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Changes in hepatic vitamin K1 levels after prophylactic administration to the newborn
M Guillaumont1, L Sann, M Leclercq
1Laboratory of Clinical Pharmacology, Hôpital Debrousse, Lyon, France.
Insights
Newborn infants have poor hepatic vitamin K1 (phylloquinone) storage, risking deficiency. Supplementation significantly boosts liver vitamin K1 levels, though concentrations decline rapidly, sustained elevated storage is observed.
Area of Science:
- Pediatric Nutrition
- Biochemistry
- Neonatal Health
Background:
- Newborn infants are at risk for vitamin K deficiency due to low initial hepatic stores.
- Vitamin K1 (phylloquinone) is crucial for neonatal hemostasis and development.
- Understanding hepatic vitamin K concentrations is vital for assessing deficiency risk.
Purpose of the Study:
- To quantify hepatic vitamin K (phylloquinone, vitamin K1-epoxide, menaquinones) concentrations in newborns.
- To evaluate the efficacy of vitamin K1 supplementation on hepatic storage in infants.
- To assess the duration of elevated hepatic vitamin K1 levels post-supplementation.
Main Methods:
- Analysis of hepatic vitamin K concentrations in 18 infants (1-8 days old).
- Comparison between supplemented and unsupplemented infant groups.
- Measurement of phylloquinone, vitamin K1-epoxide, and menaquinones in liver tissue.
Main Results:
- Unsupplemented infants had very low hepatic phylloquinone (< 1 microgram) and no detectable menaquinones.
- Vitamin K1 supplementation resulted in very high initial hepatic concentrations (> 60 micrograms/g).
- Hepatic vitamin K1 levels decreased rapidly post-supplementation, but storage remained elevated after 5 days.
Conclusions:
- Hepatic phylloquinone storage at birth is inadequate, placing newborns at potential deficiency risk.
- Prophylactic oral vitamin K1 administration leads to satisfactory liver uptake but rapid clearance.
- Despite rapid decline, vitamin K1 supplementation ensures significantly higher hepatic storage in newborns.
Abstract:
We undertook a study of hepatic concentrations of vitamin K (vitamin K1 or phylloquinone, vitamin K1-epoxide, and menaquinones) in 18 infants, ages 1-8 days, with or without vitamin K1 supplementation. The infants who had no supplementation had a total hepatic storage ranging between 0.1 and 0.9 micrograms. Also, hepatic storage of phylloquinone was poor (< 1 microgram) when compared with daily requirements. Moreover, we did not detect any menaquinone in the livers of these infants in our study. The prophylaxis applied to the other infants was very efficient. Hepatic vitamin K1 concentrations, obtained < 24 h after administration, were very high (62.8-93.5 micrograms/g). Vitamin K1-epoxide concentrations were high, which proved the efficiency of the vitamin K cycle. In contrast, the decrease in vitamin K1 concentrations was also very rapid, since the median value after 48 h was 8.4 micrograms/g and only 2.9 micrograms/g 5 days after administration. However, hepatic total storage after 5 days in one infant with vitamin K1 supplementation was much higher (112 micrograms) than in infants who had not received supplementation. In conclusion, hepatic phylloquinone storage at birth was poor (< 1 microgram). The newborn infant might be in a situation of potential deficiency. After prophylactic oral administration of phylloquinone, uptake by the liver was quite satisfactory, but concentrations dropped quickly. However, phylloquinone hepatic storage remained elevated (112 micrograms) after 5 days.