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Mannose-binding lectin in chronic hepatitis C in children
Agnieszka Balbina Dzwonek1, Teresa Woźniakowska-GĘsicka, Małgorzata Wiśniewska-Ligier
11Department of Paediatrics, Polish Mother's Memorial Hospital, Research Institute , Łódź , Poland.
Insights
Mannose-binding lectin (MBL) deficiency in children with chronic hepatitis C is linked to poorer response to antiviral therapy. Lower MBL levels were observed in non-responders, suggesting MBL
Area of Science:
- Immunology
- Hepatology
- Pediatrics
Background:
- Chronic hepatitis C is a significant liver disease in children.
- Mannose-binding lectin (MBL) plays a role in innate immunity.
- MBL genetic variations and serum levels may influence disease progression and treatment outcomes.
Purpose of the Study:
- To examine the association between MBL genetic polymorphisms and phenotype in pediatric chronic hepatitis C.
- To determine the impact of MBL status on the effectiveness of antiviral therapy in children.
Main Methods:
- Study included 54 children (2.5-18 years) with chronic hepatitis C.
- Treatment involved interferon-α alone or with ribavirin.
- MBL genotypes and serum MBL levels were assessed pre-therapy and correlated with treatment response.
Main Results:
- Lower serum MBL levels were found in non-responders (IFN-NR) compared to sustained responders (IFN-SR) (p=0.04).
- MBL2 polymorphisms were more frequent in non-responders, though not statistically significant (p=0.08).
- Elevated ALT and AST levels correlated with the A/O MBL genotype.
Conclusions:
- MBL deficiency, indicated by genotype and phenotype, may negatively impact chronic hepatitis C progression in children.
- MBL deficiency appears to reduce the efficacy of antiviral therapy in pediatric patients.
Objective:
To investigate effect of mannose-binding lectin (MBL) genetic polymorphisms and phenotype in chronic hepatitis C and its impact on response to antiviral therapy in children.
Methods:
Fifty four children with chronic hepatitis C, aged 2.5-18 years were enrolled. Forty-five children were treated with interferon-α (IFN-α) alone (n = 2) or IFN-α and ribavirin (n = 43). Twenty-one children who responded to antiviral therapy were defined as sustained responders to therapy (IFN-SR). Before therapy, MBL genotypes and serum MBL levels (by ELISA) were determined. MBL genotype distribution and levels were correlated to disease characteristics and response to therapy.
Results:
Children with chronic hepatitis C who did not respond to antiviral therapy (IFN-NR) presented more frequently MBL2 polymorphisms, although this did not reach significance (p = 0.08). MBL levels were significantly lower in children classified as IFN-NR when compared to children defined as IFN-SR (1.623 ng/ml vs. 3.699 ng/ml), (p = 0.04). Serum activity levels of ALT and AST were higher in children with A/O MBL genotype when compared to group with A/A genotype (p < 0.05).
Conclusions:
Our findings suggest negative effect of MBL deficiency (defined by genotype and phenotype) on progression of chronic hepatitis C in children and response to antiviral therapy.
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