Pilot study of HLA alloimmunization after transfusion with pre‐storage leucodepleted blood products in aplastic anaemia

• Published in: British journal of haematology 1997-06, Vol.97 (3), p.677-684
• Main Authors: KILLICK, S. B., WIN, N., MARSH, J. C. W., KAYE, T., YANDLE, A., HUMPHRIES, C., KNOWLES, S. M., GORDON‐SMITH, E. C.
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Aged; Aged, 80 and over; Anemia, Aplastic - therapy; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; aplastic anaemia; Biological and medical sciences; Blood Component Transfusion - adverse effects; Blood Group Incompatibility - etiology; Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis; Female; HLA antibodies; HLA Antigens - immunology; Humans; leucodepletion; Male; Medical sciences; Middle Aged; Pilot Projects; Prognosis; transfusions; Transfusions. Complications. Transfusion reactions. Cell and gene therapy
• ISSN: 0007-1048; 1365-2141
• DOI: 10.1046/j.1365-2141.1997.812721.x

We have performed a pilot study to examine the incidence of alloimmunization using pre‐storage leucocyte‐depleted blood products (PLDP) in 16 previously transfused aplastic anaemia (AA) patients with no detectable HLA antibodies. A further eight AA patients with HLA antibodies received HLA‐matched PLDP. Leucodepleted apheresed platelets were obtained using either Cobe spectra or Haemonetics system with an integral pall filter. Pall BPF4 filters were used for red cell preparation. Patients’ sera were tested for HLA antibodies using lymphocytotoxicity (LCT). Patients who were HLA antibody negative by LCT at study entry were further tested with enzyme‐linked immunoassay (ELISA). Out of 16 patients, two (12%) formed anti‐HLA antibodies with a median follow‐up of 9 months (range 1–15), but did not display platelet refractoriness to random donor platelets. Two patients were inadvertently transfused with non‐leucodepleted blood products when later referred back to their local hospital. Both subsequently demonstrated HLA antibodies by LCT and became platelet refractory. These results contrast with a 50% incidence of HLA alloimmunization in a control group of AA patients transfused prior to this study with non‐PLDP. HLA antibodies could no longer be detected by LCT in follow‐up of three out of eight patients with HLA antibodies at study entry. Only one patient experienced non‐haemolytic febrile transfusion reactions (NHFTR). We conclude that PLDP reduce the risk of alloimmunization even in previously transfused AA patients, PLDP are associated with a low incidence of NHFTR, and all new AA patients should receive PLDP from diagnosis.