Produção Nacional
Revisado por pares
Delayed-Onset Hepatic Encephalopathy Induced by Zolpidem: A Case Report
2008; Elsevier BV; Volume: 63; Issue: 4 Linguagem: Inglês
10.1590/s1807-59322008000400028
ISSN1980-5322
AutoresVitor Carlos Santos da Silva, Paulo Lisboa Bittencourt, Sylvania Pinho, Andréa Cavalcanti, Cláudio Celestino Zollinger,
Tópico(s)Drug-Induced Hepatotoxicity and Protection
ResumoHepatic encephalopathy (HE) is a complex neuropsychiatric disorder associated with either hepatocellular insufficiency and/or the presence of porto-systemic shunts. It is thought to be induced by altered neurotransmission mediated by enhanced gamma-aminobutyric acid (GABA)-induced inhibitory tone.1–3 The use of benzodiazepines are generally avoided in patients with advanced chronic liver disease (CLD) because they enhance GABA-mediated neurotransmission. Zolpidem is a non-benzodiazepine hypnotic that selectively binds to the omega-1 GABA-benzodiazepine receptor complex. Although it theoretically has the same propensity to induce HE, its shorter half-life when compared to commonly prescribed benzodiazepines like diazepam, alprazolam and clonazepan, makes it a reasonable choice for subjects with CLD.4 We report a patient with CLD with a rapidly induced grade IV HE attributed to zolpidem that was promptly reversed by flumazenil.
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