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Rh positive (+) denotes presence of D antigen.

The number of antigenic sites on RBCs varies

with genotype. Prevalence of genotype varies with the population. Rh negative (d/d)
individuals comprise 15% of Caucasians, 5.5% of African Americans, and <1% of Asians. A
sensitized Rh negative mother produces anti-Rh IgG antibodies that cross the placenta. Risk
factors for antibody production include 2nd (or later) pregnancies*, maternal toxemia,
paternal zygosity (D/D rather than D/d), feto-maternal compatibility in ABO system and
antigen load.

The severity of the disease is variable and it may result in fetal hydrops, fetal anemia,
developmental problems, and even intrauterine death. Since the 1960s, routine antenatal
prophylaxis with anti-RhD immunoglobulin in the third trimester to prevent rhesus
sensitization for all RhD-negative pregnant women, regardless of the rhesus status of the
baby, has been standard in many countries as recommended by most clinical guidelines (1,2).
Anti-RhD immunoglobulin is given antenatally in the third trimester and repeated postpartum
prophylaxis within 72 h of delivery is offered only to RhD-negative women who have given
birth to an RhD-positive baby.
(Is the management of Rh-Rh incompatibility with noninvasive fetal Rh genotyping
for targeted prophylaxis cost-effective in the Turkish population?
Emine DEMREL1, Sefa KELEK1,*, Emre EKMEKC1, Mustafa ENGL1, Raziye
R1, Melahat ATASEVER2
1Department of Obstetrics and Gynecology, Faculty of Medicine, zmir Ktip elebi
University, zmir, Turkey 2Department of Obstetrics and Gynecology, Faculty of Medicine,
Giresun University, Giresun, Turkey)

The following step should be the assessment of fetal Rh D status to determining if the
pregnancy is at risk for the development of hemolytic disease of the fetus and newborn. In
fact, if the fetus is Rh D-negative doesnt require any intervention irrespective of maternal
antibodies titers. When paternity is certain, if the father is Rh D negative the fetus is also Rh
D negative. If the father is Rh D positive, he can be either homozygous or heterozygous for
the D allele. If he is homozygous for the D allele, the fetus is Rh D positive (3,4). However, if
the paternal phenotype is D antigen positive and his genotype is heterozygous, fetal antigen
status should be determined by amniocentesis at 15 weeks gestation (by PCR of fetal cells).
Chorionic villus sampling is possible as well but it has the disadvantage of potentially
worsening of maternal antibodies titers due to possible fetomaternal hemorrhage.

The most common causes of maternal Rh alloimmunisation are blood transfusion and
antepartum or intrapartum fetomaternal hemorrhage (abdominal trauma, abortion, ectopic
pregnancy, invasive obstetric procedures, placental abruption, external cephalic version). The
risk of alloimmunization is affected by several factors, including the degree of fetomaternal
hemorrhage and maternal immune respons.

In case of first affected pregnancy, Rh alloimmunizated women should undergo determination

of their anti-D antibody titers. In general, women with titers higher than 1:4 should be
considered Rh alloimmunized. Titers tend to correlate more reliably with the severity of fetal
disease in the first sensitized pregnancy than in subsequent pregnancies. These are usually
performed monthly until 24 weeks of gestation, after which time titers should be repeated
every 2 weeks. If titers remain below the critical titer, delivery can occur at term. A critical
titer is defined as the titer associated with a significant risk for fetal hydrops.
Fetal detailed ultrasonography assessment has an essential role in diagnosis and management
of fetal anemia. The sonographic findings in case of hydrops include ascites, pleural and
pericardial effusions and edema. Several other sonographic findings have been proposed as
possible indicators of fetal hydrops (polyhydramnios, increased placental thickness,
myocardial and bowel dilatation) but none of these has proven to be predictive of fetal

Fetal blood sampling by cordocentesis, is the only definitive approach in diagnosing of fetal
anemia and acidosis by direct measurement of the fetal hemoglobin and acid-base status.
When fetal hematocrits is less than 30%, the only therapeutic option is intrauterine fetal
transfusion (13,14).The source of red cells for intrauterine transfusion is typically a blood
type O, RhD-negative, cytomegalovirus- negative donor. Some centers prefer to use maternal
blood as the source of red cells. Units are irradiated to prevent graft-versus-host reaction and
processed through a leukocyte-poor filter. The purpose of intrauterine transfusion is to
maintain the fetal hemoglobin value at more than 9 g/dL. Serial intrauterine transfusions, if
required, are usually performed until 34 weeks gestation, because after this time the risk of
the procedure is greater than benefits. (Obstetric
management in
Rh alloimmunizated pregnancy)



Carmelina Cuschieri
A special project submitted in partial fulfillment of the requirements for the diploma of

Health Science

Medical Laboratory Science


An antigen is any agent capable of binding specifically to components of the immune

response, such as lymphocytes and antibodies. They are present on the surface of red cells,
white cells and platelets. Some of these antigens are shared by cells of different types, while
others are found only on one type of cell. An antigen-antibody reaction that involves red cells
leads to their destruction or agglutination. An antigen can be any foreign organic substance
that is large enough to stimulate the production of antibodies. Antigens may be proteins,
polysaccharides or any combination of biochemical molecules, such as glycoproteins,
lipoproteins and nucleoproteins. An antigen must have one or more antigenic sites, known as
epitopes, to which antibodies can bind. The important point is that antigens must be foreign
materials that the body does not recognize as self antigens. Before antibodies can be made,
a foreign molecule and the antibody-producing cell have to bind.

Factors important in determining actual antibody production include the following:

i. the amount of antigen reaching the antibody-producing cell and its nature,
ii. the number of times the antigen is present in the tissues,
iii. the time before the antigen is destroyed or eliminated,
iv. the way by which the antigen is introduced into the body, and
v. the composition of the animal or patient being immunized.

Antibodies are produced by B lymphocytes. Maturation culminates with migration of the B

cells to the reticulo-endothelial tissues of the body including the lymph nodes and parts of the
spleen, bone marrow, liver, gastrointestinal tract and other tissues. Antibodies are a
miscellaneous mixture of serum globulins and share the ability to bind individually to
specific antigens. Those serum globulins with antibody activity are known as
immunoglobulins (Ig). All immunoglobulin molecules have common structural features. The
part of the molecule that binds to the corresponding antigen is different in each
immunoglobulin. The basic structure of an immunoglobulin consists of two identical light (L)
chains and two identical heavy (H) chains.

When a Rhesus antigen is introduced in the body, through transfusion or pregnancy, a

corresponding Rhesus antibody is formed in response to it, but the degree of response varies
widely. It has been shown that some Rhesus negative people (about 30 percent), known as
non-responders, fail to produce anti-D in spite of repeated injections with Rhesus positive
blood. Those persons who produce anti-D after several injections will have low titre levels,
while those responding after a single injection of Rhesus positive blood generally acquire
high titres. It was also noted that those who respond to a low dose initially, often fail to
respond to a high dose later, and vice versa. A similar situation occurs during pregnancy.
Some Rhesus negative mothers may give birth to several Rhesus positive newborns without
forming anti-D, while others become immunized at the end of the first or second pregnancy.

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