Plasma vitamin K1 and proteins induced by vitamin K absence (PIVKA) were assayed simultaneously 1-4 days and 29-35 days after delivery in three groups of infants: breast-fed not receiving vitamin K at birth (n = 12), bottle-fed without vitamin K administration at birth (n = 7) and breast-fed receiving 1 mg vitamin K1 administered by intramuscular injection at birth (n = 13). The bottle-fed infants had a significantly higher vitamin K1 plasma level than breast-fed infants who did not receive vitamin K1 at birth. Extremely high levels of vitamin K were obtained 1-4 days after intramuscular administration. At the age of 1 month, breast-fed infants had the same plasma vitamin K1 concentration whether or not they had received vitamin K1 supplements. Decarboxy prothrombin (PIVKA-II) a reliable indicator of biochemical vitamin K deficiency, was found in 5 out of 12 breast-fed and in 2 out of 6 bottle-fed infants who had not received supplemental vitamin K1 after birth. In a separate study, we followed up to 90 days after birth a larger group if infants. PIVKA-II was found with significantly greater frequency in breast-fed infants receiving no vitamin K than in breast-fed infants receiving 1 mg vitamin K intramuscularly at birth, or in bottle-fed infants without extra vitamin K1. These data form a strong argument for routine vitamin K prophylaxis after birth for all breast-fed infants. The optimum dose and manner of administration require further study.

There were no differences in symptoms comparing children with and without D fragilis infection. Furthermore, no relation was found between clinical and microbiological response after treatment for D. fragilis. This retrospective study suggests that there is no association between chronic AP and D. fragilis infection.

PIVKA-II (Protein Induced by Vitamin K Absence) is abnormal des-carboxylated prothrombin, which is present in vitamin K deficiency or in patients using warfarin. With a sensitive method for PIVKA-II, biochemical vitamin K deficiency can be established before clinical symptoms occur. We give an overview of methods used to detect PIVKA-II, and four selected methods are inter-compared: (a) measuring total factor II including PIVKA-II by using Echis carinatus snake venom as an activator of prothrombin; (b) measuring PIVKA-II by using snake venom as an activator of factor II after adsorption of functional factor II onto barium sulfate; (c) electrophoresis-immunofixation method; and (d) enzyme immunoassay. We found d to be the most sensitive and reliable method for PIVKA-II.

SummaryAssessments of the vitamin K status in newborns and their mothers by means of des-γ-carboxy-prothrombin (PIVKA II) measurement have given equivocal results. Part of the variability could be attributed to differences in sensitivity (i.e. the ability to detect small concentrations) and validity (i.e. ability to detect vitamin K deficiency) of the methods applied. None of these methods have yet been validated with respect to plasma vitamin K1. In 22 healthy mother/infant pairs PIVKA II was determined using three different assays including ratio Xa/ecarin (Xa/ec), crossed immunoelectrophoresis (CIE), and an ELISA with a monoclonal antibody (MAB). The results were compared with conventional clotting tests and plasma vitamin K1. The following results were obtained:Cord blood: Clotting tests within age-related normal ranges; PIVKA II detection rates: 0/22 (Xa/ec), 1/22 (CIE), 4/22 (MAB); plasma vitamin K1: undetectable in 20/22.Mothers: Clotting tests all within normal range; PIVKA II detection rates: 1/22 (Xa/ec), 0/22 (CIE), 5/22 (MAB); plasma vitamin K1 (pg/ml) for all mothers (median; range): 186; 55–833; for PIVKA II positive mothers: 213; 59–699.PIVKA II detectability in newborns and mothers was not correlated. The results show an increase in sensitivity for PIVKA II detection in the order of MAB ≫CIE >Xa/ec. Due to the very low plasma vitamin K1 at birth, no correlation was possible between cord PIVKA II detectability and plasma vitamin K1. However, in mothers at term PIVKA II MAB appears to be unrelated to the vitamin K status.

Protein C antigen levels were measured in the plasma of healthy full term infants by electroimmunoassay. During the first three months of life (on day four, at one month, two months and three months of age) protein C antigen levels were compared in breast-fed and bottle-fed infants. None of the two groups of infants received vitamin K at birth. Only at the age of three months there was a significant difference between the groups. Unexpectedly infants, who were breast-fed, had a higher protein C level at three months of age. Levels were also measured in 15 healthy children between one and three years of age. The antigen levels increase with age to reach adult values at about three years of age.