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Fatal thrombotic microangiopathy after a single dose of gemcitabine as fourth-line palliative treatment for metastasized ductal breast carcinoma

gemcitabine is a nucleoside analogue which was first approved in 1996 for the treatment of locally advanced or metastatic pancreatic carcinoma. it is currently used for the treatment of a wide range of malignancies. Primary side effects are myelosuppression, mild liver function abnormalities and flulike symptoms. A rare, but serious complication of gemcitabine treatment is thrombotic microangiopathy (tMA). tMA is a disorder characterized by generalized microvascular occlusion by platelet thrombi, leading to organ damage particularly in the brain, kidneys and heart. injury to the endothelial cell is the central and likely inciting factor in the sequence of events leading to tMA. Classically it presents with Coombs negative hemolytic anemia, thrombocytopenia, fever, renal insufficiency and neurological symptoms. Hypertension and pulmonary symptoms can also occur. in the spectrum of clinical presentations of tMA a distinction is made between thrombotic thrombocytopenic purpura (ttP), with a predominance of neurological symptoms, and the hemolytic-uremic syndrome (HUs), with predominantly renal insufficiency. severe deficiency of plasma ADAMts-13 activity is more specific for ttP [1,2]. the distinction between ttP and HUs is, however, not always clear. in the present article we will therefore refer to the syndrome as tMA. it is very rare for tMA to develop as a complication of gemcitabine treatment already at low cumulative doses or after short treatment duration. in this