Transcript ABO Antibodies

ABO/Rh Blood Group System
A . Amirzargar
Carl Landsteiner:
1. Discovered the ABO Blood Group System in 1901
2. He and five co-workers began mixing each others
red blood cells and serum together and
inadvertently performed the first forward and
reverse ABO groupings.
3. Landsteiners Rule: If an antigen is present on a
patients red blood cells the corresponding antibody
will NOT be present in the patients plasma, under
‘normal conditions’.
Blood group systems
Each system represents either a single gene or a
cluster of two or three closely linked homologous
genes
ABO Blood Group System


The ABO Blood Group System was the first
to be identified and is the most significant
for transfusion practice.
It is the ONLY system that the reciprocal
(antithetical) antibodies are consistently and
predictably present in the sera of people who have
had no exposure to human red cells.
Major ABO Blood Groups
ABO
Group
Antigen
Present
Antigen
Missing
Antibody
Present
A
A
B
Anti-B
B
B
A
Anti-A
O
None
A and B
Anti-A,B
AB
A and B
None
None
Forward Grouping
Definition: Determination of ABO antigens found on patient red
blood cells using reagent antisera.
Patient Red Cells Tested With:
Patient
Anti-A
Anti-B
Interpretation
1
0
0
O
2
4+
0
A
3
0
4+
B
4
4+
4+
AB
Reverse Grouping
Definition: Determination of ABO antibodies found in patient
serum using reagent red blood cells.
Patient Serum Tested With:
Patient
A1 Cells
B Cells
Interpretation
1
4+
4+
O
2
0
4+
A
3
4+
0
B
4
0
0
AB
Reaction of Cells
Tested With:
Reaction of Serum
Tested Against:
ABO
Group
% US
White
Pop.
% US
Black
Pop.
Anti-A
Anti-B
A Cells
B Cells
1.
0
0
+
+
O
45
49
2.
+
0
0
+
A
40
27
3.
0
+
+
0
B
11
20
4.
+
+
0
0
AB
4
4
H Antigen
The H gene on ch. 19 near the Se gene, codes for an enzyme (fucosylytranferase)
that adds a Fucose to the terminal sugar of a Precursor Substance (PS*). The
biochemical structure below constitutes the H Antigen. (h gene is an amorph.)
H gene acts on a
Precursor
substance(PS)*
by adding
Fucose
*PS = oligosaccharide chain
attached to either glycosphingolipid, Type 2 chain (on RBC) or
glycoprotein, Type 1 chain (in
secretions)
H antigen is the foundation upon
which A and B antigens are built.
A and B genes code for
enzymes that add an
immunodominant sugar to the
H antigen.
Formation of the
A Antigen
The A gene codes
for an enzyme that
adds GalNAc
(N-Acetyl-D
galactosamine)
to the terminal
sugar of the
H Antigen.
This biochemical structure
constitutes the A antigen.
Formation of the
B Antigen
B gene codes for an
enzyme that adds
D-Galactose
to the terminal sugar
of the H Antigen.
This biochemical structure
constitutes the B Antigen.
The H antigen is found on
the rbc when you have the Hh
or HH genotypes but NOT
with the hh genotype.
The A antigen is found on
the rbc when you have the
Hh, HH, and A/A, A/O or A/B
genotypes.
The B antigen is found on
the rbc when you have the
Hh, HH, and B/B, B/O or
A/B genotypes.
ABO Genetics
Genes at three separate loci control the
OCCURRENCE and LOCATION of A and B
antigens
Hh genes – H and h alleles

1.
–
–
H allele codes for a fucosyltransferase enzyme
that adds a fucose on Type 2 chains (primarily)
to form the H antigen onto which A and B
antigens are built on red blood cells.
h allele is a silent allele (amorph)
• A, B and H antigens are built on
oligosaccharide chains of 4
types. The most common
forms are Type 1 and Type 2.
Type 1: #1 carbon of Gal is
attached to the #3 carbon of
GlcNAc.
Type 2: #1 carbon of Gal is
attached to the #4 carbon of
GlcNAc.
ABO Genetics
2. Se genes – Se and se alleles
–
–
Se allele codes for a fucosyltransferase enzyme that
adds fuscos onto Type 1 chains (primarily) in
secretory glands. Controls expression of H antigens
in secretions (i.e. saliva, body fluids, etc.)
se allele is an amorph
3. ABO genes – A, B and O alleles
–
A and B alleles code for glycosyltransferase enzymes
that add a sugar onto H antigens to produce A and B
antigens
H Ag concentration in ABO
17
Amount of H Antigen According
to Blood Group
• Blood Group O people
have red blood cells rich
in H antigen. Why?
Greatest
Amount of H
Neither the A or B genes
have converted the H
antigens to A or B antigens
- just a whole bunch of H!
O > A2 > B > A2B > A1 > A1B
Least
Amount of H
Bombay (Oh) Phenotype




