Red Blood Cell Alloimmunization in Pregnancy

Division of Maternal-Fetal Medicine, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7516, USA.
Seminars in Hematology (Impact Factor: 3.27). 08/2005; 42(3):169-78. DOI: 10.1053/j.seminhematol.2005.04.007
Source: PubMed


Red blood cell (RBC) alloimmunization in pregnancy continues to occur despite the widespread use of both antenatal and postpartum Rhesus immune globulin (RhIG), due mainly to inadvertent omissions in administration as well as antenatal sensitization prior to RhIG given at 28 weeks' gestation. Additional instances are attributable to the lack of immune globulins to other RBC antigens. Evaluation of the alloimmunized pregnancy begins with the maternal titer. Once a critical value [32 for anti-Rh(D) and other irregular antibodies; 8 for anti-K and -k] is reached, fetal surveillance using serial Doppler ultrasound measurements of the peak velocity in the fetal middle cerebral artery (MCA) is standard. In the case of a heterozygous paternal phenotype, amniocentesis can be performed to detect the antigen-negative fetus that requires no further evaluation. MCA velocities greater than 1.5 multiples of the median necessitate cordocentesis, and if fetal anemia is detected, intrauterine transfusion therapy is initiated. A perinatal survival of greater than 85% with normal neurologic outcome is now expected. Future therapies will target specific immune manipulations in the pregnant patient.

