BIOAVAILABILITY OF PHYLLOQUINONE FROM AN INTRAVENOUS LIPID EMULSION

This randomized, controlled study evaluated the bioavailability of phy lloquinone from an intravenous lipid emulsion. A mild vitamin K defici ency was induced in 12 healthy adult men and women by dietary restrict ion of phylloquinone (40 mu g/d, days 1-11) and by administration of w arfarin (1.0 mg/d, days 5-11). On day 11, subjects received a 500-mL i ntravenous solution of either lipid or saline, both of which contained 154 mu g phylloquinone. Bioavailability was assessed by serial measur ements of plasma phylloquinone, vitamin K-1-2,3-epoxide, PIVKA-II (pro teins induced by vitamin K absence or antagonists-II), and percentage undercarboxylated osteocalcin. As a result of vitamin K deficiency and minidose warfarin, vitamin K-1-2,3-epoxide, PIVKA-II, and percentage undercarboxylated osteocalcin increased significantly between days 1 a nd 11 (P = 0.05, 0.016, and 0.001, respectively). With the infusions, plasma phyloquinone increased in both groups (P = 0.001). After the in fusions vitamin K-1-2,3-epoxide decreased in both groups (P = 0.002). Changes in plasma phylloquinone and vitamin K-1-2,3-epoxide were no di fferent in the two groups (mean areas under the curves +/- SEM: 116 +/ - 13 nmol.NL for the saline group and 102 +/- 20 nmol.h/L for the lipi d group for phylloquinone; 38.6 +/- 7.5 nmol.h/L for the saline group and 31.3 +/- 9.0 nmol.h/L for the lipid group for vitamin K-1-2,3-epox ide). PIVKA-II decreased significantly from baseline values (P = 0.005 ) in both groups after the infusions. intravenous lipid reversed the e ffects of minidose warfarin and of dietary restriction of phylloquinon e on hemostasis and vitamin K nutritional status. This reversal was no different from that seen with the infusion of phylloquinone in a sali ne solution.