Homozygous inheritance of the h gene (hh) results in
the inability to form the H antigen and subsequently
the A or B antigens.
This is referred as the Bombay or Oh phenotype due to
the location of its discovery.
This phenotype has no H, A or B antigens on the red
blood cell membrane, only an abundant amount of
precursor substance.
They also have anti-H, anti-A and Anti-B. What blood
type can we safely transfuse?
ABO Antigens in Secretions

Secretions:
–

Body fluids including plasma, saliva, synovial fluid, etc.
Blood Group Substance: Soluble antigen
–
Soluble antigen found in the secretions not bound to a
membrane such as a rbc or epithelial cell.
Soluble blood group substances (A, B and H) can be
found in the secretions. This is controlled by the H and
Se genes.
FORMATION OF ABO ANTIGENS IN
SECRETIONS
Se/se
PS1
H/H
PS2
genes
A/O
H Ag
genes
A, H Ag
genes
From left to right is the gene interactions
necessary for the production of ABH antigens
in secretions. Must have Se gene (78% of
population) for ABO Ag’s to be in secretions.
FORMATION OF ABO ANTIGENS IN
SECRETIONS
Se/se
PS1
H/H
PS2
genes
O/O
H Ag
genes
H Ag
genes
Inheritance of the O/O genotype results in the
presence of only H antigen in the secretions.
LACK OF ABO ANTIGENS IN SECRETIONS
Se/se
PS1
h/h
PS2
genes
A/O
PS2
genes
PS2
genes
Two mechanisms exist that account for a
LACK of ABO antigens in secretions:
Either se/se or h/h genotypes.
LACK OF ABO ANTIGENS IN SECRETIONS
se/se
PS1
H/h
PS1
genes
A/O
PS1
genes
PS1
genes
Two mechanisms exist that account for a
LACK of ABO antigens in secretions:
Either se/se or h/h genotypes.
ABO Antibodies


Generally IgM class antibodies.
ABO Antibody Development: Hypothesis
–
Immune response following exposure to
environmental antigens (such as bacterial cell
walls) similar to A and B antigens during infancy
results in production of ABO antibodies.
Remember, babies have a tendency to put
EVERYTHING into their mouths…
ABO Antibodies




For Group A and Group B persons the
predominant antibody class is IgM
For Group O people the dominant antibody class is
IgG (with some IgM)
React best at room temperature (22-24oC) or
below in vitro.
Activates complement to completion at 37oC
–

Can cause acute hemolytic transfusion reactions
RBC Immune form: Predominantly IgG
Which ABO blood group presents a higher risk for
Hemolytic Disease of the Newborn? Why?


Group O - because the dominant immunoglobulin
class is IgG, which crosses the placenta.
Group A and B can but only the immune form. Which
means that only after exposure to foreign ABO
antigens will the mother make immune anti-A or antiB that is predominantly IgG.
ABO Antibodies


Time of appearance:
Generally present within first 4-6 months of life
– Do we perform a reverse grouping on newborns
(<4-6 months of age) and cord blood?
– If there are anti-A or anti-B antibodies in newborn serum where did
they most likely originate? What source?
ABO antibody titers with age:
– Reach adult level at 5-10 years of age
– Level off through adult life
– Begin to decrease in later years: >65 years of age
ABO Antibodies
Group O Phenotype

Anti-A,B Antibody
–

Inseparable anti-A and anti-B antibody. If we add A
cells to anti-A,B serum all of the antibody activity is
removed, not just anti-A!!
RBC immune Anti-A,B
–
When exposed to Group A or B antigens (or both)
Group O persons will have an immune response that
results in the production of separate immune anti-A
and/or anti-B antibodies. This could be seen in a
fetomaternal bleed of a Group O mom with a Group A
baby. (Hemolytic Disease of the Newborn)
ABO Antibodies
Group B or O phenotype

Have both anti-A and Anti-A1 antibodies
Anti-A

Reacts with both A1 and A2 red blood cell antigens
Anti-A1


Reacts only with A1 antigens on red blood cells
A2 and A2B phenotypes can make anti-A1 antibodies.
What is clinical significance? Thermal range is up to
25oC - not usually clinically significant. Can cause an
ABO discrepancy.
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ABO Antibodies

Is there a reagent anti-A1 antisera?
 NO!!

