Bioavailability of phylloquinone from an intravenous lipid emulsion.

This randomized, controlled study evaluated the bioavailability of phylloquinone from an intravenous lipid emulsion. A mild vitamin K deficiency was induced in 12 healthy adult men and women by dietary restriction of phylloquinone (40 μg/d, days 1-11 and by administration of warfarin (1.0 mg/d, days 5-11). On day 11, subjects received a 500-mL intravenous solution of either lipid or saline, both of which contained 154 μg phylloquinone. Bioavailability was assessed by serial measurements of plasma phylloquinone, vitamin K 1 -2,3-epoxide. PIVKA-II (proteins 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 and 11 (P = 0.05, 0.016. and 0.001, respectively). With the infusions, plasma phylloquinone increased in both groups (P = 0.001). After the infusions 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 different in the two groups (mean areas under the curves ± SEM: 116 ± 13 nmol. h/L for the saline group and 102 ± 20 nmol. h/L for the lipid 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-epoxide). PIVKA-II decreased significantly from baseline values (P = 0.005) in both groups after the infusions. Intravenous lipid reversed the effects of minidose warfarin and of dietary restriction of phylloquinone on hemostasis and vitamin K nutritional status. This reversal was no different from that seen with the infusion of phylloquinone in a saline solution.