Quetiapine-induced thrombotic microangiopathy in a patient on maintenance dialysis
- PDF / 797,447 Bytes
- 6 Pages / 595.276 x 790.866 pts Page_size
- 65 Downloads / 161 Views
CASE REPORT
Quetiapine‑induced thrombotic microangiopathy in a patient on maintenance dialysis Miki Takahashi1 · Akihito Deguchi1 · Hiromu Nishihara1 · Mea Asou1 · Tomohiko Asakawa1 · Makoto Araki1 Received: 27 July 2020 / Accepted: 17 September 2020 © Japanese Society of Nephrology 2020
Abstract 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 Quetiapine · ADAMTS13 · Thrombotic microangiopathy · Hemodialysis
Introduction Thrombotic microangiopathy (TMA) is a clinicopathological syndrome characterized by microangiopathic hemolytic anemia, consumptive thrombocytopenia, and organ dysfunction due to microvascular thrombi. Thrombotic thrombocytopenic purpura (TTP), a typical example, is triggered by decreased ADAMST13 activity. Many diseases other than TTP have been found to cause TMA, and they are now often classified by etiology, such as infection and complement abnormalities. Antipsychotics used for the treatment of schizophrenia and delirium are often prescribed not only by psychiatrists, but also by internists. Quetiapine is a widely used atypical * Makoto Araki [email protected] 1
Department of Internal Medicine, Suwa Central Hospital, 4300 Tamagawa, Chino‑shi, Nagano‑ken 391‑8503, Japan
antipsychotic due to its low frequency of dopamine-related side effects. Quetiapine rarely causes immune-mediated TMA. We experienced a case of TMA caused by quetiapine an
Data Loading...