But there is Dolichos biflorus, a plant lectin
that has anti-A1 activity when diluted properly.
This is not an antibody, but a chemical that
acts like an antibody in that it specifically
agglutinates A1 red blood cells.

ABO Subgroups

ABO Phenotypes that differ in the amount of antigen
carried on red cell and saliva, for secretors: There are
fewer Ag sites!

Subgroups are the results of less effective
glycosyltransferase enzymes – just not as good at
attaching the immunodominant sugar to the H antigen.

Subgroups of A are more common than Subgroups of B.
ABO Subgroups

80% of all Group A’s are A1 and about 19%
are A2.
–
–
–

A1’s have 4-6 times the # of antigen sites on the
RBC surface than A2’s.
Both react strongly with reagent Anti-A but…
Only A1 cells are agglutinated with Dolichos
biflorus plant lectin and not A2 cells.
The remainder of the Subgroups of A have
even weaker expression of A antigen.
Rh Blood Group System

Currently
–
–
–
5 common antigen
three nomenclatures
two theories of inheritance
Rh antigen
Rh antigene
Antigens





Rho ( D )
rh’ ( C )
hr’ ( c )
rh’’ ( E )
hr’’ ( e )
Rho (D) antigen




A very potent antigen (50% may form
antibody to exposure)
85% positive - Rh positive
15% negative - Rh negative
no allele found
Inheritance

Fisher - Race
–
–
–
Rh antigens produced under the control of three
sets of allelic genes at closely linked locus
Nomenclature is C, D, E, c, e
Certain combinations of the antigens that are
inherited more often than others
41
Fisher-Race



There are 8 gene
complexes at the Rh
locus
Fisher-Race uses
DCE as the order
It is often written
alphabetically as CDE
DCe
dCe
DcE
dCE
Dce
dcE
DCE
dce
** Sometimes “d” is written just to
indicate that D is absent
42
Weak D Phenotype

Most D positive rbc’s react macroscopically with Reagent
anti-D at immediate spin
–
–

These patients are referred to as Rh positive
Reacting from 1+ to 3+ or greater
HOWEVER,
some D-positive rbc’s DO NOT react
(do NOT agglutinate) at Immediate Spin using Reagent
Anti-D.
These require further testing (37oC and/or AHG) to
determine the D status of the patient.
Weakened Antigens


The Rh-Hr system has a number of antigens
that are suppressed by other antigens or only
a weakened form of the antigens are present
Weakened D antigen
–
–
–
often does not react with initial spin
may require 37o incubation or antiglobulin test to
detect sensitization
two forms - inherited or suppression by C antigen
in the trans position
Weak D Mechanism’s
There are three mechanisms that account for
the Weak D antigen.
1.
2.
3.
Genetically Transmissible
Position Effect
Partial D (D Mosaic)
Genetically Transmissible

The RHD gene codes for weakened expression
of D antigen in this mechanism.
–
–



D antigen is complete, there are just fewer D Ag
sites on the rbc. Quantitative!
Common in Black population (usually Dce
haplotype). Very rare in White population.
Agglutinate weakly or not at all at immediate
spin phase.
Agglutinate strongly at AHG phase.
Can safely transfuse D positive blood
components.
Position Effect
(Gene interaction effect)

C allele in trans position to D allele
–
Example: Dce/dCe, DcE/dCE
In both of these cases the C allele is in the trans
position in relation to the D allele.

D antigen is normal, C antigen appears to be
crowding the D antigen. (Steric hindrance)

Does NOT happen when C is in cis position

Example: DCe/dce
Can safely transfuse D positive blood components.
–
Position Effect
C in trans position to D:
Dce/dCe
Weak D
C in cis position to D:
DCe/dce
48
NO weak D
Partial D (D Mosaic)

Missing one or more PARTS of the D antigen
–

D antigen comprises many epitopes
PROBLEM
–
Person types D positive but forms alloanti-D that
reacts with all D positive RBCs except their OWN.
Partial D: Multiple epitopes make up D antigen. Each
color represents a different epitope of the D antigen.
A.
B.
Patient B lacks
one D epitope.
The difference between Patient A and Patient B is a single
epitope of the D antigen. The problem is that Patient B can make
an antibody to Patient A even though both appear to have the
entire D antigen present on their red blood cell’s using routine antiD typing reagents..
D Mosaic/Partial D

