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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\u2010year\u2010old man was electively admitted for a tracheostomy. A total of 14.5\u00a0g paracetamol was given over four days. He developed a severe ALF and died 11\u00a0days after admission. Pharmacogenetic screening showed absent CYP2D6 metabolism and increased CYP1A2 activity, which may have increased the formation of toxic intermediate metabolite, N\u2010acetyl\u2010p\u2010benzo\u2010quinone 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\u2010induced 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.<\/jats:p>","DOI":"10.1111\/bcpt.13389","type":"journal-article","created":{"date-parts":[[2020,1,24]],"date-time":"2020-01-24T17:54:34Z","timestamp":1579888474000},"page":"47-51","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Fatal liver failure after therapeutic doses of paracetamol in a patient with Duchenne muscular dystrophy and atypical pharmacogenetic profile of drug\u2010metabolizing enzymes"],"prefix":"10.1111","volume":"127","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2744-6390","authenticated-orcid":false,"given":"Yvonne Elisabeth","family":"Lao","sequence":"first","affiliation":[{"name":"Norwegian National Unit for CBRNE Medicine Department of 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