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BACKGROUND: Type I allergic reactions such as urticaria-like manifestations constitute a large percentage of transfusion-related adverse events. Along with donor factors, patient factors might be involved in these reactions. Sera from some patients with chronic idiopathic urticaria show histamine-releasing activity (HRA). Sera from patients who develop Type I allergic reaction might possess HRA. STUDY DESIGN AND METHODS: Pretransfusion serum samples were collected. Mast cells were cultured from peripheral blood CD34+ cells and mixed with the serum samples. Cells with elevated intracytoplasmic Ca2+ concentrations were monitored using flow cytometry to evaluate Ca2+ influx–inducing activity (CaIA) in serum. The amount of histamine released into the supernatant was measured using an enzyme immunoassay kit to evaluate HRA. In some assays, cells were incubated with pertussis toxin (Ptx). RESULTS: CaIA values were higher (p < 0.05) in sera from patients with reactions (27.68 ± 20.38 [n = 145]; range, 0.49-84.90) than in sera of patients without reactions (10.70 ± 6.50 [n = 54]; range, 2.67-36.97) and control sera (9.67 ± 5.88 [n = 107]; range, 1.11-25.68). No difference in CaIA was found between patients with (27.38 ± 20.46 [n = 88]) and without (28.38 ± 20.59 [n = 57]) skin manifestations. However, CaIA was higher (p < 0.05) in patients with pure urticaria (mean, 30.58 ± 21.3 [n = 30]; range, 70.43-4.1) than in patients with fever alone (mean, 18.61 ± 14.71 [n = 18]; range, 45.94-3.19). Levels of HRA were higher (p < 0.001) in CaIA-positive sera than in CaIA-negative sera. Both CaIA and HRA were blocked by Ptx. CONCLUSION: Elevated CaIA and HRA in pretransfusion sera might be attributable to adverse reactions, especially to urticaria-like manifestation. The Gi protein–coupled receptor complexes on mast cells and its ligand must be involved. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor regarding the donor reactions among African-American and Caucasian first-time whole-blood donors, published in the August 2005 issue of "Transfusion."

Anti-CD36 isoantibody in blood recipients is reported to cause refractoriness to platelet (PLT) transfusions and posttransfusion purpura–like syndrome. There are few reports, however, about the effects of passively transfused blood products containing this isoantibody on recipients. A 67-year-old Japanese woman underwent brain surgery. On the 6th postoperative day, the patient experienced tightness of the chest and nausea after receiving a transfusion of fresh frozen plasma (FFP). When she manifested hypotension, the transfusion was discontinued. No cutaneous manifestation was observed. The patient's condition gradually improved soon after the administration of steroids. Her pretransfusion PLT count was 17.1 × 104 perµL. It decreased to 1.9 × 104 perµL 12 hours after transfusion and recovered to 15.4 × 104 perµL 8 days after transfusion. The donor of the FFP had a Type I CD36 deficiency. Flow cytometric analysis identified anti-CD36 isoantibody in the FFP. The cross-match between the patient's PLTs and the FFP was positive. The FFP induced the aggregation of PLTs derived from healthy adults. This is the first reported case of life-threatening adverse effects and thrombocytopenia caused by passively transfused anti-CD36 isoantibody. The possibility of passive infusion of this antibody should be considered in the evaluation of life-threatening transfusion reactions followed by thrombocytopenia. [ABSTRACT FROM AUTHOR]