found a preterm birth rate of 50 percent in mice that were genetically altered to lack the TP53 gene. Inflammation produced a premature birth rate of 100 percent.
The relationship to human preterm births is in the chemistry. The same gene defect and inflammation were found in human females that experienced preterm births.
The high incidence of preterm births in developed countries were due inflammation caused by chronic diseases like diabetes and hypertension while high rates of preterm births in less developed countries were the result of inflammation caused by disease. The defect in the TP53 gene was common to all women who experienced preterm births regardless of the country they lived in.
The researchers found that an injection of small amounts of a combination of rapamycin and progesterone was successful in preventing preterm births in mice. The treatment produced no side effects for mothers or offspring. Progesterone is presently used as a preventative for preterm births in humans. Similar testing is planned for women who are at higher risk for preterm birth.