Abstract
Rituximab (RTX), a monoclonal antibody against the B-cell marker CD20, is commonly used as a treatment for antibody-mediated diseases or B-lymphocyte-mediated diseases. Destruction of B cells may reverse the disease course in many conditions; however, patients who are treated with RTX cannot respond appropriately to de novo infection due to lack of B lymphocytes. Here, we report one such case. A 7-year-old renal allograft recipient presented with severe anemia due to parvovirus infection after RTX treatment. The patient had focal segmental glomerulosclerosis and had received cadaveric kidney transplantation 6 months previously. She was treated with high-dose steroid for acute rejection and RTX for Epstein Barr Virus infection 3 months previously. At presentation, her hemoglobin level was 5.4 g/dL and leukocyte and platelet counts were normal. She had microcytic normochromic anemia and high viral load of parvovirus B19(70,578 copies/mL). Intravenous immunoglobulin ($200mg/kg{\cdot}d$) treatment controlled the progression of anemia and parvovirus infection. De novo parvovirus infection during the B lymphocyte-depletion period may have precipitated the severe anemia in this case. Close monitoring of infection is required after RTX therapy.
