Dear Sir: A 25-year-old woman was diagnosed in 1996 with thrombocytopenic purpura and ileocolonic Crohn’s disease. She tested positive for antiplatelet antibodies, and her bone marrow examination showed increased cellularity and megakaryocytic hyperplasia consistent with immune-mediated thrombocytopenia. Her thrombocytopenia was refractory to corticosteroid treatment and splenectomy but responded to intravenous immune globulin (IVIG). She received several courses of IVIG for thrombocytopenic episodes over the following years but was later complicated by infusion reactions that necessitated discontinuation of treatment. Her Crohn’s disease was treated intermittently with corticosteroids, antibiotics, and mesalamine. She was intolerant to 6-mercaptopurine, methotrexate, and 6-thioguanine. She continued to have intermittent symptoms of diarrhea, bleeding, and abdominal pain. In 2000, the patient developed severe thrombocytopenia (platelet count 5000/dL). She received 4 weekly infusions of the anti-CD2O monoclonal antibody, rituximab, with gradual recovery of the platelet count. However, the symptoms of diarrhea, abdominal pain, and rectal bleeding persisted if not worsened. Over the following year, she was treated with antibiotics, budesonide, and experimental therapies for her Crohn’s disease with temporary success. The patient was offered a colectomy but she refused. Rituximab is a chimeric monoclonal antibody directed against the CD2O antigen expressed on most B cells and is used to treat B-cell non-Hodgkin’s lymphoma.1 Rituximab is highly effective in depleting B-lymphocytes in vivo, and it may take as long as 1 year for peripheral blood B-lymphocytes to recover. More recently, it has been reported for the treatment of posttransplant lymphoproliferative disease (PTLD) and immune-mediated thrombocytopenia related to graft-versus-host disease.2,3 Such treatment would presumably eliminate B cells producing antiplatelet antibodies. Immune-mediated thrombocytopenia has been occasionally associated with inflammatory bowel disease (IBD), particularly ulcerative colitis.4 This is a report of successful and sustained response to anti-CD2O antibody treatment, rituximab, for IBD-associated thrombocytopenia. This case also suggests that therapies directed against B-lymphocytes may not be effective for the treatment of human IBD, they may possibly be detrimental. In animal models, colitis is mediated by T lymphocytes that are reactive to bacterial antigens. In the T cell receptor(TCR / ) knockout model of colitis, B-lymphocytes were shown to have a protective role because TCR / mice backcrossed with immunoglobulin and B-lymphocyte deficient mice developed more severe colitis, whereas transfer of B-lymphocytes ameliorated the disease.5