If the patient is transfused with D positive red
cells, they may develop an anti-D
alloantibody* to the part of the antigen
(epitope) that is missing
Missing
portion
RBC
RBC
51
*alloantibody- antibody produced with specificity other than self
Weak-D Determination:
Donor Blood

When testing Donor Blood for the D antigen,
testing is required through all phases.
–

We need to know the D Status of all Donor
Blood. Why?
–

Weak-D testing is REQUIRED
Main problem is Rh Negative women of child bearing
age and pediatric patients.
Donor RBCs are labelled Rh positive if any
part of the D antigen is present on the red blood
cell membrane.
Unusual Phenotypes
D-Deletion
Rh null
53

No reaction when RBCs are tested with anti-E,
anti-e, anti-C or anti-c

Requires transfusion of other D-deletion red
cells, because these individuals may produce
antibodies with single or separate specificities(
anti-Hr0 or anti-Rh17)

Red cells that lack C/c or E/e antigens may
demonstrate stronger D antigen activity
Written as D- - or -D-

54
D-Deletion
Rh Null

Lack all Rh antigens

The lack of antigens causes the red cell membrane
abnormalities
Immunized idividuals have anti-Rh29( “Total Rh” or Rh29)


2 Rh null phenotypes:
– Regulatory type– gene inherited(Xºr)
(X¹r is a normal regulator gene) the Rh gene are inherited
but not expressed.
Amorph type –Result from the r amorph gene
RHD gene is absent, lack of expression of the RHCE gene
–
55
Rh Antibodies





Most antibodies react at 37o and require a
coombs procedure to demonstrate the
reaction.
Some react at saline and room temperature
Most are IgG
None fix Complement
All are important in HDN and HTR
Rh System Antibodies
1.
React optimally
1.
37oC and AHG Phases
2.
RBC Immune
2.
Transfusion or pregnancy,
IgG, HDN, HTR, etc.
3.
Clinically Significant
3.
Will result in shortened red
cell survival - need to
transfuse antigen negative
blood
Rh typing



Normal typing for Rh antigens only includes
typing for Rho (D).
The result of this typing determines the Rh
status of the cells (Rh - positive or Rh negative). Other antigens are identified for
genotyping
Some Rh typing sera is diluted in high protein
solutions and may require a negative control.
HEMOLYTIC DISEASE
OF THE NEWBORN
HDN: THE DISEASE





Caused by blood group system or HLA
maternal/fetal incompatibility (mother has IgG1 or
IgG3 Abs to Ag on baby RBCs)
With Rh HDN, previous matherno-fetal bleeds
usually the stimulus for Ab production; with other
HDNs, stimulus may be unclear
Begins in utero
Range of severity from asymptomatic --> mild
anemia --> kernicterus --> stillborn
ABO, Rh, and Kell groups most commonly
involved
Categories of HDN
1.
Rh System
Antibodies
1.
Most severe form of HDN.
•
•
2.
3.
Other Blood
Group Antibodies
ABO Antibodies
Anti-D
Less common due to RhIg
1.
Anti-K, -Fya, -s, etc.
2.
Least severe. Group O mom
with A or B fetus. Most
common form of HDN.
ABO vs. Rh HDN
Rh
ABO
Mother
Negative
Group O
Infant
Positive
A or B (AB)
Occurrence in first born
5%
40-50%
Stillbirth and or hydrops
Frequent
Rare
Severe Anemia
Frequent
Rare
DAT
Positive
Pos or Negative
Spherocytes
None
Present
Exchange Transfusion
Frequent
Infrequent
Phototherapy
Adjunct to exchange
Often only treatment









Risk is also increased in pregnancies complicated by :
placental abruption
spontaneous or therapeutic abortion
Toxemia
after cesarean delivery
ectopic pregnancy
Amniocentesis
chorionic villus sampling
cordocentesis

After sensitization, maternal anti-D antibodies cross the
placenta into fetal circulation and attach to Rh antigen on
fetal RBCs, which form rosettes on macrophages in the
reticuloendothelial system, especially in the spleen.

