title: An elevated neutrophil-lymphocyte ratio is associated with adverse outcomes following single time-point paracetamol (acetaminophen) overdose: a time-course analysis.
abstract: BACKGROUND
  The innate immune system is profoundly dysregulated in paracetamol (acetaminophen)-induced liver injury. The neutrophil-lymphocyte ratio (NLR) is a simple bedside index with prognostic value in a number of inflammatory conditions.
  
  
  OBJECTIVE
  To evaluate the prognostic accuracy of the NLR in patients with significant liver injury following single time-point and staggered paracetamol overdoses.
  
  
  METHODS
  Time-course analysis of 100 single time-point and 50 staggered paracetamol overdoses admitted to a tertiary liver centre. Timed laboratory samples were correlated with time elapsed after overdose or admission, respectively, and the NLR was calculated.
  
  
  RESULTS
  A total of 49/100 single time-point patients developed hepatic encephalopathy (HE). Median NLRs were higher at both 72 (P=0.0047) and 96 h after overdose (P=0.0041) in single time-point patients who died or were transplanted. Maximum NLR values by 96 h were associated with increasing HE grade (P=0.0005). An NLR of more than 16.7 during the first 96 h following overdose was independently associated with the development of HE [odds ratio 5.65 (95% confidence interval 1.67-19.13), P=0.005]. Maximum NLR values by 96 h were strongly associated with the requirement for intracranial pressure monitoring (P<0.0001), renal replacement therapy (P=0.0002) and inotropic support (P=0.0005). In contrast, in the staggered overdose cohort, the NLR was not associated with adverse outcomes or death/transplantation either at admission or subsequently.
  
  
  CONCLUSIONS
  The NLR is a simple test which is strongly associated with adverse outcomes following single time-point, but not staggered, paracetamol overdoses. Future studies should assess the value of incorporating the NLR into existing prognostic and triage indices of single time-point paracetamol overdose.
authors.affiliation: aGastroenterology Department, The James Cook University Hospital, Middlesbrough bDivision of Clinical and Surgical Sciences, University of Edinburgh, Edinburgh, UK.
authors.forename: Darren G
authors.initials: DG
authors.lastname: Craig
authors.forename: Laura
authors.initials: L
authors.lastname: Kitto
authors.forename: Sara
authors.initials: S
authors.lastname: Zafar
authors.forename: Thomas W D J
authors.initials: TW
authors.lastname: Reid
authors.forename: Kirsty G
authors.initials: KG
authors.lastname: Martin
authors.forename: Janice S
authors.initials: JS
authors.lastname: Davidson
authors.forename: Peter C
authors.initials: PC
authors.lastname: Hayes
authors.forename: Kenneth J
authors.initials: KJ
authors.lastname: Simpson
mesh_terms: D000082:Acetaminophen / Q000506:poisoning*; D000328:Adult; D018712:Analgesics, Non-Narcotic / Q000506:poisoning*; D056486:Chemical and Drug Induced Liver Injury / Q000175:diagnosis / Q000276:immunology / Q000601:surgery; D062787:Drug Overdose / Q000175:diagnosis* / Q000276:immunology; D005260:Female; D006501:Hepatic Encephalopathy / Q000139:chemically induced / Q000175:diagnosis / Q000276:immunology; D006801:Humans; D007958:Leukocyte Count; D017114:Liver Failure, Acute / Q000139:chemically induced / Q000175:diagnosis / Q000276:immunology / Q000601:surgery; D016031:Liver Transplantation; D008214:Lymphocytes / Q000473:pathology*; D008297:Male; D009504:Neutrophils / Q000473:pathology*; D011379:Prognosis; D012189:Retrospective Studies; D016019:Survival Analysis; D018746:Systemic Inflammatory Response Syndrome / Q000139:chemically induced / Q000175:diagnosis / Q000276:immunology; D014218:Triage / Q000379:methods
chemical_list: D018712:Analgesics, Non-Narcotic; D000082:Acetaminophen