Role of inflammation and infection in the pathogenesis of human acute liver failure: Clinical implications for monitoring and therapy

Table 2 Proposed biomarkers in acute liver failure with an immune basis

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.