Thrombotic microangiopathy associated with Valproic acid toxicity

Abstract Background Thrombotic microangiopathy (TMA) is a serious, sometimes life-threatening disorder marked by the presence of endothelial injury and microvascular thrombi. Drug-induced thrombotic microangiopathy (DI-TMA) is one specific TMA syndrome that occurs following drug exposure via drug-de...

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Main Authors: Sean A. Hebert, Timothy P. Bohan, Christian L. Erikson, Rita D. Swinford
Format: Article
Language:English
Published: BMC 2017-08-01
Series:BMC Nephrology
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12882-017-0677-4
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author Sean A. Hebert
Timothy P. Bohan
Christian L. Erikson
Rita D. Swinford
author_facet Sean A. Hebert
Timothy P. Bohan
Christian L. Erikson
Rita D. Swinford
author_sort Sean A. Hebert
collection DOAJ
description Abstract Background Thrombotic microangiopathy (TMA) is a serious, sometimes life-threatening disorder marked by the presence of endothelial injury and microvascular thrombi. Drug-induced thrombotic microangiopathy (DI-TMA) is one specific TMA syndrome that occurs following drug exposure via drug-dependent antibodies or direct tissue toxicity. Common examples include calcineurin inhibitors Tacrolimus and Cyclosporine and antineoplastics Gemcitabine and Mitomycin. Valproic acid has not been implicated in DI-TMA. We present the first case of a patient meeting clinical criteria for DI-TMA following admission for valproic acid toxicity. Case presentation An adolescent male with difficult to control epilepsy was admitted for impaired hepatic function while on valproic acid therapy. On the third hospital day, he developed severe metabolic lactic acidosis and multiorgan failure, prompting transfer to the pediatric intensive care unit. Progressive anemia and thrombocytopenia instigated an evaluation for thrombotic microangiopathy, where confirmed by concomitant hemolysis, elevated lactate dehydrogenase (LDH), low haptoglobin, and concurrent oliguric acute kidney injury. Thrombotic thrombocytopenic purpura was less likely with adequate ADAMTS13. Discontinuing valproic acid reversed the anemia, thrombocytopenia, and normalized the LDH and haptoglobin, supporting a drug-induced cause for the TMA. Conclusion To the best of our knowledge, this is the first report of drug-induced TMA from valproic acid toxicity.
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spelling doaj.art-bf86dc3a1eec4950aafee5fa5cb4baeb2022-12-22T01:53:21ZengBMCBMC Nephrology1471-23692017-08-011811410.1186/s12882-017-0677-4Thrombotic microangiopathy associated with Valproic acid toxicitySean A. Hebert0Timothy P. Bohan1Christian L. Erikson2Rita D. Swinford3Department of Internal Medicine and Pediatrics, Division of Nephrology, McGovern Medical School at The University of Texas Health Science Center at Houston (UTHealth), Children’s Memorial Hermann HospitalPediatric Neurology, Memorial Hermann Texas Medical Center, Children’s Memorial Hermann HospitalDepartment of Pediatrics, Division of Critical Care Medicine, Texas Children’s HospitalDepartment of Pediatrics, Division of Nephrology, McGovern Medical School at The University of Texas Health Science Center at Houston (UTHealth), Children’s Memorial Hermann HospitalAbstract Background Thrombotic microangiopathy (TMA) is a serious, sometimes life-threatening disorder marked by the presence of endothelial injury and microvascular thrombi. Drug-induced thrombotic microangiopathy (DI-TMA) is one specific TMA syndrome that occurs following drug exposure via drug-dependent antibodies or direct tissue toxicity. Common examples include calcineurin inhibitors Tacrolimus and Cyclosporine and antineoplastics Gemcitabine and Mitomycin. Valproic acid has not been implicated in DI-TMA. We present the first case of a patient meeting clinical criteria for DI-TMA following admission for valproic acid toxicity. Case presentation An adolescent male with difficult to control epilepsy was admitted for impaired hepatic function while on valproic acid therapy. On the third hospital day, he developed severe metabolic lactic acidosis and multiorgan failure, prompting transfer to the pediatric intensive care unit. Progressive anemia and thrombocytopenia instigated an evaluation for thrombotic microangiopathy, where confirmed by concomitant hemolysis, elevated lactate dehydrogenase (LDH), low haptoglobin, and concurrent oliguric acute kidney injury. Thrombotic thrombocytopenic purpura was less likely with adequate ADAMTS13. Discontinuing valproic acid reversed the anemia, thrombocytopenia, and normalized the LDH and haptoglobin, supporting a drug-induced cause for the TMA. Conclusion To the best of our knowledge, this is the first report of drug-induced TMA from valproic acid toxicity.http://link.springer.com/article/10.1186/s12882-017-0677-4Thrombotic microangiopathyDrug-induced thrombotic MicroangiopathyValproic acid toxicityCase report
spellingShingle Sean A. Hebert
Timothy P. Bohan
Christian L. Erikson
Rita D. Swinford
Thrombotic microangiopathy associated with Valproic acid toxicity
BMC Nephrology
Thrombotic microangiopathy
Drug-induced thrombotic Microangiopathy
Valproic acid toxicity
Case report
title Thrombotic microangiopathy associated with Valproic acid toxicity
title_full Thrombotic microangiopathy associated with Valproic acid toxicity
title_fullStr Thrombotic microangiopathy associated with Valproic acid toxicity
title_full_unstemmed Thrombotic microangiopathy associated with Valproic acid toxicity
title_short Thrombotic microangiopathy associated with Valproic acid toxicity
title_sort thrombotic microangiopathy associated with valproic acid toxicity
topic Thrombotic microangiopathy
Drug-induced thrombotic Microangiopathy
Valproic acid toxicity
Case report
url http://link.springer.com/article/10.1186/s12882-017-0677-4
work_keys_str_mv AT seanahebert thromboticmicroangiopathyassociatedwithvalproicacidtoxicity
AT timothypbohan thromboticmicroangiopathyassociatedwithvalproicacidtoxicity
AT christianlerikson thromboticmicroangiopathyassociatedwithvalproicacidtoxicity
AT ritadswinford thromboticmicroangiopathyassociatedwithvalproicacidtoxicity