Alloimmunisation

Alloimmunisation occurs as a result of an immune response after exposure to foreign antigens after blood transfusion, pregnancy or tissue transplant. This gives rise to alloantibodies against red cells, human leucocyte antigen (HLA) or human platelet antigen (HPA).(1)

Alloimmunisation against red cells results in an acute or delayed haemolytic transfusion reaction and haemolytic disease of the newborn. Approximately 1% of red cell transusions is associated with alloantibody formation (1) but may be much higher (up to 30%) in patients who are frequently transfused such as those with sickle cell disease and thalassaemia.(2)

HLA and HPA antibody formation may lead to platelet refractoriness where less than an expected rise in platelet count is seen after a platelet transfusion.(3) This may occur in about 20-70% of patients receiving multiple platelet transfusions.(4) Post-transfuson purpura can also occur as a consequence of development of HPA and HLA antibodies.

Alloimmunisation against HLA antigen is also implicated in transplant rejection, febrile non-haemolytic reaction and in TRALI.
 

Investigation

Obtain patient history of any previous transfusions, transplantations or pregnancies.

Perform an antibody screen tests on the patient’s plasma to detect clinically significant red cell antibodies, HLA or HPA antibodies.
 

What to do?

Treatment depends on the type and severity of the transfusion reaction with most reactions being mild. Alloimmunisation cannot be completely prevented. In Australia, all cellular blood products are leucodepleted where most white cells are removed by filtration to reduce the risk of HLA sensitisation. RhD immunoglobulin is also given to pregnant women who are RhD negative to prevent haemolytic disease of the newborn. To reduce the risk of TRALI plasma for FFP and cryoprecipitate is only accepted from males and apheresis platelets from males and nulliparous women only.

If a red cell alloantibody is identified, antigen-negative blood is warranted if further transfusion is needed.

With patients on long term transfusion support, eg patients with thalassaemia, giving phenotyped matched blood early in their chronic support may reduce the risk of further antibody development.(2)
 

References
  1. Fung MK, Grossman BJ, Hillyer CD, Westhoff CM (ed).      Non-infectious complications of blood transfusion. Chapter 27, AABB Technical Manual, 18th edition. AABB, Bethesda, 2014.
  2. Chou ST, Liem RI, Thompson AA.  Challenges of alloimmunization in patients with haemoglobinopathies.  BJH 2012;159(4):394-404.
  3. Hod E, Schwartz J.  Platelet transfusion refractoriness.  BJH 2008;142(3):348-360.
  4. Fung MK, Grossman BJ, Hillyer CD, Westhoff CM (ed).      Non-infectious complications of blood transfusion. Chapter 19, AABB Technical Manual, 18th edition. AABB, Bethesda, 2014.