RT Book, Section
A1 Fasano, Ross M.
A1 Hendrickson, Jeanne E.
A1 Luban, Naomi L.C.
A2 Prchal, Josef T.
A2 Lichtman, Marshall A.
SR Print(0)
ID 1184013664
T1 Alloimmune Hemolytic Disease of the Fetus and Newborn
T2 Williams Hematology The Red Cell and Its Diseases
YR 2022
FD 2022
PB McGraw Hill
PP New York, NY
SN 9781264269075
LK hemonc.mhmedical.com/content.aspx?aid=1184013664
RD 2024/04/16
AB SUMMARYAlloimmune  hemolytic  disease  of  the  fetus  and  newborn  (HDFN)  is  caused  by  the  action  of  transplacentally  transmitted  maternal  immunoglobulin  (Ig)  G  antibodies  on  paternally  inherited  antigens  present  on  fetal  red  cells  but  absent  on  the  maternal  red  cells.  Maternal  IgG  antibodies  bind  to  fetal  red  cells,  causing  hemolysis  or  suppression  of  erythropoiesis.  As  a  consequence,  anemia,  extramedullary  hematopoiesis,  and  neonatal  hyperbilirubinemia  may  result,  with  severe  cases  resulting  in  fetal  loss  or  neonatal  death  or  disability.  Collaboration  among  maternal–fetal  medicine  specialists,  hematologists,  transfusion  medicine  physicians,  radiologists,  and  neonatologists  has  substantially  reduced  perinatal  mortality  and  morbidity  resulting  from  hemolytic  disease  of  the  fetus  and  newborn.  Antenatal  diagnostic  methods  identify  at  risk  fetuses  and  assess  disease  severity  in  affected  fetuses.  After  birth,  phototherapy  and  exchange  transfusions  prevent  serum  bilirubin  from  rising  to  levels  that  could  produce  bilirubin  encephalopathy  and  resultant  brain  damage  (kernicterus),  remove  maternal  antibody,  and  replace  circulating  fetal  red  blood  cells  with  those  negative  for  the  implicated  antigen(s).  Rho(D)  immunoglobulin  (RhIg)  has  successfully  prevented  alloimmune  hemolytic  disease  resulting  from  rhesus  D  sensitization  in  many  at  risk  infants,  but  there  is  not  enough  RhIg  available  to  distribute  to  all  women  at  risk  worldwide,  and  no  prophylactic  therapy  exists  as  of  this  writing  to  prevent  alloimmune  hemolytic  disease  resulting  from  other  red  cell  antibodies.  Advances  in  immunohematology  and  molecular  biology  may  offer  new  avenues  for  prevention  and  treatment  in  the  future.