Cannabidiol/lithium interaction
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Cannabidiol/lithium interaction Renal dysfunction and lithium toxicity: case report
A 13-year-old boy developed lithium toxicity during concomitant treatment with cannabidiol and lithium secondary to cannabidiol-induced renal dysfunction during treatment of Lennox-Gastaut syndrome (LGS) [routes and time to reactions onset not stated]. The boy with LGS (started at 18 months of age), autism, history of two previous epilepsy surgeries and history of vagus nerve stimulator (VNS; at the age of 11 years), presented to a comprehensive epilepsy clinic for transfer care. He had undergone full corpus callosotomy (at the age of 4 years) and left frontal lobe resection (at the age of 7 years). He experienced seizures several times a week, and his prior medications included rufinamide, levetiracetam, lacosamide, topiramate, oxcarbazepine, lamotrigine and valproic acid. At presentation, he had been receiving clobazam and felbamate for over 4 months at stable doses. He met the criteria for autism spectrum disorder with comorbidities including associated aggressive and self-harmful behaviours, severe intellectual disability and sleep difficulties. At baseline, he was non-verbal and incontinent, but with full strength and ambulation. Several months prior to the initiation of cannabidiol, he was transitioned to the psychiatry service during a hospitalisation. During prior hospitalisation, he had increasing lethargy and aggressiveness, and bupropion, pregabalin and amantadine were discontinued. He continued to receive a complex regimen of psychoactive medications, including lithium 600mg every morning, 300mg every evening and 600mg every night/bedtime along with perphenazine, trazodone and quetiapine. Upon presentation, to the epilepsy clinic, cannabidiol was recommended to improve his seizure control and possibly behaviour control, on which his psychiatrist agreed. He started receiving cannabidiol 5 mg/kg/day, divided into twice a day. His clobazam dose was reduced by 25% due to potential interaction with cannabidiol. However, after the increase in cannabidiol dose to 10 mg/kg/day as scheduled, he showed symptoms of weakness, lethargy, decreased oral intake and unsteadiness. Hence, he was admitted to the hospital. At this point, his clobazam dose was reduced by 50%. The parents reported that after taking his midday doses of lithium, clonidine and felbamate, he would become lethargic, tired and off balance. On evaluation, he was afebrile but somnolent. When awake, he was ataxic compared to baseline. All other laboratory tests were unremarkable. However, his lithium level was markedly elevated to 2.4 mmol/L (baseline 1–1.3 mmol/L). His creatinine levels increased from 0.6 mg/dL (before the initiation of cannabidiol) to 0.75 mg/dL (2 weeks after the initiation of cannabidiol). Neurology and psychiatry was consulted. He was thought to have lithium toxicity due to drug-drug interaction secondary to cannabidiol-induced renal dysfunction. The boys lithium treatment was stopped, and midday doses of felbamate and clobazam were held. H
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