TRALI: correlation of antigen-antibody and monocyte activation in donor-recipient pairs.

BACKGROUND: TRALI may be a severe reaction associated with transfusion of plasma-containing blood components. TRALI has usually been associated with antibodies against granulocytes and HLA class I antigens, but more recently with antibodies against HLA class II and monocytes. TRALI cases were investigated to determine correlation between antigen and antibody. Additionally, activation of monocytes by TRALI serums was studied. STUDY DESIGN AND METHODS: Sixteen cases of TRALI were investigated. All patients were typed for HLA antigens. Implicated donors were screened for HLA antigens and antibodies against granulocytes and monocytes. In 6 cases, recipient monocyte activation was measured in vitro after incubation with TRALI and control serums. In four cases, monocyte activation was measured after incubation of TRALI serums against a panel of monocytes of known HLA antigen type. RESULTS: In 14 of the 16 cases (87.5%), antigen-antibody correlation was identified. TRALI monocytes, incubated with implicated TRALI serum (n = 6), expressed significantly greater cytokine and tissue factor (p < 0.05, repeated-measures ANOVA) than controls. Panel monocytes incubated with TRALI serum showed increased expression of cytokine and/or tissue factor when corresponding antigen was present. CONCLUSION: In most cases of TRALI, a correlation between antigen and antibody can be identified. Activation of monocytes and their subsequent release of cytokines may play a role in the pathogenesis of TRALI.

Early diagnosis and successful treatment of a patient with transfusion-associated GVHD with autologous peripheral blood progenitor cell transplantation.

BACKGROUND: Transfusion-associated GVHD (TA-GVHD) is an uncommon complication of blood transfusion. Diagnosis of TA-GVHD is difficult, and it is usually rapidly fatal. There are few documented sur- vivors of TA-GVHD. CASE REPORT: A 61-year-old woman with chronic lymphocytic leukemia (CLL) was treated with fludarabine followed by combination chemotherapy and high-dose radioimmunotherapy and peripheral blood progenitor cell (PBPC) rescue. She was transfused with nonirradiated blood components at an outside hospital and presented 10 days later with rash, elevated liver enzymes, and progressive pancytopenia. Skin biopsy was consistent with GVHD, and HLA typing of lymphocytes from the patient demonstrated mixed chimerism. The patient was treated with solumedrol and cyclosporin A, followed by high-dose cyclophosphamide and antithymocyte globulin and autologous PBPC infusion. She had rapid engraftment, resolution of skin rash, and normalization of liver function abnormalities. She is in good health with normal blood counts and no evidence of CLL 34 months after transplantation. CONCLUSION: TA-GVHD occurs in the setting of an immunocompromised recipient receiving nonirradiated blood components. A typical presentation includes skin rash, liver function abnormalities, and pancytopenia. Demonstration of mixed chimerism by HLA typing facilitated diagnosis in this patient. High-dose immunosuppression, facilitated by the availability of autologous PBPCs, resulted in a successful outcome.