A multi-centre safety and efficacy trial of a preterm infant formula supplemented with long chain polyunsaturated fatty acids (LCP) (48 weeks PCA analysis)

LCP supplementation of premature infant formula has been shown to produce plasma and erythrocyte lipid profiles similar to human milk (HM)-fed preterm infants. Previous studies reported decreased growth with LCP supplemented formula. This prospective, double-blind, randomised, controlled, parallel trial compared safety, growth and phospholipid fatty acid (PFA) levels in preterm infants fed preterms formula with (L+) or without (Lo) LCP. The study consisted of Phase I: enrolment to 40 weeks (wk) postconceptual age (PCA); and Phase II: 40 to 48 wk PCA. Infants (birth weight 750-2000 g, 0-28 days of age) were fed L+ or L preterm formula, 24 Kcal/oz during Phase I, and 20 Kcal/oz during Phase II. A control group was exclusively HM-fed preterms who, if weaned at the end of Phase I, received L. HM and formula intake were unrestricted. Weight (wt), length (Lt), head circumference (OFC) and upper mid-arm circumference (MAC), and phospholipid profiles were measured at 40 and 48 wk PCA. Adverse events were monitored. 183/288 infants completed Phase II. There were no difference in growth rates between formula groups. At 48 wk PCA, mean PFA levels in infants fed L+ were similar to HM-fed and were significantly higher than the L fed group. Adverse events were similar between the 2 formula groups. The number of infants who were discontinued because of an adverse event was similar among all groups. In conclusion the LCP preterm infant formula is safe, support normal growth and maintains phospholipid profiles similar to HM-fed infants.(AU)

Activity of the alternative pathway of complement in the newborn infant.

Levels of C3, properdin, factor B, and C3 to C9 activity were markedly reduced in cord sera taken from 94 normal newborn infants. Nevertheless, cord serum supported complete activation of its own alternative pathway by zymosan or CoF. Lysis of a target cell, however, was defective; nearly 75% of cord sera had reduced rabbit erythrocyte CH50 titers. These were partially increased by the addition of factor B and properdin, and totally restored by adding factor B, properdin, and C3 to C9. Therefore, although the alternative pathway of the neonate is intact, it appears to be limited in its ability to generate an adequate number of stable and active enzymatic sites on a target cell membrane.