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. Author manuscript; available in PMC: 2023 Oct 15.
Published in final edited form as: Semin Liver Dis. 2022 Aug 24;42(3):362–378. doi: 10.1055/s-0042-1755274

Table 1.

Clinical and laboratory features of the different etiologies of acute liver failure

Clinical feature Etiology of ALF, N = 2,614
Paracetamol, N = 1,195 Ischemia, N = 181 DILI, N = 283 AI-ALF, N = 173 HBV, N = 188 HAV, N = 39 Pregnant, N = 27 All others, N = 528
Age (median years) 37 53 47 46 45 50 31 40
Gender (% female) 75 58 67 81 45 44 100 64
Jaundice-coma (median days) 1 2 12 16 8 4 7 7
HE grade ≥ 3 (%) 54 56 36 27 51 54 54 44
ALT (median IU/L) 3,780 2,311 654 404 1,410 2,229 43 758
Bilirubin (median mg/dL) 4.3 3.8 19.6 22.8 19.2 12.0 9.0 16.2
Transplanted* (%) 9 2 39 57 40 33 4 36
Transplant-free survival* (%) 65 57 24 14 19 51 78 22
Overall survival* (%) 72 58 58 63 53 77 82 55

Abbreviations: AI, autoimmune; ALF, acute liver failure; ALT, alanine aminotransferase; DILI, drug-induced liver injury; HAV, hepatitis A virus; HBV, hepatitis B virus; HE, hepatic encephalopathy.

Note: Striking differences are seen between the two hyperacute etiologies (paracetamol and ischemia) and all other etiologies in terms of time from onset to failure, liver laboratory values, and outcomes.

*

indicates outcome 21 days after admission for ALF to the study site hospital