Abstract
An abnormal lipoprotein (LP), detected in plasma during total parenteral nutrition, has been shown to be similar to LPX observed in cholestasis and in familial lecithin-cholesterol-acyl-transferase (LCAT) deficiency. However, the conditions which facilitate the appearance of LPX during total parenteral nutrition are unclear; potential determining factors could be lipid input, plasma lipid levels, and/or inhibition of LCAT activity. An investigation was conducted on 12 patients receiving total parenteral nutrition for 3 wk by simultaneously evaluating plasma LPX (via a quantitative method) as well as total cholesterol, phospholipids (PL), triglycerides (TG), apolipoprotein B, and LCAT activity. Daily total nonprotein calories (40 kcal/kg body weight) and nitrogen input (250 mg/kg body weight) were fixed in this study. Three 7-day periods were defined: during periods 1 and 3, lipid emulsion (10 or 20% Intralipid) and glucose were given as nonprotein calories (glucose-lipid periods); in period 2, glucose was administered alone as the sole source of nonprotein energy (glucose period) so that the total energy input was not modified. During periods 1 and 3, the patients were randomly assigned to receive either 9 g (period 1) and 12 g (period 3) of PL/day for 7 days, or 12 and 9 g of PL/day. By infusing either 10 or 20% Intralipid, TG input was varied concomitantly so that the subjects received 75, 100, or 150 g/day in periods 1 and 3. During the glucose-lipid periods, plasma LPX was measurable from the 2nd day and increased progressively. Its increment was closely related to a rise in unesterified cholesterol and PL (r = 0.7; p < 0.05). These increases in cholesterol and PL were largely incorporated into LPX. In contrast, TG was decreased independently of LPX levels. LPX concentrations were dependent on PL input since the LPX increment was significantly higher when 12 g rather than 9 g of PL were infused daily. TG input had no such effect. LPX was not correlated with either LCAT activity or apolipoprotein B levels which did not yield any significant variation during the entire study. In the glucose period, there was a significant decrease in LPX (half life: 2-4 days), cholesterol, and PL, while TG was increased. Our study suggests that different types of discontinuous total parenteral nutrition can induce varying patterns of the plasma lipid profile. The LPX level and the rise of cholesterol and PL were related to PL input but not to TG input or to inhibition of LCAT activity. The increase of unesterified plasma cholesterol was higher than expected after low cholesterol input, indicating that the excess cholesterol may be partly endogenous in origin. (Journal of Parenteral and Enteral Nutrition 8:529-534, 1984)
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