title: Persistently elevated troponin I in paracetamol hepatotoxicity: association with liver injury, organ failure, and outcome.
abstract: BACKGROUND
  An elevated troponin I (TnI) is associated with a poorer prognosis during critical illness.
  
  
  OBJECTIVE
  Our aims were to determine whether significant paracetamol-induced hepatotoxicity was associated with an elevated TnI; if this elevation was persistent and was associated with worse clinical outcomes.
  
  
  METHODS
  In this retrospective cohort study, the requirement for orthotopic liver transplantation (OLT) or death and/or the development of multiorgan failure (MOF) was evaluated for 48 consecutive patients admitted to the Royal Infirmary of Edinburgh (a university tertiary referral centre) with acute liver injury or acute liver failure secondary to paracetamol overdose.
  
  
  RESULTS
  TnI was elevated (≥ 0.05 ng/L) in 13/48 patients (27%). This appeared to be sustained for at least 6 days which has not been shown previously in the context of Acute Liver Injury (ALI). Elevated TnI was strongly associated with MOF, with the requirement for inotropic support being the strongest predictor (p = 0.003, OR 9.00, 95% CI 2.13-37.98). TnI elevations also correlated strongly with Acute Physiology and Chronic Health Evaluation (APACHE) II scores (p = 0.0006, r = 0.482, 95% CI 0.22-0.68) and with interleukin 6 (IL-6) levels (p = 0.0001, r = 0.55, 95% CI 0.29-0.73). Although a raised TnI was associated with a markedly increased risk of death or orthotopic liver transplant (p = 0.005, OR 7.73, 95% CI 1.87-32.05) on univariate analysis, this was primarily seen in the context of MOF (SOFA score p = 0.003, OR 1.23, 95% CI 1.07-1.41) and was not an independent predictor of death. There was no correlation between TnI or outcome with other cardiac biomarkers and markers of cardiovascular risk.
  
  
  CONCLUSIONS
  An elevated TnI in the context of acute liver injury or liver failure following paracetamol overdose is associated with a significantly worse patient outcome but it is not an independent prognostic factor. Further studies should be undertaken to investigate the mechanism behind this elevated troponin association.
authors.affiliation: Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Little France, Edinburgh EH16 4SA, UK.
authors.forename: J K
authors.initials: JK
authors.lastname: Moore
authors.forename: D G
authors.initials: DG
authors.lastname: Craig
authors.forename: E A
authors.initials: EA
authors.lastname: Pryde
authors.forename: S W
authors.initials: SW
authors.lastname: Walker
authors.forename: G J
authors.initials: GJ
authors.lastname: Beckett
authors.forename: P C
authors.initials: PC
authors.lastname: Hayes
authors.forename: K J
authors.initials: KJ
authors.lastname: Simpson
mesh_terms: D018806:APACHE; D000082:Acetaminophen / Q000506:poisoning*; D000293:Adolescent; D000328:Adult; D000368:Aged; D018712:Analgesics, Non-Narcotic / Q000506:poisoning*; D015415:Biomarkers / Q000097:blood; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood* / Q000175:diagnosis / Q000209:etiology / Q000401:mortality / Q000601:surgery; D016009:Chi-Square Distribution; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D017114:Liver Failure, Acute / Q000097:blood* / Q000175:diagnosis / Q000209:etiology / Q000401:mortality / Q000601:surgery; D016031:Liver Transplantation; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000097:blood / Q000209:etiology / Q000401:mortality; D015999:Multivariate Analysis; D016017:Odds Ratio; D063305:Organ Dysfunction Scores; D011379:Prognosis; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D012606:Scotland; D013997:Time Factors; D019210:Troponin I / Q000097:blood*; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D018712:Analgesics, Non-Narcotic; D015415:Biomarkers; C508600:IL6 protein, human; D015850:Interleukin-6; D019210:Troponin I; D000082:Acetaminophen