%0 Journal Article
%T Mitomycin-C-Induced TTP/HUS Treated Successfully with Rituximab: Case Report and Review of the Literature
%A Gunjan Shah
%A Hanah Yamin
%A Hedy Smith
%J Case Reports in Hematology
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/130978
%X Microangiopathic hemolytic anemia (MAHA), thrombocytopenia, fever, renal failure, and neurologic symptoms comprise the cardinal features of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome. Etiologies can include medications, infections, cancers, or transplantation. We present a patient with a history of rectal cancer treated with mitomycin-C who developed MAHA, acute kidney injury, and thrombocytopenia 6 months after completing therapy and to did not respond the plasmapheresis or steroids. She was treated with four weekly doses of rituximab with full recovery. 1. Introduction Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) encompass a spectrum of thrombotic microangiopathies classically associated with microangiopathic hemolytic anemia, thrombocytopenia, fever, renal failure, and neurologic symptoms. Further classification occurs based on the predominance of the cardinal features (with a greater degree of renal failure suggesting HUS and neurologic disease suggesting TTP), associated symptoms (diarrhea with typical HUS), level of the serum metalloprotease ADAMTS13 (low in TTP), and etiology. Secondary etiologies can include medications, infections, cancers, or transplantation. Several chemotherapeutic agents including mitomycin-C and gemcitabine and targeted therapies including bevacizumab and sunitinib have been implicated. We describe the case of a woman with mitomycin-C- (MMC-) induced TTP treated successfully with rituximab after failing a course of plasmapheresis and steroids. 2. Case Presentation A 73-year-old woman was referred for hematologic evaluation when she was found to be anemic and thrombocytopenic on preoperative labs for a hernia repair. She was found to have evidence of microangiopathic hemolytic anemia with acute kidney injury and admitted to her local hospital where she was transfused for a hemoglobin of 7.1£¿g/dL. She was transferred to our hospital for consideration of plasmapheresis. On admission, her hemoglobin was 11£¿g/dL, platelet count 74,000£¿/uL, creatinine 1.48£¿mg/dL, lactate dehydrogenase (LDH) 372£¿IU/L, and haptoglobin 2£¿mg/dL. D-dimer was mildly elevated and fibrinogen was normal making DIC unlikely. Her systolic blood pressure was elevated to 160, which had previously been normal. Past medical and surgical history included squamous cell anal carcinoma diagnosed 10 months previously and being treated with a diverting loop colostomy, radiation therapy, 5-FU, and mitomycin-C. She also had macular degeneration, paroxysmal atrial fibrillation, hypothyroidism, osteopenia, and back
%U http://www.hindawi.com/journals/crihem/2013/130978/