The clinical data of 112 patients with hepatitis B virus (HBV)- and non-HBV-related
liver failure admitted to the intensive care unit (ICU) of the Fifth People's Hospital of Wuxi were collected from January to December 2020. The relevant etiologies of acute, subacute, acute-on-chronic, subacute-on-chronic, chronic subtype
liver failure were analyzed. The efficacies of
artificial liver support systems in the treatment of various subtypes of
liver failure were also compared. The correlation of various indicators was analyzed by Spearman correlation analysis, the risk factors affecting the prognosis of patients with
liver failure were analyzed by multivariate Logistic regression equation, and receiver operator characteristic curve (ROC curve) of subjects was plotted to evaluate the predictive value of each risk factor for the prognosis of patients with
liver failure.
RESULTS: Among the 112
liver failure patients, 63 were caused by
hepatitis B and 49 were caused by non-
hepatitis B. The
liver failure caused by
hepatitis B was 6 times higher than for men than for women, which was higher than that of non-HBV
liver failure group (1.33 times).
Antithrombin III (AT III) and total
bilirubin (TBil) levels of subacute
liver failure were higher than those of pre-
liver failure in the HBV
liver failure group [AT III: (59.33±14.57)% vs. (35.66±20.72)%, TBil (μmol/L): 399.21±112.94 vs. 206.08±126.96, both P < 0.05]. The levels of AT III in patients with pre-
liver failure and
chronic liver failure in the non-HBV
liver failure group were significantly higher than those with
acute liver failure [(58.33±15.28)%, (44.00±19.10)% vs. (31.33±7.57)%, both P < 0.05], patients with
acute liver failure had significantly lower level of TBil than pre-
liver failure (μmol/L: 107.83±49.73 vs. 286.20±128.92, P < 0.05), the TBil levels in patients with subacute and
acute-on-chronic liver failure were also significantly higher than that in pre-
liver failure group (μmol/L: 417.27±118.60, 373.00±187.00 vs. 286.20±128.92, both P < 0.05). Patients with subacute
liver failure, subacute-on-
chronic liver failure and
chronic liver failure in the non-HBV failure group were significantly longer than those in
acute liver failure (days: 36.00±8.31, 27.52±11.71, 27.72±22.71 vs. 11.00±1.41, all P < 0.05). There was no statistically significant difference in the case fatality rate of using the
artificial liver support system between the HBV failure group and the non-HBV failure group (55.6% vs. 50.0%, P < 0.05), the levels of AT III in the two groups of surviving patients were significantly higher than that of the dead [HBV
liver failure group: (36.20±6.26)% vs. (27.33±8.87)%, non-HBV
liver failure group: (41.06±4.16)% vs. (28.71±12.35)%, both P < 0.01]. Correlation analysis showed that there was a clear positive correlation between AT III and TBil in the dead patients of HBV
liver failure group and the survival and death patients of non-HBV
liver failure group (r values were 0.069, 0.341, 0.064, and P values were 0.723, 1.196 and 0.761, respectively); there was a significant inverse correlation between AT III and TBil in the HBV
liver failure group (r = -0.105, P = 0.745). Multivariate Logistic regression analysis showed that AT III was an independent risk factor affecting the prognosis of patients with non-HBV
liver failure [odd ratio (OR) = 1.023, 95% confidence interval (95%CI) was -0.001 to 0.001, P = 0.007]. TBil was an independent risk factor affecting prognosis of patients with HBV
liver failure (OR = 1.005, 95%CI was -0.002 to -7.543, P = 0.033). The analysis of ROC curve showed that AT III had a predictive value for the prognosis of patients with non-HBV
liver failure, the area under the ROC curve (AUC) = 0.747, the 95%CI was 0.592-0.902, P = 0.009. When the optimal truncation value was 39.5%, its sensitivity and specificity were 83.33% and 56.25%, respectively.
CONCLUSIONS: