The administration of parcnteral fat emulsion—Intralipid, a preparation rich in the essential fatty acid (EFA), linoleic acid, is widely used as an integral part of therapy for sick infants along with total parenteral nutrition (TPN). EFAs serve as precursors for prostaglandin (PGs). We measured tissue lipid composition and the excretion of the major urinary metabolite of prostaglandins E1 and E2, 7α-hydroxy-5, 11 diketotetranor-prostane-1, 16 dioic acid (PGE-M) in three infants who received TPN with Intralipid for prolonged periods and compared these values with control infants. Linoleic acid is incorporated into the major lipid classes of the plasma, RBC, and tissues in the infants receiving Intralipid. Concomitantly with the increase in the relative concentration of linoleate, a decrease in the higher polyunsaturated fatty acid homologue, arachidonate is apparent. However, the sum of the two EFAs, linoleate and arachidonate, is similar in red blood cells (RBC) and tissue phospholipids of control infants and in infants who received Intralipid. A significant difference between the PGE-M excretion in the group of infants before and after the administration of Intralipid also is apparent (P < 0.05). Differences in the urinary excretion of PGE-M are seen between the control group and the infants receiving Intralipid (P < 0.05). PGE-M excretion after the administration of Intralipid is similar to that obtained from infants with EFA-deficiency.
Speculation The increase in the relative concentration of linoleic acid in plasma, RBC, and major tissue lipid classes and a concomitant decrease in the level of the higher EFA homologue arachidonate after the administration of Intralipid may indicate a competition between these EFAs for esterification and storage in tissue lipids, a balanced content of the intake of the linoleic and linolenic acids, a rapid turnover of the long chain polyunsaturated fatty acids or a combination of these factors. The decrease in PGE-M excretion in patients receiving high content of linoleic acid is most likely related to a decrease in the precursor EFA, arachidonate, although an inhibiting effect of linoleic acid on prostaglandin synthesis is possible. Further investigation is needed into the pathophysiologic consequences of increased linoleic acid consumption as well as decreased PG biosynthesis and turnover in sick infants.