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The development of anti-HLA antibodies in multiply transfused preterm infants
A R Bedford Russell1, R P Rivers, N Davey
1St Mary's Hospital Medical School, London.
Insights
Preterm infants receiving multiple blood transfusions can develop antihuman leucocyte antigen antibodies (aHLAA). Using leukocyte filters during transfusions prevented aHLAA development in this study.
Area of Science:
- Immunology
- Neonatology
- Transfusion Medicine
Background:
- Multiple blood transfusions are common in preterm infants.
- Preterm infants may develop antihuman leucocyte antigen antibodies (aHLAA) after transfusions.
- The impact of leukocyte filtration on aHLAA development in this population is not fully understood.
Purpose of the Study:
- To prospectively investigate the development of aHLAA in multiply transfused preterm infants.
- To determine if leukocyte filtration of blood products can prevent aHLAA formation.
Main Methods:
- Prospective randomized study of 57 preterm infants requiring at least two blood transfusions.
- Infants were randomized to receive either whole blood or leukocyte-filtered blood.
- Antihuman leucocyte antigen antibodies (aHLAA) were monitored via microlymphocytotoxicity assay in maternal, cord, and infant blood samples.
Main Results:
- Data were analyzed for 42 infants (19 filtered, 23 unfiltered).
- None of the infants receiving leukocyte-filtered blood developed aHLAA.
- Seven infants in the unfiltered group developed aHLAA.
Conclusions:
- Multiply transfused preterm infants possess the capacity to develop antibodies against HLA.
- Leukocyte filtration of blood products appears to be an effective strategy for preventing aHLAA development in these infants.
Abstract:
The development of antihuman leucocyte antigen antibodies (aHLAA) in response to multiple transfusions in preterm infants was studied prospectively. Fifty seven infants requiring a minimum of two blood transfusions were recruited after obtaining informed written parental consent. They were randomised to receive either whole blood or blood that had been passed through a leucocyte filter. Anti-HLAA were sought in maternal and cord blood so as to ensure that any aHLAA detected after transfusion had not been passively transferred antenatally, and in 1 ml samples drawn monthly from the baby, at least 10 days from a previous transfusion, until discharge from hospital. Anti-HLAA were detected by microlymphocytotoxicity assay. Results were obtained in 42 babies, 19 in the filter and 23 in the no filter group. Fifteen babies had to be excluded because of protocol violation or because they died. None of the babies receiving filtered blood developed aHLAA, but seven babies in the no filter group developed aHLAA. In conclusion, multiply transfused preterm infants have the ability to elaborate antibodies to HLA and leucocyte filters may prevent this.
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