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Abstract: SA-PO217

Gemcitabine-Induced Thrombotic Microangiopathy Treated with Eculizumab in a Patient with Pancreatic Cancer: A Case Report

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Madken, Mohit, Brigham and Women's Hospital, Boston, Massachusetts, United States
  • Gupta, Shruti, Brigham and Women's Hospital, Boston, Massachusetts, United States
  • Mount, David B., Brigham and Women's Hospital, Boston, Massachusetts, United States

Thrombotic microangiopathies (TMA) are characterized clinically by the presence of microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and ischemic organ injury. Drug-induced thrombotic microangiopathy (DITMA) is often under-recognized and under-reported. The incidence of gemcitabine-induced TMA (GITMA) has been reported to be between 0.02% and 2.2%.

Case Description

67-year-old female with history of DM, Hypertension, CKD (B/L creat 1.8-2.0), Ca Pancreas s/p Whipple`s on neoadjuvant chemotherapy (FOLFIRINOX followed by Gemcitabine/Abraxane) was admitted with history of frequent falls and worsening left upper and lower limb weakness for 3 days. She had received gemcitabine with cumulative dose of 15,000 mg/m2 for the preceding 1 year, with last dose 2 months prior to her presentation. On admission, her BP was 170/90 mm Hg, serum creatinine 3.5 mg/dl, serum albumin 3.1 g/dl, worsening anemia (hemoglobin 7.1 g/dl), thrombocytopenia (platelet count 89,000/mm3), LDH 447 IU/L, with schistocytes on blood film. Urinalysis revealed RBC casts with urine microalbumin-creatinine 2400 mg/gm. ANA, ANCA, hepatitis B and C serologies were negative and complements normal. A diagnosis of GITMA was onsidered and she was stabilized with conservative measures. She was started on treatment with Eculizumab with which her renal functions improved with stable Hb.


TMA occurring in a patient with a malignancy can be either malignancy or drug-induced. Mechanism of drug-induced TMA can be direct endothelial damage (type 1, dose dependent) or immune-mediated through the development of drug-dependent autoantibodies (type 2, none-dose dependent). Treatment of drug-induced TMA includes supportive therapy and withdrawal of the drug. Eculizumab has shown promise as an effective therapy for GITMA.