Lacosamide-Induced Thrombotic Microangiopathy

Introduction: Drug-induced thrombotic microangiopathy is a life-threatening condition that is characterized by anemia, thrombocytopenia, and acute kidney failure without ADAMTS13 deficiency. Many drugs have been identified to cause TMA including quinine, antimicrobials, and cancer therapies. In this case we will describe a rare case of lacosamide induced TMA Case Description: An 84-year-old female who presented to the hospital with intracranial hemorrhage. She then underwent craniotomy and was intubated for seizure. The patient was then started on lacosamide and valproic acid for her seizures. On admission hemoglobin was 13 and platelets were 250. 6 days into her admission, schistocytes started appearing on automated differential. Also, her hemoglobin dropped to 7.5 and platelets count gradually dropped until they reached a nadir of 54. Peripheral smear showed schistocytes, D-Dimer was positive, RPI was low, LDH was mildly elevated, but she had normal pt/INR, fibrinogen. Creatinine increased from 0.7 to 1.4 and the patient remained non oliguric. Nephrology team was consulted for AKI and MAHA. ADAMTS13 level was collected, lacosamide was held and valproic acid was continued. The patient was started on 60 IV methyl prednisone every eight hours. She also received 2 units of fresh frozen plasma. Three sessions of plasma exchange were performed. ADAMTs 13 came back at 50% making the diagnosis of drug induced thrombotic microangiopathy (DITMA) more likely. Patient platelets improved back to baseline. She was then stable and was discharged home. Discussion: The patient in this case started having signs of TMA 6 days after starting lacosamide, which improved after discontinuation of the medication. ADAMTS13 of 50% differentiated between drug induced TMA and TTP. DITMA can sometimes be challenging to diagnose, especially in the ICU setting. Although literature on lacosamide induced TMA is scarce, this case sheds the importance of keeping TMA as a differential in the setting of new onset thrombocytopenia and anemia after starting new medications.

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Journal
Journal of the American Society of Nephrology
Published
2024-10-01
DOI
https://doi.org/10.1681/asn.2024fnxnhpjg
Citations
1
Primary Topic
Acute Myeloid Leukemia Research
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article
Field-Weighted Citation Impact
0.45
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article

Lacosamide-Induced Thrombotic Microangiopathy

Zeid Khitan, Khaled Al-Baqain, Said Sharawi
1 citations
Journal of the American Society of Nephrology
Acute Myeloid Leukemia Research
0.45
article

Lacosamide-Induced Thrombotic Microangiopathy

Zeid Khitan, Khaled Al-Baqain, Said Sharawi
article en
1 citations

Abstract

Introduction: Drug-induced thrombotic microangiopathy is a life-threatening condition that is characterized by anemia, thrombocytopenia, and acute kidney failure without ADAMTS13 deficiency. Many drugs have been identified to cause TMA including quinine, antimicrobials, and cancer therapies. In this case we will describe a rare case of lacosamide induced TMA Case Description: An 84-year-old female who presented to the hospital with intracranial hemorrhage. She then underwent craniotomy and was intubated for seizure. The patient was then started on lacosamide and valproic acid for her seizures. On admission hemoglobin was 13 and platelets were 250. 6 days into her admission, schistocytes started appearing on automated differential. Also, her hemoglobin dropped to 7.5 and platelets count gradually dropped until they reached a nadir of 54. Peripheral smear showed schistocytes, D-Dimer was positive, RPI was low, LDH was mildly elevated, but she had normal pt/INR, fibrinogen. Creatinine increased from 0.7 to 1.4 and the patient remained non oliguric. Nephrology team was consulted for AKI and MAHA. ADAMTS13 level was collected, lacosamide was held and valproic acid was continued. The patient was started on 60 IV methyl prednisone every eight hours. She also received 2 units of fresh frozen plasma. Three sessions of plasma exchange were performed. ADAMTs 13 came back at 50% making the diagnosis of drug induced thrombotic microangiopathy (DITMA) more likely. Patient platelets improved back to baseline. She was then stable and was discharged home. Discussion: The patient in this case started having signs of TMA 6 days after starting lacosamide, which improved after discontinuation of the medication. ADAMTS13 of 50% differentiated between drug induced TMA and TTP. DITMA can sometimes be challenging to diagnose, especially in the ICU setting. Although literature on lacosamide induced TMA is scarce, this case sheds the importance of keeping TMA as a differential in the setting of new onset thrombocytopenia and anemia after starting new medications.

Journal of the American Society of NephrologyVol. 35(10S)
Marshall University (US)
Openalex Percentile: Top 31%
Acute Myeloid Leukemia Research
0.45
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Lacosamide-Induced Thrombotic Microangiopathy — Zeid Khitan, Khaled Al-Baqain, et al. · Journal of the American Society of Nephrology (2024) | TGRS Research Map | TGRS