• norsk
    • English
  • norsk 
    • norsk
    • English
  • Logg inn
Vis innførsel 
  •   Hjem
  • Fakultet for helsevitenskap (HV)
  • HV - Institutt for naturvitenskapelige helsefag
  • Vis innførsel
  •   Hjem
  • Fakultet for helsevitenskap (HV)
  • HV - Institutt for naturvitenskapelige helsefag
  • Vis innførsel
JavaScript is disabled for your browser. Some features of this site may not work without it.

Fatal liver failure after therapeutic doses of paracetamol in a patient with Duchenne muscular dystrophy and atypical pharmacogenetic profile of drug-metabolizing enzymes

Lao, Yvonne Elisabeth; Molden, Espen; Kringen, Marianne K.; Annexstad, Ellen Johanne; Sæverud, Håvard Andreassen; Jacobsen, Dag; Hovda, Knut Erik
Journal article, Peer reviewed
Accepted version
Thumbnail
Åpne
Lao_et_al-2020-Basic__Clinical_Pharmacology__Toxicology.pdf (1.356Mb)
Permanent lenke
https://hdl.handle.net/10642/9496
Utgivelsesdato
2020-01-24
Metadata
Vis full innførsel
Samlinger
  • HV - Institutt for naturvitenskapelige helsefag [361]
Originalversjon
Lao Y, Molden, Kringen, Annexstad, Sæverud, Jacobsen, Hovda. Fatal liver failure after therapeutic doses of paracetamol in a patient with Duchenne muscular dystrophy and atypical pharmacogenetic profile of drug-metabolizing enzymes. Basic & Clinical Pharmacology & Toxicology. 2020;127(1):47-51   https://doi.org/10.1111/bcpt.13389
Sammendrag
Paracetamol has a good safety profile, but pharmacogenetic differences in drug-metabolizing enzymes

may have an impact on its risk of hepatotoxicity. We present a case of fatal acute liver failure (ALF) after

therapeutic doses of paracetamol in a patient with Duchenne muscular dystrophy, where

pharmacogenetic screening was conducted.

This 30-year-old man was electively admitted for a tracheostomy. A total of 14.5 g paracetamol was given

over four days. He developed a severe ALF and died 11 days after admission. Pharmacogenetic screening

showed absent CYP2D6 metabolism and increased CYP1A2 activity, which may have increased the

formation of toxic intermediate metabolite, N-acetyl-p-benzo-quinone imine (NAPQI). He also had

decreased function of UGT2B15, which increases the amount of paracetamol available for metabolism to

NAPQI. Having a reduced muscle mass and thus a reduced glutathione levels to detoxify produced NAPQI

may add to the risk of toxicity.

This case may indicate that pharmacogenetic variability is of potential relevance for the risk of

paracetamol-induced hepatotoxicity in patients with neuromuscular diseases. Further studies should

investigate if pharmacogenetic screening could be a tool to detect potentially increased risk of

hepatotoxicity in these patients at therapeutic doses of paracetamol, and hence provide information for

selection of analgesic treatment.
Utgiver
Wiley
Serie
Basic & Clinical Pharmacology & Toxicology;Volume 127, Issue 1, July 2020
Tidsskrift
Basic & Clinical Pharmacology & Toxicology

Kontakt oss | Gi tilbakemelding

Personvernerklæring
DSpace software copyright © 2002-2019  DuraSpace

Levert av  Unit
 

 

Bla i

Hele arkivetDelarkiv og samlingerUtgivelsesdatoForfattereTitlerEmneordDokumenttyperTidsskrifterDenne samlingenUtgivelsesdatoForfattereTitlerEmneordDokumenttyperTidsskrifter

Min side

Logg inn

Statistikk

Besøksstatistikk

Kontakt oss | Gi tilbakemelding

Personvernerklæring
DSpace software copyright © 2002-2019  DuraSpace

Levert av  Unit