Balkan Journal of Medical Genetics

DETERMINATION OF FETAL RHESUS D STATUS BY MATERNAL PLASMA DNA ANALYSIS
Aykut A1,*, Onay H1, Sagol S2, Gunduz C3, Ozkinay F1, Cogulu O1
*Corresponding Author: Ayça Aykut, M.D., Ph.D., Department of Medical Genetics, Ege University Faculty of Medicine, 35100, Bornova, Izmir, Turkey; Tel.: +90-232-390-3961; Fax: +90-232-390-3971; E-mail: aycaaykut@hotmail.com
page: 33

INTRODUCTION

Rhesus D (RhD) alloimmunization still remains the major cause of severe hemolytic disease in fetuses and newborns (HDFN), which may lead to anemia, hydrops fetalis and intrauterine fetal death. The incidence of HDFN has been reduced by anti- RhD prophylaxis at the 28th and 34th week of gestation. Therefore, the demonstration of fetal D status is very important in the management of HDFN. Accurate prediction of the fetal RhD type provides prenatal prophylaxis in RhD-negative women with an RhD-positive fetus (about 40.0%) from unnecessary administration of anti D. The most common cause of RhD negativity is the absence of the RHD gene [1]. Consequently, most genotyping strategies are based on detecting the presence or absence of the RHD gene. An RhD status of the fetus can be detected by invasive methods of prenatal diagnostic tests such as amniocentesis and chorionic villus sampling (CVS) that require fetal tissue but may result in miscarriage or risk of increased maternal sensitization because of complications attributed to CVS or amniocentesis. Recent studies have focused on new non invasive prenatal diagnostic techniques such as circulating fetal nucleic acids in maternal plasma to develop reliable non invasive tests for clinical prenatal diagnosis for RhD status of the fetus [2-8]. In this study, we assessed the feasibility of fetal gender and RHD genotyping in the plasma samples of RhD-negative pregnant women by using primers and probes targeted toward the SRY gene and exons 7 and 10 of the RHD gene.

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