Hepatic involvement in dengue Fever in children
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Updated: May 17, 2026

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Kalenahalli Jagadishkumar1, Puja Jain, Vaddambal G Manjunath
1Department of Pediatrics, JSS Medical College, JSS University, Mysore, India.
Insights
Dengue infection frequently causes liver dysfunction in children, particularly in severe Dengue Hemorrhagic Fever and Dengue Shock Syndrome cases. Early consideration of dengue is vital for children with fever, jaundice, and tender hepatomegaly in endemic areas.
Area of Science:
- Pediatric Infectious Diseases
- Hepatology
- Virology
Background:
- Hepatic dysfunction is a common complication in dengue infection.
- Liver injury in children with dengue ranges from mild transaminase elevation to severe jaundice.
Purpose of the Study:
- To assess the spectrum of hepatic involvement in pediatric dengue infection.
- To characterize clinical and biochemical liver abnormalities in children with dengue.
Main Methods:
- Studied 110 serologically confirmed dengue fever cases in children (2 months - 14 years).
- Excluded malaria, enteric fever, Hepatitis A, and Hepatitis B through relevant investigations.
- Assessed hepatic functions clinically and biochemically, categorizing cases into Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF), and Dengue Shock Syndrome (DSS).
Main Results:
- Hepatomegaly (79%) and hepatic tenderness (56%) were prevalent.
- Elevated liver enzymes were common: AST (93%), ALT (78%), AP (57%).
- Jaundice (4.5%), prolonged PT (20%), reduced albumin (66%), and abnormal ultrasound (65%) were also observed.
Conclusions:
- Hepatic dysfunction was more pronounced in DHF and DSS groups compared to DF.
- Approximately 17.27% of children experienced >10 fold increase in liver enzymes.
- Clinical signs like hepatomegaly or tenderness did not correlate with the severity of liver function abnormalities.
Objective:
Hepatic dysfunction is common in dengue infection and the degree of liver dysfunction in children varies from mild injury with elevation of transaminases to severe injury with jaundice. This study was undertaken to assess the spectrum of hepatic involvement in dengue infection.
Methods:
110 children with serologically positive dengue fever aged between 2 months - 14 years were studied for their hepatic functions both clinically and biochemically after excluding malaria, enteric fever, Hepatitis A and Hepatitis B with relevant investigations.
Findings:
All cases were grouped into DF (Dengue fever), DHF (Dengue hemorrhagic fever) and DSS (Dengue shock syndrome) according to WHO criteria. The spectrum of hepatic manifestations included hepatomegaly (79%), hepatic tenderness (56%), jaundice (4.5%), raised levels of aspartate transaminase (AST)(93%), alanine transaminase (ALT)(78%), alkaline phosphatase (AP) (57%), prolonged prothrombin time (PT) (20%), reduced levels of serum albumin (66%) and abnormal abdomen ultrasound (65%).
Conclusion:
Hepatic dysfunction was observed more in DHF and DSS group compared to DF group. About 17.27% of children had >10 fold increase in the liver enzymes. There was no correlation between the degree of hepatic enlargement or hepatic tenderness with the abnormalities of liver functions. Any child with fever, jaundice and tender hepatomegaly in geographical areas where dengue is endemic, the diagnosis of dengue infection should be strongly considered.
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