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. Author manuscript; available in PMC: 2023 Nov 24.
Published in final edited form as: Hepatology. 2021 Aug;74(2):937–949. doi: 10.1002/hep.31767

Table 1.

Demographics and baseline clinical features of the study population based upon etiology.

ALI* ALF
N Non-APAP (N=41) APAP (N=49) N Non-APAP (N=50) APAP (N=49)
Age (yrs) 90 48.0±26.0 33.0±19.0 99 52.0±22.2 38.0±19.0
Gender (% Female) 90 18(43.9) 34(69.4) 99 25(50.0) 31(63.3)
Race (% White) 90 27(65.9) 36(73.5) 99 40(80.0) 46(93.9)
INR 87 2.4±1.0 3.1±1.9 94 3.1±2.6 3.4±3.0
Platelet (x109/L) 85 173.0±91.0 149.5±74.0 95 118.0±138.0 126.5±87.8
Bilirubin (mg/dl) 89 10.8±9.7 2.7±2.8 94 7.4±13.4 4.5±4.4
Creatinine (mg/dl) 88 1.0±1.0 0.9±0.5 98 2.1±2.0 1.7±1.9
Fibrinogen (mg/dl) 23 190.0±91.0 200.0±73.2 44 172.0±103.0 177.0±133.0
aPTT (sec) 41 44.0±16.1 32.1±6.0 70 42.7±20.9 33.7±17.9
RRT at Admission (%) 90 0(0.0) 2(4.1) 99 17(34.0) 16(32.7)
Hepatic Encephalopathy (% grade 3/4) 96 26(54.2) 26(54.2)
SIRS (Present) 35 6(60.0) 12(48.0) 75 28(77.8) 30(76.9)

APAP, acetaminophen; RRT, renal replacement therapy; SIRS, systemic inflammatory response syndrome.

*

Ten patients (4 APAP and 6 non-APAP) presented as ALI but developed hepatic encephalopathy (ALF) during the study (“converters”); one ALI patient had liver injury of unknown etiology. Baseline data of these patients were omitted from this table.