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Maternal chronic hepatitis B virus does not affect neonatal biotinidase activity
George D Vlachos1, Kleopatra H Schulpis, Evangelos Papakonstantinou
1First Department of Obstetrics and Gynecology, Alexandra Hospital, Athens University Medical School, Athens, Greece.
Acta Paediatrica (Oslo, Norway : 1992)
|February 5, 2008
Summary
Maternal chronic hepatitis B virus (HBV) infection significantly reduces biotinidase activity in mothers but not in their newborns. Biotin supplementation may be beneficial for mothers with HBV to prevent symptoms from impaired biotin recycling.
Area of Science:
- Hepatology
- Biochemistry
- Neonatal Medicine
Background:
- Biotinidase activity is intrinsically linked to liver function.
- Chronic hepatitis B virus (HBV) infection can impact maternal liver health.
Purpose of the Study:
- To investigate the effect of maternal chronic HBV infection on neonatal biotinidase activity.
- To assess potential correlations between HBV infection markers, liver function, and biotinidase levels.
Main Methods:
- A comparative study involving 23 pregnant women with HBV and 28 healthy controls.
- Laboratory analysis included serological HBV markers, liver function tests, and biotinidase activity measurement via HPLC.
- Cord blood samples were collected from newborns for laboratory examinations.
Main Results:
- Mothers with chronic HBV exhibited significantly decreased biotinidase activity compared to controls.
- Transaminase levels were moderately elevated in infected mothers, while albumin levels remained comparable.
- Neonatal biotinidase activity was not significantly different between groups, despite the presence of maternal HBV markers in neonates.
- Biotinidase activity showed an inverse correlation with transaminases but not with HBV DNA or albumin levels.
Conclusions:
- Maternal chronic HBV infection leads to reduced biotinidase activity in mothers but not in their neonates.
- The findings suggest that biotin supplementation could be a preventive measure for mothers with HBV to address potential biotin recycling impairments.
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