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PubMedDate not supplied

Alpha1-antitrypsin deficiency with fatal intracranial hemorrhage in a newborn.

A 4-week-old boy had a fatal intracranial hemorrhage resulting from vitamin K deficiency. The infant had received no vitamin K prophylaxis and was exclusively breastfed. At autopsy, examination of the liver showed cholestasis and fibrosis. DNA was isolated from a blood spot on a Gutherie sample card obtained from the infant for routine metabolic screening. This DNA was used for alpha1-antitrypsin genotyping studies. Genotyping studies identified homozygosity for the point mutation 9989G-->A, confirming a diagnosis of alpha1-antitrypsin deficiency (ZZ phenotype), and resulted in appropriate screening of siblings born after this child's death. Alpha1-antitrypsin deficiency should be considered in the differential diagnosis of infants with late hemorrhagic disease of the newborn. Use of blood from the metabolic screening card as a source of DNA allowed confirmation of this diagnosis after the infant's death.

Brain↗
PubMed1995

Vitamin K deficiency bleeding in infants and children.

The historical term "hemorrhagic disease of the newborn," which is used as a synonym for vitamin K deficiency bleeding (VKDB) in infancy, preferably should be abandoned, since neonatal bleeding is often not due to vitamin K (VK) deficiency and VKDB may occur after the neonatal period. VKDB is a form of bleeding that is caused by reduced activity of VK-dependent coagulation factors (II, VII, IX, X), has normal or even increased activity of VK-independent coagulation factors, and responds to VK. Acarboxy proteins are present. In a bleeding infant a prolonged one-stage prothrombin time (a decreased Quick value, which means prothrombin time expressed as percent of normal) in association with a normal (or increased) fibrinogen level and platelet count is almost diagnostic of VKDB. The diagnosis is proven, if administration of VK is followed by a shortening of the prothrombin time (after only 30 minutes) or cessation of bleeding. Classification is by age of onset as early, classic, and late form of VKDB. Rare cases of VKDB occur also after week 15; therefore the upper age limit should be 6 months and not 3 months. In idiopathic VKDB the cause (ther than breast-feeding) is unknown. In secondary VKDB additional factors can be demonstrated, such as poor intake or absorption of VK and increased consumption of VK. Most often cholestasis is present. Postnatal VK provides effective protection from the classic and late form of VKDB. The classic form can be prevented equally well by a single oral dose of 1 mg VK after birth as by parenteral VK. Parenteral prophylaxis appears to be more effective in preventing the late form, especially in patients with hepatobiliary disease. The protection achieved by single oral prophylaxis can be improved by repeated oral administration. In addition to reducing the incidence of VKDB, VK prophylaxis also reduced the proportion of intracranial hemorrhages and increases the age at onset of bleeding, parenteral prophylaxis being more effective than single oral prophylaxis in this respect. Because of the potential risks (cancer?) associated with extremely high levels of VK (20,000-fold the normal value for healthy newborns) and the possibility of injection injury, parenteral VK has been questioned as the first choice of prophylaxis for normal neonates. These disadvantages do not apply to oral prophylaxis. The major disadvantage of oral prophylaxis, namely, its lesser reliability in terms of intake and absorption, could be largely overcome by repeated administration. Although VK prophylaxis seems to be necessary only for breast-fed infants, breast-feeding should be promoted. As VK is involved not only in coagulation but also in carboxylation with multiple effects, care should be taken to avoid any excessive deviation from the physiologic conditions, that prevail in the fully breast-fed healthy mature infant, with low VK levels in the postnatal period. Repeated (daily or weekly) oral doses of VK are closer to physiologic conditions than single parenteral bolus doses, which expose neonates to excessively high VK levels. The incidence of intracranial VKDB can be reduced if the grave significance of warning signs is recognized (icterus, failure to thrive, feeding problems, minor, bleeding, diseases with cholestasis) or if a simple test for acarboxy proteins (similar to the Guthrie test) would be applicable. Whether or not the more reliable absorption of the new mixed micellar preparation of VK could reduce the protective oral dose of VK prophylaxis has to be evaluated.

Child↗
PubMed1995

[Efficacy of oral administration of a micellaar solution of vitamin K during the neonatal period].

BACKGROUND: Oral administration of vitamin K to neonates is quite satisfactory for preventing hemorrhagic disease of the newborn. The aim of this study is to test efficacy of a micellar solution of vitamin K at birth. POPULATION AND METHODS: Thirty full term infants, exclusively breast-fed during the first month of life, were included in this study. Seven of them (control group Cos) were given oral supplementation with 5 mg vitamin K1, cremophor; 15 other infants were given oral supplementation with 3 mg micellar solution of vitamin K1 (group MMos) and 7 were given an intramuscular injection of 1.5 mg micellar solution of vitamin K1 (group MMim). Prothrombin time activity and plasma vitamin K concentration were measured in the cord blood, 24 +/- 12 hours and 1 month after supplementation. RESULTS: No hemorrhage was seen and tolerance to vitamin K was good in the 3 groups. Mean prothrombin time activity was 54% in the cord blood, around 55% and 75%, 24 hrs and 1 month after supplementation, respectively; only one infant had low value (41%) by 1 month despite normal plasma vitamin K concentration. Two infants had low plasma vitamin K1 concentration by the second control despite normal prothrombin time activity; one belonged to the MMos group and the other to the Cos group. Mean values of plasma vitamin K1 concentration were higher by 1 month in the MMos group. CONCLUSION: A unique dose of micellar solution of vitamin K given orally at birth seems effective to prevent hemorrhagic disease.

Administration, Oral↗
PubMed1995

[Effects of the administration of vitamin K on the activity of Factor II, VII and X in healthy newborns].

The study was designed to know the effect of oral vitamin K (VK) treatment, on clotting factors II-VII-IX-X and the protein induced by VK absence from factor II (PIVCA II) on full term infants. Seventy healthy newborns were studied and each was randomly placed in one of two groups: Group A, newborns that received human milk and milk formula (mixed feeding)and group B, newborns that were exclusively breast fed. These groups were also divided in two subgroups: I received 2mg of VK1 orally and II (control) did not receive VK. Clotting activity of the coagulation factors and PIVCA II was determined from blood plasma obtained immediately after birth and 48 hours after VK administration. Basal activity of the factors analyzed was similar in all groups with values ranging from 25% to 40%. After 48 hours a significant increase in all factors studied and a decrease of PIVKA II was observed in those children who received oral VK. The results suggest that oral VK effectively increases VK dependent factors and prevents the risk of hemorrhagic disease in the newborn, with the advantage of being less traumatic and less risky to the infant than intramuscular VK.

Factor VII↗