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Published on: June 26, 2020
A novel, bedside, etiology specific prognostic model (Peds-HAV) in hepatitis A induced pediatric acute liver failure
Bikrant Bihari Lal1, Vikrant Sood1, Pandey Snehavardhan1
1Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, 110070, India.
Insights
A new Peds-HAV model accurately predicts death in children with Hepatitis A-induced acute liver failure. This simple, bedside tool uses three objective parameters to guide transplant listing decisions.
Area of Science:
- Hepatology
- Pediatric Gastroenterology
- Virology
Background:
- Hepatitis A virus (HAV) is a leading cause of pediatric acute liver failure (PALF) in developing nations.
- Developing an etiology-specific prognostic model for HAV-induced PALF is crucial for patient management.
Purpose of the Study:
- To develop and validate a prognostic model specifically for pediatric acute liver failure caused by Hepatitis A virus.
- To identify independent predictors of mortality in children with HAV-induced PALF.
Main Methods:
- A cohort of children with HAV-induced PALF was analyzed.
- A prognostic model (Peds-HAV) was derived using independent predictors of 28-day outcomes (death or native liver survival).
- The model was validated prospectively in an independent cohort.
Main Results:
- Hepatitis A accounted for 45.9% of PALF cases.
- The Peds-HAV model identified Grade 3-4 hepatic encephalopathy (HE), INR > 3.1, and jaundice-to-HE interval > 10 days as predictors of death.
- The model demonstrated high sensitivity (83.3-90%) and specificity (81.4-92.6%) in predicting death in both derivation and validation cohorts.
Conclusions:
- The Peds-HAV model is a simple, dynamic, and etiology-specific prognostic tool for HAV-induced PALF.
- Its optimal sensitivity and specificity support its use as a criterion for liver transplant listing in these patients.
Background:
Hepatitis A virus (HAV) is the commonest cause of pediatric acute liver failure (PALF) in developing countries. Our objective was to develop and validate a HAV-etiology specific prognostic model in PALF.
Methods:
All children with HAV induced PALF (IgM HAV reactive) were included. Outcome was defined at day 28. Only those with death or native liver survival were included. The model (Peds-HAV) was derived using the independent predictors of outcome and validated in a prospective independent cohort.
Results:
Hepatitis A accounted for 131 (45.9%) of total 285 PALF. After excluding 11 children who underwent liver transplant, 120 children (74 survivors and 46 death) were included. The first 75 patients formed the derivation cohort and the next 45 patients formed the prospective validation cohort. In the derivation cohort, INR: OR 2.208, (95% CI 1.321-3.690), p = 0.003, grade of hepatic encephalopathy (HE): OR 3.078, (95% CI 1.017-9.312), p = 0.047 and jaundice-to-HE interval: OR 1.171, (95% CI 1.044-1.314), p = 0.007 were independent predictors of death. The final model comprised three criteria: (1) presence of grade 3-4 HE, (2) INR greater than 3.1, and (3) jaundice to HE interval more than 10 days. Presence of 2 or more of these criteria predicted death with 90% sensitivity, 81.4% specificity and 84.9% accuracy. Peds-HAV model was superior to existing prognostic models. In the validation cohort, Peds-HAV model predicted death with 83.3% sensitivity and 92.6% specificity.
Conclusion:
Peds-HAV model is a simple, bedside, dynamic, etiology (HAV) specific prognostic model based on 3 objective parameters with optimum sensitivity and specificity, hence should be used as liver transplant listing criteria in HAV induced PALF.
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