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Published on: April 17, 2017
Is HCV infection associated with liver steatosis also in children?
Antonietta Giannattasio1, Maria Immacolata Spagnuolo, Angela Sepe
1Department of Pediatrics, University Federico II, Naples, Italy.
Insights
Steatosis (fatty liver) affects a quarter of children with chronic hepatitis C (CHC). Children with steatosis show more severe fibrosis and a lower sustained response to interferon therapy.
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Viral Hepatitis Research
Background:
- The prevalence and clinical significance of steatosis in pediatric chronic hepatitis C (CHC) are not well-established.
- Understanding steatosis in children with CHC is crucial for disease management and treatment outcomes.
Purpose of the Study:
- To analyze the prevalence of steatosis in children diagnosed with CHC.
- To investigate the relationship between steatosis and clinical features, laboratory findings, and interferon treatment response in pediatric CHC patients.
Main Methods:
- Retrospective evaluation of 64 pediatric patients with CHC who underwent liver biopsy.
- Assessment of steatosis, necroinflammation, fibrosis, and body mass index (BMI).
- Analysis of interferon treatment response in patients with and without steatosis.
Main Results:
- Twenty-five percent of children with CHC exhibited mild to moderate steatosis.
- Steatosis was not significantly associated with BMI, but patients with steatosis showed a trend towards higher fibrosis scores (P<0.05).
- Children with steatosis had significantly lower rates of sustained response to interferon therapy (23%) compared to those without steatosis (53%).
Conclusions:
- Histological steatosis is present in approximately 25% of children with CHC, potentially independent of metabolic factors.
- Pediatric CHC patients with steatosis may experience more advanced fibrosis.
- Steatosis in pediatric CHC is associated with a poorer sustained virologic response to interferon therapy.
Background/Aims:
Prevalence and significance of steatosis in children with chronic hepatitis C are not well defined. We analysed the prevalence of steatosis in children with chronic hepatitis C and its relationship with clinical, laboratory features and response to interferon.
Methods:
Sixty-four consecutive children with CHC undergoing liver biopsy were retrospectively evaluated.
Results:
Twenty-five percent of children showed mild to moderate steatosis. Only one child was infected by genotype 3. Body mass index did not significantly differ between children with and without steatosis. Although no significant difference in necroinflammatory and fibrosis scores between children with and without steatosis was found, 3 (18.7%) of 16 patients with steatosis and only one (2.1%) of 48 patients without steatosis had a fibrosis score >2 (P<0.05). Forty-seven children (13 with steatosis) received interferon after liver biopsy. A sustained response was observed in 3 (23%) children with steatosis and in 18 (53%) without steatosis.
Conclusions:
Histological evidence of steatosis is detectable in a quarter of children with CHC. Differently from adults, genotypes other than 3 may be associated with steatosis independently from classical metabolic risk factors. Children with steatosis seem to have more severe fibrosis and lower rates of sustained response to interferon therapy compared to children without steatosis.
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