Quetiapine has been reported to cause immune-mediated thrombotic microangiopathy (TMA), although few cases have been reported thus far. A 71-year-old man with autosomal dominant polycystic kidney disease on maintenance dialysis was hospitalized with a hemorrhagic basal ganglia stroke, and was treated with 25 mg quetiapine for delirium from day 4 of admission. There was no worsening of consciousness, fever, diarrhea, or elevated blood pressure during the hospitalization. Gingival bleeding appeared on day 35, and the platelet count on day 38 was 0.5 × 104/μL (13.2 × 104/μL on day 16). The presence of 1% schistocytes, high LDH level, inability to measure haptoglobin, negative direct Coombs test, and normal prothrombin time and activated partial thromboplastin time indicated TMA. We considered an exclusionary diagnosis of drug-induced TMA, because of normal ADAMTS13 activity, no evidence of complement activation and the absence of Shiga toxin or symptoms of collagen disease or cancer. Quetiapine was the most likely causative factor; however, all drugs, including heparin, were discontinued or changed. Due to persistent microbleeding, platelet transfusions were performed several times. After only quetiapine was discontinued, the platelet count recovered smoothly to 3.1 and 7.2 × 104/μL on days 45 and 72, respectively; LDH and fibrinogen levels normalized on day 47. All medications, except quetiapine, were restarted sequentially after day 47, without subsequent thrombocytopenia. Platelet activation predominantly by a drug-dependent antibody might be the etiology of quetiapine-induced TMA. Plasmapheresis may not be necessary for quetiapine, because of its unproven efficacy in drug-induced TMA.
Keywords: ADAMTS13; Hemodialysis; Quetiapine; Thrombotic microangiopathy.