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31 January 2024 : Case report  Belgium

[In Press] Unconjugated Hyperbilirubinemia in Acetaminophen-Related Acute Liver Failure

Unusual clinical course, Challenging differential diagnosis, Diagnostic / therapeutic accidents, Management of emergency care, Adverse events of drug therapy

Marie Philippart1BE, Jean-Baptiste Mesland1C, Vincent Haufroid2D, Christine Collienne1D, Philippe Hantson12ABCDEF

DOI: 10.12659/AJCR.942703

Am J Case Rep In Press; DOI: 10.12659/AJCR.942703  

Available online: 2024-01-31, In Press, Corrected Proof

Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule

Abstract

BACKGROUND
In the absence of liver transplantation, the natural history of acetaminophen-induced liver failure is characterized by a progressive increase of liver function tests, including bilirubin mainly as its conjugated form. The presence of high levels of unconjugated bilirubin is more unusual; its etiology is unclear and its prognostic factor has been poorly investigated.
CASE REPORT
A 52-year-old man with a history of chronic analgesics, alcohol, and illicit drug abuse developed acute liver failure in relationship with the ingestion of largely supra-therapeutic doses of acetaminophen over the days preceding admission. The patient received the classical N-acetylcysteine treatment regimen for acetaminophen overdose. Clinical course was characterized by a progressive worsening of the neurological condition, evolving to grade IV encephalopathy. Coagulation disorders persisted, with factor V level <10%. He fulfilled the criteria for liver transplantation, but this option was rejected after a careful psychiatric evaluation. Laboratory investigations revealed a progressive increase in serum unconjugated bilirubin until his death. As evidence for hemolysis was lacking, acquired deficit in bilirubin glucuronidation appeared likely and diagnosis of Gilbert’s syndrome was excluded.
CONCLUSIONS
After the exclusion of other causes of high unconjugated bilirubin levels, the progressive increase in unconjugated bilirubin can reflect a persistent defect in bilirubin conjugation in relationship with liver centrilobular injury, but the relationship with acetaminophen-glucuronidation is not known and there are insufficient data to affirm that the ratio unconjugated/conjugated bilirubin could be used as a prognostic factor.

Keywords: Acetaminophen; Drug Overdose; Gilbert Disease; UGT1A1 Enzyme

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American Journal of Case Reports eISSN: 1941-5923
American Journal of Case Reports eISSN: 1941-5923