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English Abstract
Journal Article
[Fetal D gene in maternal plasma should be examined in all immunized Rh(-) pregnant women to avoid invasive procedures].
Ginekologia Polska 2006 May
UNLABELLED: We have recently developed and published a noninvasive determination of fetal RhD status by examination of cell-free DNA in maternal plasma. The predictive value of the procedure of fetal testing, already published by us, was 99,6%.
AIM: To assess the necessity of RhD fetal testing in immunized Rh(-) mothers with Rh(+) partners.
MATERIAL: Rh(-) mothers with anti-D antibodies, their partners and children.
METHODS: Molecular: RHD gene examination by real-time polymerase chain reaction; analysis of control genes present in the father but not in the mother. Serological: titre of anti-D antibodies, Rh phenotypes.
RESULTS: Among 53 Rh(+) partners of immunized Rh(-) pregnant women, 56,6% were homozygous and 43,6%--heterozygous. The latter ones might have had either Rh(+) or Rh(-) children; in fact, in 52,2% of fetuses the D gene was not detected. Among fetuses of homozygous fathers (based on their phenotypes) 2 fetuses, to our surprise, occured to be Rh(-); however the subsequent genotyping showed that both fathers were heterozygous. The titres of anti-D in both groups of mothers with Rh(-) and Rh(+) fetuses were very similar.
CONCLUSIONS: The examination of fetal D gene by noninvasive method should be performed in each alloimmunised Rh(-) mother if her partner is Rh(+). The prediction of RhD fetal status based on the fathers phenotype can be misleading, thus may result in unnecessary invasive method.
AIM: To assess the necessity of RhD fetal testing in immunized Rh(-) mothers with Rh(+) partners.
MATERIAL: Rh(-) mothers with anti-D antibodies, their partners and children.
METHODS: Molecular: RHD gene examination by real-time polymerase chain reaction; analysis of control genes present in the father but not in the mother. Serological: titre of anti-D antibodies, Rh phenotypes.
RESULTS: Among 53 Rh(+) partners of immunized Rh(-) pregnant women, 56,6% were homozygous and 43,6%--heterozygous. The latter ones might have had either Rh(+) or Rh(-) children; in fact, in 52,2% of fetuses the D gene was not detected. Among fetuses of homozygous fathers (based on their phenotypes) 2 fetuses, to our surprise, occured to be Rh(-); however the subsequent genotyping showed that both fathers were heterozygous. The titres of anti-D in both groups of mothers with Rh(-) and Rh(+) fetuses were very similar.
CONCLUSIONS: The examination of fetal D gene by noninvasive method should be performed in each alloimmunised Rh(-) mother if her partner is Rh(+). The prediction of RhD fetal status based on the fathers phenotype can be misleading, thus may result in unnecessary invasive method.
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