TY - JOUR
T1 - Obstetric outcome after RhD and Kell testing
AU - Lipitz, S.
AU - Many, A.
AU - Mitrani-Rosenbaum, S.
AU - Carp, H.
AU - Frenkel, Y.
AU - Achiron, R.
PY - 1998
Y1 - 1998
N2 - The study was conducted to report on the use of molecular biology methods and pregnancy outcome in women sensitized to either Rhesus D (RhD) or Kell 1 (K1) antigens. Paternal RhD genotype was determined by DNA amplification of an RhD-specific sequence from single sperm cells. Paternal Kell phenotype was determined by serologic assays using peripheral blood samples, and the fetal RhD or Kell-type status were established by the polymerase chain reaction (PCR) with amniotic cells. Thirteen women (14 pregnancies, one with twins) sensitized to RhD and four sensitized to K1 antigens, comprised the study group, All had paternal heterozygosity to either D or K1 antigens. Nine fetuses were RhD positive and five were RhD negative, An additional woman under went early spontaneous abortion. The nine RhD-positive fetuses underwent a total of 41 invasive procedures. One fetus with hydrops fetalis died in utero after intrauterine blood transfusion. All the remaining RhD-positive fetuses were delivered after 33 weeks gestation, and all those who were RhD negative were delivered at term. Four women were sensitized to the K1 antigen; in three, the fetus was found to be K1 negative, and in one, K1 positive, necessitating intrauterine blood transfusion. In all cases, the results of RhD or Kl genotype analyses from amniotic fluid were compatible with fetal/neonatal red blood cell RhD or Kell phenotypes. In conclusion, the use of molecular biology techniques represents a major advance in the clinical management of RhD and Kell alloimmunization.
AB - The study was conducted to report on the use of molecular biology methods and pregnancy outcome in women sensitized to either Rhesus D (RhD) or Kell 1 (K1) antigens. Paternal RhD genotype was determined by DNA amplification of an RhD-specific sequence from single sperm cells. Paternal Kell phenotype was determined by serologic assays using peripheral blood samples, and the fetal RhD or Kell-type status were established by the polymerase chain reaction (PCR) with amniotic cells. Thirteen women (14 pregnancies, one with twins) sensitized to RhD and four sensitized to K1 antigens, comprised the study group, All had paternal heterozygosity to either D or K1 antigens. Nine fetuses were RhD positive and five were RhD negative, An additional woman under went early spontaneous abortion. The nine RhD-positive fetuses underwent a total of 41 invasive procedures. One fetus with hydrops fetalis died in utero after intrauterine blood transfusion. All the remaining RhD-positive fetuses were delivered after 33 weeks gestation, and all those who were RhD negative were delivered at term. Four women were sensitized to the K1 antigen; in three, the fetus was found to be K1 negative, and in one, K1 positive, necessitating intrauterine blood transfusion. In all cases, the results of RhD or Kl genotype analyses from amniotic fluid were compatible with fetal/neonatal red blood cell RhD or Kell phenotypes. In conclusion, the use of molecular biology techniques represents a major advance in the clinical management of RhD and Kell alloimmunization.
KW - Fetal haemolytic disease
KW - Kell
KW - RhD
UR - http://www.scopus.com/inward/record.url?scp=0031832157&partnerID=8YFLogxK
U2 - 10.1093/humrep/13.6.1472
DO - 10.1093/humrep/13.6.1472
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AN - SCOPUS:0031832157
SN - 0268-1161
VL - 13
SP - 1472
EP - 1475
JO - Human Reproduction
JF - Human Reproduction
IS - 6
ER -