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Prolonged coma due to amitriptyline overdose and genetic polymorphism: a case report.

Tijs van de Wint1, Aurelia H M de Vries Schultink2, Arend Jan Meinders3

  • 1Department of Anesthesiology, Intensive Care and Pain Management, St. Antonius Hospital, Amsterdam, The Netherlands. t.van.de.wint@antoniusziekenhuis.nl.

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A tricyclic antidepressant overdose, specifically amitriptyline, caused prolonged coma in a patient with a cytochrome P450 2D6 poor metabolizer status. This case highlights unexpected toxicological presentations and genetic factors influencing drug metabolism.

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Area of Science:

  • Toxicology
  • Pharmacogenetics
  • Clinical Neurology

Background:

  • Reduced consciousness often stems from toxic causes, though the source isn't always apparent.
  • Tricyclic antidepressants (TCAs) are a less common cause of toxic-induced unconsciousness.

Observation:

  • A 76-year-old female presented with unexplained unconsciousness.
  • Initial diagnostics, including a drug abuse screen, were inconclusive.
  • Cardiac (intraventricular conduction delay, QRS widening) and EEG abnormalities suggested a drug-induced effect.

Findings:

  • Heteroanamnesis and lab confirmation revealed amitriptyline intoxication.
  • High amitriptyline levels and cytochrome P450 2D6 poor metabolizer status correlated with prolonged coma.
  • The patient remained comatose for several days due to the severe overdose and impaired drug metabolism.

Implications:

  • This case underscores the importance of considering TCAs in unexplained comatose states.
  • Genetic variations (CYP2D6 poor metabolizer) significantly impact TCA toxicity and duration.
  • Awareness of TCA overdose and pharmacogenetic interactions is crucial for clinical management.