Vitamin K Deficiency Bleeding in Infancy.

Shunsuke Araki,Akira Shirahata

doi:10.3390/nu12030780

Abstract

Vitamin K is essential for the synthesis of few coagulation factors. Infants can easily develop vitamin K deficiency owing to poor placental transfer, low vitamin K content in breast milk, and poor intestinal absorption due to immature gut flora and malabsorption. Vitamin K deficiency bleeding (VKDB) in infancy is classified according to the time of presentation: early (within 24 h), classic (within 1 week after birth), and late (between 2 week and 6 months of age). VKDB in infancy, particularly late-onset VKDB, can be life-threatening. Therefore, all infants, including newborn infants, should receive vitamin K prophylaxis. Exclusive breastfeeding and cholestasis are closely associated with this deficiency and result in late-onset VKDB. Intramuscular prophylactic injections reduce the incidence of early-onset, classic, and late-onset VKDB. However, the prophylaxis strategy has recently been inclined toward oral administration because it is easier, safer, and cheaper to administer than intramuscular injection. Several epidemiological studies have shown that vitamin K oral administration is effective in the prevention of VKDB in infancy; however, the success of oral prophylaxis depends on the protocol regimen and parent compliance. Further national surveillance and studies are warranted to reveal the optimal prophylaxis regimen in term and preterm infants.

Highlights

Vitamin K is a fat-soluble vitamin and a necessary cofactor for the synthesis and activation of coagulation factors II, VII, IX, and X and proteins C and S in the liver [1]
We have previously reported that vitamin K levels in umbilical blood were extremely low and that newborn infants have few vitamin K
A frequent single nucleotide polymorphism (SNP)—G-1639A—within the vitamin K epoxide reductase complex 1 (VKORC1) promoter has been identified as a major determinant of coumarin sensitivity, reducing the activity of vitamin K epoxide reductase enzyme to 50% of that of the wild GG type

Summary

Introduction

Vitamin K is a fat-soluble vitamin and a necessary cofactor for the synthesis and activation of coagulation factors II (prothrombin), VII, IX, and X (vitamin K-dependent coagulation factors) and proteins C and S in the liver [1]. (Figure 1B), indicating that the activity level of vitamin K 2, 3-epoxide reductase in infants was lower than that in adults, and the reuse of vitamin K in the liver was decreased. A frequent single nucleotide polymorphism (SNP)—G-1639A—within the VKORC1 promoter has been identified as a major determinant of coumarin sensitivity, reducing the activity of vitamin K epoxide reductase enzyme to 50% of that of the wild GG type. VKORC1 genetic variants and VKDB in Japan are lacking, the low enzyme activity of vitamin K epoxide reductase might be associated with VKDB in infancy because of the ethnic differences in the incidence of VKDB in infancy. VKDB is a hemostatic disorder in which the coagulation parameters can be rapidly managed by vitamin K supplementation

Epidemiology and Classification of VKDB

Diagnosis of VKDB in Infancy

Treatment of VKDB in Infancy

Findings

Prevention of VKDB in Infancy and Prophylaxis Guidelines