ABO Blood Group
There are 4 common blood groups in the ABO system: A, B, AB, and O.
- These blood groups are defined by the presence of specific antigens on RBCs.
- Blood group A: antigen A
- Blood group B: antigen B
- Blood group AB: antigens A and B
- Blood group O: no antigens
- A and B antigens consist of specific carbohydrate sugars:
- N-acetylgalactosamine for the A antigen
- D-galactose for the B antigen
- Both of these sugars bind to and modify the H antigen on the surface of RBCs.
- If the H antigen is left unmodified, the resulting blood group is O.
- There are over 80 ABO alleles: The most common are A1, A2, B1, O1, O1v, and O2.
Blood-type frequencies vary in different racial/ethnic groups. The ABO blood type is inherited in an autosomal codominant fashion:
- The A and B alleles are codominant.
- The O allele is recessive.
|Mother A||Mother B||Mother O|
|A + A||A|
|A + O||A|
|A + B||AB|
|B + B||B|
|B + O||B|
|O + O||O|
Individuals will naturally develop antibodies (Abs) against the ABO antigens they do not have:
- Individuals with blood group A have anti-B Ab.
- Individuals with blood group B have anti-A Ab.
- Individuals with blood group O will have both anti-A and anti-B Abs.
These Abs can elicit a hemolytic response upon encountering their respective antigen:
- An ABO-incompatible blood transfusion can be fatal.
- A universal RBC donor has type O blood.
- A universal plasma donor has type AB blood.
Blood groups are associated with differential risk to certain diseases. Blood group O may have ↓ risk for:
- Pancreatic cancer
- Thromboembolic disease
Rh factor (Rhesus factor) is an RBC surface antigen.
- Encoded by the 2 genes RHD and RHCE:
- ↑ Polymorphism: Numerous genetic rearrangements produce distinct Rh antigens.
- 50 Rh group antigens (5 are important)
- 85% of people carry the D allele: They are Rh+.
- 15% do not carry it: They are Rh–.
- Rh– persons do not carry anti-Rh Ab unless they are exposed to Rh+ RBCs.
Anti-Rh Abs occur when:
- Rh– blood is transfused into Rh+ person:
- Causes an acute hemolytic reaction
- Results in a mild hemolytic anemia
- Rh– pregnant mother is exposed to Rh+ fetal RBCs:
- Secondary to fetomaternal hemorrhage from abortion, trauma, invasive obstetric procedures, or normal delivery
- Mother produces Abs against the baby’s RBCs.
- Abs are IgG and cross the placenta.
- Abs can cause hemolysis to the fetus (also called hemolytic disease of the newborn or erythroblastosis fetalis).
- Anti-D Ig is administered to sensitized women after pregnancy to avoid this reaction.
If fetus is Rh+ and the mother Rh–, serial monitoring during pregnancy is needed and is accomplished by:
- Serial indirect Coombs test in mother
- Measurement of fetal blood flow velocity in middle cerebral artery by Doppler
Other Blood Groups
- 3rd most potent immunogenic antigen after ABO and Rh system
- 25 Kell antigens have been discovered.
- Defined by the immune Ab anti-K
- Anti-K Ab causes:
- Severe hemolytic disease of the fetus and newborn
- Hemolytic transfusion reactions
- Duffy antigen was 1st isolated from a patient with hemophilia.
- Also known as Fy glycoprotein
- 2 alleles exist:
- There are 4 possible phenotypes:
- Nonspecific receptor for chemokines and the malaria parasite Plasmodium vivax
- Associated Abs are IgG and can cause hemolytic transfusion reactions.
- Kidd antigen (Jk antigen) acts as an urea transporter in RBC and renal endothelium.
- 3 antigens have been identified to date:
- Kidd Ab can cause severe transfusion reactions.
Complications of Blood Transfusion
Complications of blood transfusion can be acute (minutes to hours) or delayed (days to months).
- Hemolytic reaction:
- Due to IgM antibodies against RBCs
- Typically of the ABO group
- Delayed: IgG antibodies are not present during transfusion but develop later.
- Due to aged RBCs
- Improper storage
- Transfusion along noncompatible medications
- Transfusion through small-bore IV tubes
- Viral: HIV, hepatitis C virus, hepatitis B virus, human T-lymphotropic virus 1 or 2
- Allergic reaction:
- Mild: hives, pruritus
- Severe, leading to anaphylaxis:
- GI symptoms
- Systemic organ failure
- Due to sensitization to antigens in the donor unit, especially plasma proteins
- Transfusion-related acute lung injury (TRALI):
- Within 6 hours after transfusion
- Causes noncardiogenic pulmonary edema with severe hypoxemia
- Diagnosis requires no other risk factors for acute lung injury.
- Due to activation of recipient’s immune system by anti-HLA or anti-neutrophil Ab
- Acute febrile nonhemolytic reaction:
- ↑ Body temperature by 1°F (-17°C) within 24 hours after blood transfusion
- More frequent with:
- Repeated transfusions
- Due to release of Ab-mediated endogenous pyrogens and cytokines
- Circulatory overload:
- Due to rapid transfusion of large volume of blood products
- ↑ Risk:
- Underlying cardiopulmonary disease
- Renal failure
- Chronic anemia
- Elderly patients
- Signs and symptoms include:
- ↑ HR, dyspnea, cough
- ↑ Central venous pressure, widened pulse pressure
- Chest radiography shows cardiomegaly and pulmonary edema.
- Iron overload:
- In patients who receive blood long term and regularly
- 1 unit of RBC = 200 mg of iron
- Iron accumulation can occur and is toxic for tissues and organs.
- Management: iron chelation
- Graft-versus-host disease:
- Due to proliferation of donor’s lymphocytes, which attack recipient’s tissues and organs
- Symptoms include:
- Rash, fever, diarrhea, liver dysfunction, and pancytopenia
- Symptoms occur 1–6 weeks after transfusion
- Fatal in > 90% of cases
- ↑ Risk in:
- History of Hodgkin disease
- History of stem cell transplantation
- History of solid tumors treated with cytotoxic drugs
- Intensive chemotherapy
- Blood transfusion from relative (shared HLA haplotypes)
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