28 Reads
  • Source
    • "The use of anti-D immunoglobulin for RhD prophylaxis has led to a significant reduction in perinatal mortality and morbidity from HDFN. However, severe cases still persist and despite the widespread use of Rh (D) immune globulin, it remains to be one of the most commonly detected antibody in Rh negative females [7] [9]. In addition, there has also been a relative increase in the importance of non-Rh (D) alloimmunization as a cause of haemolytic disease of the fetus or newborn [10]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Haemolytic disease of the fetus and the newborn [HDFN] is caused by incompatibility of maternal and fetal erythrocytes. Red blood cell alloimmunization is a well-known cause of HDFN. Due to heterogeneity of populations, the spectrum of alloimmunization varies around the world. This study aimed to determine the frequency of alloimmunization in pregnant women and to determine the risk of HDFN in our population. This was a descriptive study conducted at Aga Khan University Hospital Karachi. Blood type and red cell antibody screening was determined on every pregnant woman at her first antenatal visit. Red cell antibody identification was performed on positive screening results. A total of 1000 pregnant females including 633 (63.3%) multigravida were studied. Blood type B was predominant (n = 374 or 37.4%) and D negative was observed in 136 women (13.6%). No red cell antibody was detected in 982 females (98.2%). 20 red cell antibodies were detected in 18 women (1.8%). The incidence of non-anti-D was 16/1000 [1.6%] in all pregnant females. The non-anti-D alloantibodies included anti-M (n = 3; 15%), anti-Lewis(a) (n = 3; 15%), anti C ( n = 1; 5%), anti-E (n = 1; 5%), anti-e (n = 1; 5%), anti-Lewis(b) (n = 1; 5%) and nonspecific antibodies (n = 6; 30%). The incidence of anti-D was 4/136 or 2.9% in D negative blood type. After excluding prior sensitization due to blood transfusions, risk remained was 2.2%. Antibodies of clinical significance were identified in 9 (0.9%) females. In our cohort, frequency of red cell alloimmunization during pregnancy was 1. 8% out of which 0.9% were clinically significant antibodies posing a risk for HDFN. Despite prenatal and post natal prophylaxis, risk of sensitization with D antigen in D negative women was high at 2.2%. We recommend that all pregnant women should be screened for irregular antibodies irrespective of the rhesus type. Copyright © 2014. Published by Elsevier Ltd.
    Transfusion and Apheresis Science 12/2014; 52(1). DOI:10.1016/j.transci.2014.12.002 · 0.77 Impact Factor
  • Source
    • "Cells from fetal origin were first recognized in 1893 by Schmorl [1], but in most cases, the cause of FMH IS unknown [2]. Obstetric risk factors (caesarean section, multiple pregnancy, placenta praevia, vasa praevia, miscarriage , therapeutic termination of pregnancy and manual placental extraction), in-utero therapeutic interventions procedures (external cephalic version, transfusion, surgery , amniocentesis and cordocentesis) and trauma to abdomen/placenta (motor vehicle accident, and placenta abruption) [3] [4] have majorly been implicated as possible associated factors. Some studies have suggested that * Financial disclosure: We declare that no funding/grant was received for this study and no conflict of interest or commercial relationship. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Purpose: Feto-maternal haemorrhage (FMH) is a complication of pregnancy and large FMH may lead to life-threaten-ing anaemia in the fetus or newborn. In addition, exposure of Rhesus (Rh) D negative women to small amounts of fetal Rh D positive red cells during pregnancy or delivery may result in sensitization with its attendant problems of isoim-munisation. In most cases, the cause of FMH IS unknown. Through this study, we sought to determine if placental weight & diameter have any direct relationship with incidence and severity of FMH. Methods: This was a prospective study of parturients for presence of fetal red cells in the maternal blood circulation. The prepared slide was processed as in the acid elution test described by Kleihauer-Betke. The FMH was calculated using Mollison formula. Baseline data included maternal biodata, blood group, Rh D factor, placenta weight and diameter. Data generated were analysed with Frequency tables, cross-tabulations and Odd ratio and confidence intervals as appropriate. Results: Three hundred par-turients were studied. However, only two hundred and ninety-five parturients were analysed, with five excluded due to lysed blood samples. A total of 52 parturients (17.63%) had demonstrable FMH, of which 8 (2.71%) were large FMH (>15 ml foetal cells). Both the placenta weight (P < 0.005) and diameter (P < 0.042) were significantly associated with incidence of FMH, more with placenta weight than diameter. Incidence of demonstrable FMH was 24.12% (48/199) in the group with placenta weight greater than 500 g, in contrast to 4.17% (4/96) in the group with weight of placenta be-low or equal to 500 g. All the 8 parturients with large FMH had placenta weights greater than 500 g. Placenta diameters were greater than 22 cm in 41/197 (20.81%) who had demonstrable FMH, compared with 11/98 (11.23%) whose di-ameter was less than 22 cm. Conclusion: Both the placenta weight and diameter are significant predictors of FMH in parturients. However, placenta diameter appears to be a minor predictor. These are factors that can be assessed antena-tally by ultrasonography and in conjunction with other known obstetric factors, may possibly be considered in risk-based scoring system for predicting feto-maternal haemorrhage.
    International Journal of Clinical Medicine 03/2013; 443024(03):133-136. DOI:10.4236/ijcm.2013.43024
  • Source
    • "The laboratory investigations of the immune response to blood group antigens that result from transfusion or pregnancy have taught that human red cell membranes are very pleomorphic. Moieties exist on the surface of red cells that are 'foreign' (antigenic) among humans [1] [2]. These moieties have a variety of structural and functional properties, either of which are affected by changes in their amino acid composition [3]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Antigen diversity arises from changes at the gene level that range from single nucleotide polymorphisms (SNPs) to intra- and inter-genic exchanges, inversions, insertions, and deletions. Nucleotide changes often result in amino acid difference from the wild-type gene product and with those changes new blood group antigens arise. Alternatively, there is loss of expression altogether, which is deemed the 'null' phenotype. Near complete knowledge of the genetic changes underlying the expression of blood group antigens will lead to the reality that red cell genotyping as a test-of-record. The importance of molecular testing in immunohematology necessitates appropriate training and competency programs to ensure that the highly skilled staff has the appropriate knowledge background. This review summarizes the core mechanisms for gene expression and provides a compilation of the molecular basis for blood group expression.
    Transfusion and Apheresis Science 02/2011; 44(1):53-63. DOI:10.1016/j.transci.2010.12.010 · 0.77 Impact Factor
Show more

Similar Publications