These antibody-coated RBCs are lysed by lysosomal
enzymes released by macrophages and natural killer
lymphocytes, and they are independent of the activation
of the complement system
Rh HDN



Most severe form of HDN
(Usually*) affects only 2nd or subsequent
pregnancies (mother allo-immunized at delivery
of 1st pregnancy; has pre-formed Abs during
subsequent pregnancies)
Usually Ab directed to D Ag but Abs to C, c, and
E also seen
BEFORE BIRTH




Antibodies cause destruction of the red cells
Anemia
heart failure
fetal death
Metabolism of bilirubin:




Before delivery:
Fetal bilirubin produced by the breakdown of
sensitized RBCs in fetal spleen is sefely
metabolized by the maternal liver.
After delivery:
Newborn’s liver doesn’t produce glucuronyl
transferase and cannot convert bilirubin to an
excretable form.as a result,it collects in tissues
and causes brain damage.
Metabilim of bilirubin:
HDN: SIGNS & SYMPTOMS


Anemia (Hb < 16 mg/dL) - begins in utero
Increased bilirubin - begins after birth
–
–


Baby’s liver does not conjugate bilirubin efficiently;
unconjugated (toxic) bilirubin increases as RBCs
continue to be destroyed
If > 18 mg/dL, may have to exchange transfuse
Jaundice
Hepato- and splenomegaly
AFTER BIRTH






Antibodies cause destruction of the red cells
Anemia
Heart failure
Build up of bilirubin
Kernicterus
Severe retardation
PROBLEMS FOR BABY

Anemia
–
–


heart failure
erythroblastosis
General edema
-Called hydrops fetalis and erythroblastosis fetalis
Kernicterus ( a condition with severe neural symptoms,
associated with high level of bilirubin in the blood)
–
severe retardation


Bilirubin has been postulated to cause neurotoxicity via 4 distinct
mechanisms:
(1) interruption of normal neurotransmission (inhibits phosphorylation of
enzymes critical in release of neurotransmitters)
(2) mitochondrial dysfunction

(3) cellular and intracellular membrane impairment (bilirubin acid affects
membrane ion channels and precipitates on phospholipid membranes of
mitochondria

(4) interference with enzyme activity (binds to specific bilirubin receptor sites
on enzymes).

PREVENTION

Before birth
–

Work up mother for risk and evaluation of complications
After birth
–
Rh immune globulin - IgG anti-D given to prevent primary
immunization

Before birth workup
–
–
Identify women at risk
ABO - Rh -(Du) - Antibody screen

–
–
based on results continue testing (Handout)
IgM antibodies are insignificant
IgG antibodies - titer - freeze and store retiter with a second sample - looking for
a 1:32 rise or change in titer

Before birth workup
–
titer identifies mothers who need
amniocentesis
–
titer every 4 week until 24th week - then every
2 weeks
–
amniocentesis is performed after 21st week on
high titer - high mortality
PRENATAL TESTING



Test father to see if he is Ag positive (if he is
negative, not a concern)
If Ab is significant and father is positive for
Ag, perform Ab titers (> 32 significant) on
mother’s serum
If serum Ab titer high, test amniocytes for
presence of Ag
PRENATAL TESTING



ABO/Rh type (including Dw) & Ab screen at 1st visit
If Ab screen neg., repeat at 24 weeks; if Ab screen
pos., perform Ab ID
If Ab is to IgM or IgG,
–
–
determine if IgM or IgG by treating serum with DTT (DTT
destroys IgMs)
Repeat Ab ID (using treated serum) for detection of IgGs that
the IgMs may be masking (IgMs are not a HDN concern)
Amniocentesis
Intrauterine transfusions
 Bilirubin
 Hb is below 11 g/dL
–
Usually O and compatible with mother’s antibody
–
CMV, Hb S, and leukocyte negative
–
immediate correction of anemia and resolution of fetal hydrops,
reduced rate of hemolysis and subsequent hyperinsulinemia, and
acceleration of fetal growth for nonhydropic fetuses who often are
growth retarded

Post Natal Laboratory Studies

Mother
–

ABO - Rh - Du (micro) - Antibody screen Antibody identification if necessary
Baby
–
–
–
ABO - Rh - Du - DAT for IgG antibodies - elute
DAT positive and identify antibody
CBC
Imaging studies
TREATMENT

Exchange transfusion

Phototherapy

After birth

Rh Immune Globulin
–
–
–
Give antenatal 28 -32 weeks
also after amniocentesis - IUT - abortion - ectopic
pregnancy - miscarriage
Each vial contains 300 ugm and will prevent
sensitization by 15 ml RBC or 30 ml whole blood
Rh (D) HDN: PREVENTION





