ArticleCureus2025
Prolonged Elimination of Lamotrigine After Suicidal Overdose: A Case Report.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lamotrigine (LTG) is an antiepileptic drug that stabilizes neuronal membranes by inhibiting excitatory neurotransmitter release, thereby reducing neuronal excitation. Various factors can contribute to its metabolic dysfunction. A 22-year-old female with bipolar disorder presented after intentionally ingesting 216 tablets, including LTG (4,100 mg), prescribed antipsychotics, over-the-counter cold medicine containing acetaminophen (27 g), and alcohol. She arrived at the hospital approximately one-hour post-ingestion in a confused state, with mild transaminase elevation but no significant electrocardiographic abnormalities. Initial management included activated charcoal, N-acetylcysteine therapy, and intravenous fluids. Despite these interventions, she deteriorated to a comatose state by hospital day two, accompanied by a mild skin rash later diagnosed as urticaria. Her hepatic function and consciousness gradually improved, with transaminase normalization and full neurological recovery by day six. She was discharged on day seven without residual deficits. Serial LTG serum measurements at 13, 55, and 79 hours post-ingestion (16.10 mg/L, 12.39 mg/L, and 6.84 mg/L, respectively) revealed a non-linear elimination pattern, with an estimated half-life of ~100 hours between the first two measurements. However, by the third measurement, elimination aligned with previously reported pharmacokinetics. The patient's young age, normal BMI, absence of hepatic disease, and minimal interaction potential with co-ingested antipsychotics did not explain the delayed LTG clearance. We hypothesize that hepatic metabolic pathway saturation led to this non-linear pharmacokinetic behavior. The resolution of delayed elimination corresponded with hepatic enzyme normalization. In drug overdose cases, prolonged consciousness disturbance may indicate an extended drug half-life due to metabolic dysfunction. If recovery exceeds expectations, further evaluation is warranted to identify and address potential causes.
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Registered trials
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