Table 2.
Ref. | Biomarker study population | Relevance | Finding in ALF |
Antoniades et al[75] | Monocyte HLA-DR expression | Monocytes are key in the immune dysregulation of ALF | Percentage of monocyte HLA-DR expression significantly lower in ALF patients compared with healthy controls, correlating with poor prognosis |
APAP-ALI | |||
Koch et al[76] | Soluble urokinase plasminogen activator receptor (suPAR) | suPAR related to immune activation in systemic inflammation | suPAR levels significantly increased in ALF patients, correlating with parameters reflecting hepatocyte injury |
ALF (all aetiologies) | |||
Craig et al[77] | Pentraxin-3 | Pentraxins are soluble pattern recognition receptors forming part of the humoral innate immune system | Admission levels of pentraxin-3 significantly higher in patients with APAP-ALI than those with non-APAP ALI. Pentraxin-3 levels significantly higher in APAP-ALI patients who died/required transplantation vs spontaneous survivors. |
APAP-ALI | |||
Rule et al[78] | Procalcitonin | Biomarker of bacterial infection studied in other clinical conditions | No difference in procalcitonin levels in pre-defined severity groups, non-SIRS and SIRS groups with no documented infection and no correlation with presence of infection |
ALFSG | ALF (all aetiologies) | ||
Antoniades et al[79] | Secretory Leukocyte Protease Inhibitor | Stimulates epithelial cell proliferation and modulates macrophage function | Higher SLPI levels were associated with a greater liver injury, infection and adverse outcome |
APAP-ALI | |||
Craig et al[80] | Neopterin and soluble CD163 (sCD163) | Markers of macrophage activation | Levels of both markers significantly higher in APAP-ALI compared with CLD and healthy controls. No association between biomarker level and presence of infection. |
APAP-ALI |
ALF: Acute liver failure; APAP: Acetaminophen.