Levetiracetam
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Rhabdomyolysis: case report A 22-year-old man developed rhabdomyolysis during treatment with levetiracetam for generalised tonic-clonic seizures. The man presented to the emergency department (ED) for evaluation of a new-onset single episode of generalised tonic-clonic seizure at home lasting for about 2–3 min, followed by fall and brief syncopal episode. In the ED, he was found to be completely oriented and neurologically intact without postictal confusion. He received a single dose of IV levetiracetam 500mg in the ED and was admitted for further evaluation and management. He was then started on oral levetiracetam 500mg twice daily. Imaging studies, including CT and MRI of the head, were unremarkable. An electroencephalogram (EEG) was unremarkable and did not show any focus of epileptiform activity. Neurology consultation was requested. Oral levetiracetam 500mg twice daily was continued because of previously suspected seizure-like symptoms in his history. Eight hours after the initiation of levetiracetam (i.e. 10h after hospital admission), a slight elevation in his creatine kinase (CK) was noted, which was presumed to be due to the rhabdomyolysis secondary to the seizure episode. He received IV fluids and CK levels were monitored. Despite aggressive IV hydration for almost 72h, CK levels continued to rise and reached a level above 20000 IU/L on day 5. His serum myoglobin was found to be elevated at 594 ng/mL, but there was no evidence of acute kidney injury or myoglobinuria. His serum electrolytes, including phosphorus, calcium and potassium, were within the normal limits and his urine drug screen was negative for cocaine/ amphetamines. He was not on any other medications. He remained seizure free since his hospital admission. He had no known underlying musculoskeletal disorder. He denied any recent viral respiratory tract or gastrointestinal infection. In the absence of any obvious reason to explain this unexpected and persistent increase in CK level, levetiracetam was suspected to be the cause of his rhabdomyolysis. Levetiracetam was discontinued on day 5, with CK levels peaking to 21936 IU/L about 12h after the last levetiracetam dose, followed by significant decrease in CK level to 11337 IU/L the next day. Throughout his hospital stay, he did not complain of myalgias; he remained neurologically intact and seizure free. Investigations for genetic musculoskeletal or mitochondrial disorders was not performed since he declined family history of musculoskeletal disorders. On day 6, he was discharged from the hospital without any antiepileptic medication. He was advised to follow-up with the neurologist an as outpatient within 1–2 weeks of discharge, and he reported no further seizure episodes. Repeat EEG after 14 days of hospital discharge did not show any epileptiform activity. The CK level was repeated 8 days after hospital discharge (i.e. 9 days after discontinuation of levetiracetam) and it was found to be 330 IU/L, further supporting the diagnosis of levetiracetam-induced rhabdomyolysis. Moinuddin IA. Su
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