Rh Immune Globulin is a potent solution of Anti-D
Anti-D covers D epitopes in baby RBCs in maternal
circulation
Coated cells removed by splenic macrophages
D-bearing RBCs destroyed before mother can mount
immune response
Very effective preventative treatment
Rh (D) HDN: PREVENTION

Rh Immune Globulin given to mother at 28
weeks gestation and within 72 hours of
delivery of infant if:
–
–
–

Baby is Rh positive
Rh type of fetus is unknown, and
Mother is known to be negative for Anti-D
Dosage calculated using results of the
Kleihauer-Betke test


1 Rh Immune Globulin dose protects against 30 mL
fetal whole blood
Kleihauer-Betke test
– sample from mother treated with acid then stained;
fetal cells resistant to acid, maternal cells become
ghost cells
– determine # fetal cells in first 2000 maternal cells
counted
– % fetal x 50 = Whole blood bleed

It should be considered if the total serum
bilirubin level is approaching 20 mg/dL and
continues to rise despite intense in-hospital
phototherapy.
Selection of blood for exchange
transfusion:







Group o(or ABO-compatible)
Fresh(less than 7 days old)RBCs resuspended
in fresh frozen plasma
CMV negative
Irradiate blood
HbS negative
Blood lack of Ag corresponding to maternal Ab
Compatible crossmatch with maternal serum

Exchange Transfusions Objectives
–
decrease serum bilirubin and prevent kernicterus
–
provide compatible red cells to provide oxygen
carrying capacity
–
decrease amount of incompatible antibody
–
remove fetal antibody coated red cells

The following are requirements for exchange transfusion :

Severe anemia (Hb <10 g/dL)

Rate of bilirubin rises more than 0.5 mg/dL despite
optimal phototherapy

Hyperbilirubinemia

DAT
 Potential
complications of exchange
transfusion include the following:
–
–
–
–
–
–
Cardiac - Arrhythmia, volume overload, congestive failure,
and arrest
Hematologic - Overheparinization, neutropenia,
thrombocytopenia, and graft versus host disease
Infectious - Bacterial, viral (CMV, HIV, hepatitis), and
malarial
Metabolic - Acidosis, hypocalcemia, hypoglycemia,
hyperkalemia, and hypernatremia
Vascular - Embolization, thrombosis, necrotizing
enterocolitis, and perforation of umbilical vessel
Systemic - Hypothermia
Phototherapy
 Phototherapy
–
The efficacy of phototherapy depends on the spectrum of light delivered,
the blue-green region of visible light being the most effective; irradiance
(mW/cm2/nm); and surface area of the infant exposed.
–
Nonpolar bilirubin is converted into 2 types of water-soluble
photoisomers as a result of phototherapy. The initial and most rapidly
formed configurational isomer 4z, 15e bilirubin accounts for 20% of total
serum bilirubin level in newborns undergoing phototherapy and is
produced maximally at conventional levels of irradiance (6-9
mW/cm2/nm).
Phototherapy

The structural isomer lumirubin is formed slowly, and its
formation is irreversible and is directly proportional to the
irradiance of phototherapy on skin.

Lumirubin is the predominant isomer formed during highintensity phototherapy. Decrease in bilirubin is mainly the result
of excretion of these photoproducts in bile and removal via
stool.

In the absence of conjugation, these photoisomers can be
reabsorbed by way of the enterohepatic circulation and
diminish the effectiveness of phototherapy
ABO HDN






Most common form of HDN
Mother is “O” with IgG form of Anti-A,B
Baby is “A” or “B”
May occur with 1st or subsequent pregnancies
Usually less severe than Rh HDN (babies’ A and B
Ags not fully developed)
Most cases treated only with phototherapy
ABO incompatibility

ABO incompatibility is limited to type O mothers with fetuses
who have type A or B blood

in type O mothers, the antibodies are predominantly IgG in
nature

Because A and B antigens are widely expressed in a variety of
tissues besides RBCs, only small portion of antibodies crossing
the placenta is available to bind to fetal RBCs. In addition, fetal
RBCs appear to have less surface expression of A or B
antigen, resulting in few reactive sites—hence the low
incidence of significant hemolysis in affected neonates.
ABO HDN: PREVENTION AND
TREATMENT




Not preventable as with Rh (D) HDN
Usually treatable using only phototherapy
If exchange transfusion required, use type
“O” cells and “AB” plasma
ABO HDN sometimes protects babies from
the more severe forms of Rh HDN