Inflammation-induced hepatotoxicity in humans

Shock. 2009 Feb;31(2):151-6. doi: 10.1097/SHK.0b013e31818335ff.

Abstract

Because severe sepsis is frequently complicated by multiple organ failure, it is of importance to monitor organ function. Unfortunately, conventional liver function markers are either relatively unspecific or have a long half-life, which make them poor predictors of acute liver injury. Glutathione S-transferase A1-1 (GSTA1-1) has a relatively short half-life (1 h), is more specific, and is rapidly released into the blood after liver damage. In the present study, we measured plasma GSTA1-1 levels by enzyme-linked immunosorbent assay in seven healthy volunteers after repeated experimental endotoxemia induced by 2 ng kg Escherichia coli endotoxin per day (to investigate inflammation-induced hepatic injury) and in 21 patients within 12 h after the occurrence of severe sepsis/septic shock (to investigate its ability to predict an increase of transaminases on day 7). During repeated experimental endotoxemia in healthy volunteers, TNF-alpha and IL-6 levels increased from undetectable levels to 1,425 (474-1,949) and 1,739 (989-2,047) pg mL, respectively, whereas GSTA1-1 levels did not exceed the normal range, indicating that no (sub)clinical liver injury occurs in this model of inflammation. In septic patients, GSTA1-1 levels had a specificity of 88%, resulting in a positive predictive value for liver injury of 86% and a positive likelihood ratio of 6 to indicate an increase in transaminases on day 7. Furthermore, GSTA1-1 levels did not correlate with IL-6 levels but did with dobutamine infusion rate (Spearman r = 0.94; P = 0.02), suggesting that the extent of hemodynamic instability and not the degree of inflammation could be of importance for the occurrence of liver damage. In septic shock patients, GSTA1-1 may represent a useful marker for early liver injury.

MeSH terms

  • Adult
  • Aged
  • Escherichia coli / metabolism
  • Female
  • Glutathione Transferase / blood
  • Glutathione Transferase / metabolism
  • Humans
  • Inflammation / etiology*
  • Inflammation / pathology*
  • Interleukin-6 / metabolism
  • Liver / injuries
  • Liver / pathology*
  • Liver Failure, Acute / diagnosis*
  • Liver Failure, Acute / enzymology
  • Male
  • Middle Aged
  • Sensitivity and Specificity
  • Shock, Septic / blood*
  • Shock, Septic / diagnosis
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Glutathione Transferase