n South African Journal of Obstetrics and Gynaecology - Maternal levels of free fetal DNA are elevated in pregnancies with growth restriction due to placental dysfunction : a preliminary study : research article
|Article Title||Maternal levels of free fetal DNA are elevated in pregnancies with growth restriction due to placental dysfunction : a preliminary study : research article|
|© Publisher:||Health and Medical Publishing Group (HMPG)|
|Journal||South African Journal of Obstetrics and Gynaecology|
|Author||Medhat S. Alberry, Sebastian Illanis, Deborah G. Maddocks, Sherif A. Fattah, Bernhard G. Zimmermann, Neil D. Avent and Peter W. Soothill|
|Publication Date||Apr 2007|
|Pages||60 - 63|
|Keyword(s)||Growth restriction, Maternal levels of free fetal DNA, Placental dysfunction and Pregnancies|
Objective. Fetal growth restriction (FGR) is associated with an increased risk of perinatal mortality and morbidity but can have many different causes. Non-cellular fetal DNA in maternal blood offers many opportunities for noninvasive prenatal diagnosis. It is likely that the source of the DNA is apoptosis or cell death in the placenta and that free fetal DNA (ffDNA) levels could theoretically be increased in placental dysfunction or infarction. We hypothesised that non-cellular fetal DNA levels would be increased only in the subset of FGR cases with placental dysfunction, which could explain previous contradictory reports.
Methods. We used plasma samples obtained during a previous study from pregnant women with singleton male pregnancies as controls and from women with small-for-gestational-age (SGA) infants that had been classified as having FGR due to placental dysfunction. A third group was defined as normal but small fetuses with placental function within the normal ranges indicated by Doppler studies. Twenty-two cases were identified in the third trimester of pregnancy (8 from the control group and 7 from each of the FGR and the normal small groups). DNA was extracted and the DYS14 gene of the Y chromosome was quantified by real-time quantitative polymerase chain reaction (PCR).
Results. ffDNA levels were higher in pregnancies with FGR due to placental dysfunction than in either normal pregnancies or those with SGA fetuses from causes other than placental dysfunction. There was no significant difference in the ffDNA levels between the fetuses of normal growth and those with FGR from other causes.
Conclusion. The level of ffDNA in maternal plasma is increased in pregnancies complicated by FGR secondary to placental dysfunction but not in those with small fetuses with normal placental function.
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