ACID ELUTION OF PLATELETS HLA‐CLASS I ANTIGENS IN THE TREATMENT OF A REFRACTORY PATIENT

Platelet refractoriness is a not infrequent and life-threatening complication during myelosupressive treatments for cancer. This implies the inability of transfused platelets to increase patients’ platelet counts or stop the bleeding. There are few options in supporting patients when they became refractory to platelets’ transfusions. The most common situation causing refractoriness is the development of multiple HLA-class I antibodies. Therefore the first therapeutic approach is to transfuse HLA-matched and/or cross-matched platelets. Sometimes compatible donors are not available and therefore there is no alternative. Several authors have proposed methods to overcome this problem. Using an acid treatment of platelet products, the elution of platelet HLA-class I antigens can be achieved (Kurata et al, 1989; Novotny et al, 1996a). A few patients have been treated successfully this way. Although the posttransfusion platelet counts were not very high in some reported patients, all experienced clinical improvement (Shanwell et al, 1991; Novotny et al, 1996). We present the case of a 34-year-old woman with a diagnosis of chronic myeloid leukaemia in the aplastic phase of an allogeneic bone marrow transplant. She had bruising and bowel bleeding. She was febrile, under Amphotericin B treatment, and also had splenomegaly, which are considered relevant clinical factors for platelet refractoriness. After several transfusions she became refractory to platelets. Multiple anti-HLA class I antibodies (95% reactivity in a lymphocytotoxic assay) were demonstrated in her serum. Her HLA type was A2, B18, B44, Bw4, Bw6 and only platelets from her sister – the HLA-identical bone marrow donor – gave appropriate post-transfusion increments. Our HLA-typed donor file was searched. We found two compatible donors, grade B2 and C, but the outcome of the transfusions was unsuccessful. When the sibling donor was no longer available we were unable to find more compatible donors by platelet cross-match (28 donors were crossmatched 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 room temperature, followed immediately by a wash in 500 ml of fresh frozen plasma at 4oC, and two more washes with 500 ml of an additive solution (Plasmalyte A, Baxter Healthcare). In the first two acid treatments we observed platelet clumps in the final product. In order to reduce clumping we added a 10% volume of ACD to the additive solution in the two last washes. With this measure, clumps were totally prevented, and further acid treatments were performed using the modification. The average loss of platelets due to processing was 40%. Transfusion of the eluted platelets was accomplished immediately after acid treatment (within 6 h). On two occasions a platelet cross-match was carried out with the patient’s serum and the pooled platelets, using the Capture P technique, resulting in a positive reaction before the treatment which disappeared after elution. The patient received seven transfusions of random pooled acid-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 and transfusion 6 produced only a moderate recovery. Transfusion 4 also had anacceptable 24 h ICC. The patient’s bowel bleed stopped after the first eluted platelet pool transfusion and she had no further bleeds during therapy. No adverse effects related to the procedure were noticed. British Journal of Haematology, 1998, 100, 245–246