Written by Staff Writer at CNN
Each year in the US, the Centers for Disease Control and Prevention says 20,000 babies are stillborn due to complications during pregnancy.
Now researchers from Johns Hopkins University say they’ve discovered why.
For the study, which appears in the journal Molecular Psychiatry, the team studied CEDI4 expression among members of a family with two different disorders — heparin intolerance syndrome and organ stunting.
Heparin intolerance syndrome — which can cause intense abdominal pain, constipation and loss of appetite — was associated with CEDI4 expression in the mothers’ blood, which, in turn, disrupted fetal development.
Organ stunting — which is a condition where organs such as the liver and the kidneys don’t develop normally — also occurred in the families with low CEDI4 expression in blood. This coupled with multiple stillbirths in each pregnancy, was found to be the cause.
The researchers also found that prolonged periods of blood cell deterioration was associated with stillbirths in the families of abnormal CEDI4 expression in blood.
A previous study found the rate of stillbirths in the US is less than 1% among women with normal CEDI4 expression in their blood. However, Dr. Linda Taddie from the Johns Hopkins Bloomberg School of Public Health said there was a distinct increase in stillbirths in mothers with abnormal CEDI4 expression in their blood.
“The variance in stillbirth rates across women with normal CEDI4 expression in their blood is about 1%,” she said. “So, this study sheds new light on how CEDI4 expression may affect congenital malformations and stillbirths.”
The researchers have since created a strategy to identify which patients have abnormal levels of CEDI4 in their blood. In the laboratory, they identified that circulating levels of CEDI4 differ between pre- and post-cord clamping.
“In spite of a clear link between CEDI4 expression and abnormal stillbirth and organ dysfunction, there have been many studies indicating that poor prenatal health is not the main cause of fetal death,” said Maria Tomassi, first author of the study.
“With higher levels of CEDI4 present in the blood, abnormally-expressed immune cells are more likely to have positive effects on the fetus.”
“Using gene expression analysis, we were able to pinpoint which abnormal blood CEDI4 expression families may be more likely to have premature fetal death. This study, which demonstrates the biological basis of CEDI4 status, could improve our ability to identify babies at risk of poor fetal outcomes, including premature births, as well as identify individuals with greater chances of having a normal outcome if obstetric care is optimally delivered.”