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Thursday 01 June 2006

Late humoral rejection in a cardiac transplant recipient treated with the anti-CD20 monoclonal antibody rituximab.

By: Keren A, Hayes HM, O'Driscoll G.

Transplant Proc 2006 Jun;38(5):1520-2

Humoral or vascular rejection results from a B cell-mediated production of immunoglobulin (Ig) G antibody against a transplanted organ, producing immune complex deposition on the vascular endothelium, activation of the complement cascade, generation of endothelial dysfunction, and regional ischemic injury. Antibody-mediated rejection, which may be accompanied by hemodynamic compromise, is associated with reduced long-term graft survival. Patients believed to be at an increased risk of developing humoral rejection include women, particularly those with high levels of panel reactive antibodies, cytomegalovirus seropositivity, and positive cross matches, and subjects with prior sensitization to OKT3. Treatment options for humoral rejection include plasmapheresis to lower the circulating immunoglobulin levels followed by high-dose cyclophosphamide to reduce the B-cell population. Other modalities include total lymphoid irradiation, photophoresis, splenectomy, and, for treatment failures, retransplantation. Rituximab is a chimeric humanized monoclonal antibody directed against the pan B-cell surface molecule, CD20. It is approved for the treatment of low-grade B-cell non-Hodgkin's lymphoma. It has also been used successfully for the treatment of posttransplant B-cell lymphoproliferative disease. We report a case of late humoral rejection successfully treated with rituximab.

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