Correspondence

ACID ELUTION OF PLATELETS HLA-CLASS I ANTIGENSIN THE TREATMENT OF A REFRACTORY PATIENT

Platelet refractoriness is a not infrequent and life-threaten-ing complication during myelosupressive treatments forcancer. This implies the inability of transfused platelets toincrease patients’ platelet counts or stop the bleeding.

There are few options in supporting patients when theybecame refractory to platelets’ transfusions. The mostcommon situation causing refractoriness is the developmentof multiple HLA-class I antibodies. Therefore the firsttherapeutic approach is to transfuse HLA-matched and/orcross-matched platelets. Sometimes compatible donors arenot available and therefore there is no alternative.

Several authors have proposed methods to overcome thisproblem. Using an acid treatment of platelet products, theelution of platelet HLA-class I antigens can be achieved(Kurata et al, 1989; Novotny et al, 1996a). A few patientshave been treated successfully this way. Although the post-transfusion platelet counts were not very high in somereported patients, all experienced clinical improvement(Shanwell et al, 1991; Novotny et al, 1996).

We present the case of a 34-year-old woman with adiagnosis of chronic myeloid leukaemia in the aplastic phaseof an allogeneic bone marrow transplant. She had bruisingand bowel bleeding. She was febrile, under Amphotericin Btreatment, and also had splenomegaly, which are consideredrelevant clinical factors for platelet refractoriness. Afterseveral transfusions she became refractory to platelets.Multiple anti-HLA class I antibodies (95% reactivity in alymphocytotoxic assay) were demonstrated in her serum.Her HLA type was A2, B18, B44, Bw4, Bw6 and onlyplatelets from her sister – the HLA-identical bone marrowdonor – gave appropriate post-transfusion increments. OurHLA-typed donor file was searched. We found two compa-tible donors, grade B2 and C, but the outcome of the

transfusions was unsuccessful. When the sibling donor wasno longer available we were unable to find more compatibledonors by platelet cross-match (28 donors were cross-matched and found incompatible).

Following the method proposed by Novotny et al (1996b),we treated pools of 8–10 fresh random platelets (<24 h old)with 30 ml of pH 3·0 citric acid for 10 min at roomtemperature, followed immediately by a wash in 500 ml offresh frozen plasma at 4ºC, and two more washes with 500ml of an additive solution (Plasmalyte A, Baxter Healthcare).

In the first two acid treatments we observed plateletclumps in the final product. In order to reduce clumping weadded a 10% volume of ACD to the additive solution in thetwo last washes. With this measure, clumps were totallyprevented, and further acid treatments were performed usingthe modification.

The average loss of platelets due to processing was 40%.Transfusion of the eluted platelets was accomplishedimmediately after acid treatment (within 6 h). On twooccasions a platelet cross-match was carried out with thepatient’s serum and the pooled platelets, using the Capture Ptechnique, resulting in a positive reaction before the treatmentwhich disappeared after elution.

The patient received seven transfusions of random pooledacid-treated platelets (Table I). Corrected count increments(CCI) at 1 h and 24 h were available on four occasions.Transfusions 1 and 5 had appropriate 1 h CCI andtransfusion 6 produced only a moderate recovery. Transfu-sion 4 also had anacceptable 24 h ICC.

The patient’s bowel bleed stopped after the first elutedplatelet pool transfusion and she had no further bleedsduring therapy. No adverse effects related to the procedurewere noticed.

British Journal of Haematology, 1998, 100, 245–246

245q 1998 Blackwell Science Ltd

Table I. Patient response to acid-treated platelet transfusions.

Transfusion episode

1 2 3 4 5 6 7

Platelet dose ( × 1011) 4.2 3.5 3.5 3.5 4.5 5.5 10.5Platelet pre-count × 109/l 1.0 1.0 1.0 8.0 3.0 2.0 4.01 h platelet post-count × 109/l 18.0 1.0 ND ND 27.0 16.0 ND24 h platelet post-count × 109/l 2.0 1.0 2.0 18.0 2.0 1.0 6.01 h CCI × 109/l 7.1 0.0 ND ND 9.3 4.5 ND24 h CCI × 109/l 0.4 0.0 0.5 5.0 0.0 0.0 0.3

CCI ¼ post-transfusion increment (109/l) × body surface area (m2)/no. of platelets transfused (1011). ND ¼ not done.

In conclusion, this is a feasible and useful method that canbe safely applied in refractory patients who have notresponded to classic therapeutic options.

Centro de Donacion E. CA S T RO

de Sangre, J. M U N C U N I L L

de Cruz Roja Espanola, L. BA R E A

and *Servicio de Hematologıa, R. G O N Z A L E Z

Hospital de La Princesa, M.J. F E R N A N D E Z -V I L L A LTA *Madrid, Spain

REFERENCES

Kurata, Y., Oshida, M., Take, H., Furubayashi, T., Nakao, H.,Tomiyama, Y., Kanayama, Y., Nagao, N., Okubo, Y., Yonezawa, T.& Tarui, S. (1989) New approach to eliminate HLA class I

antigens from platelet surface without cell damage: acid treatmentat pH 3·0. Vox Sanguinis, 57, 199–204.

Novotny, V.M.J., Doxiadis, I.N.N., Van Doorn, R. & Brand, A. (1996a)The kinetics of HLA class I elution and the relevance for the use ofHLA-eluted platelet transfusions. British Journal of Haematology,95, 422–426.

Novotny, V.M.J., Huizinga, T.W.J., Van Doorn, R., Briet, E. & Brand, A.(1996b) HLA class I eluted platelets as alternative for HLA-matched platelet transfusions. Transfusion, 36, 438–444.

Shanwell, A., Sallander, S., Olsson, I., Gulliksson, H., Pedajas, I. &Lerner, R. (1991) An alloimmunized, thrombocytopenic patientsuccessfully transfused with acid-treated, random-donor platelets.British Journal of Haematology, 79, 462–465.

Keywords: platelet refractoriness, HLA class I antigens, acidelution.

246 Correspondence

q 1998 Blackwell Science Ltd, British Journal of Haematology 100: 245–246