Eculizumab successfully resolved gemcitabine-induced thrombotic microangiopathy without relapse after three infusions in a patient with a CFHR1-CFHR3 homozygous deletion.
Does eculizumab improve gemcitabine-induced thrombotic microangiopathy in a patient with a homozygous deletion in CFHR1-CFHR3?
Eculizumab successfully treated gemcitabine-induced thrombotic microangiopathy in a patient with a genetic predisposition (homozygous deletion in CFHR1-CFHR3).
Absolute Event Rate: 0% vs 0%
We present here the case of a 66‐year‐old female with a history of pancreatic adenocarcinoma who was on a chemotherapeutic regimen of nanoparticle albumin‐bound paclitaxel (nab‐paclitaxel) and gemcitabine after demonstrating local progression of her disease on the regimen of 5‐fluorouracil, leucovorin, irinotecan, and oxaliplatin (FOLFIRINOX). The patient presented to clinic prior to receiving Cycle 15 of nab‐paclitaxel and gemcitabine with labs demonstrating concern for acute kidney injury and hemolytic anemia. The patient was referred for admission with renal biopsy exhibiting endothelial injury and thrombotic microangiopathy (TMA). Additionally, the patient was found to have mutations in a TMA genetic panel, raising questions on whether an existing genetic predisposition contributed to the development of gemcitabine‐induced TMA. The patient was treated with eculizumab with resolution of TMA and without relapse after three infusions.
Dziarnowski et al. (Thu,) reported a other. Eculizumab successfully resolved gemcitabine-induced thrombotic microangiopathy without relapse after three infusions in a patient with a CFHR1-CFHR3 homozygous deletion.