Pronounced growth restriction (GR) occurs after very preterm birth. The interaction between IGF-I, nutritional intake, and growth was evaluated prospectively in 64 infants with a mean (SD) GA of 25.7 (1.9) wk. Blood sampling of IGF-I and measurements of weight, length, and head circumference were performed weekly until discharge. Daily calculation of nutritional intake was performed. Standard deviation scores (SDSs) for growth parameters defined two growth phases: GR phase (birth until lowest SDS) and catch-up (CU) phase (lowest SDS until 35 gestational weeks). IGF-I concentrations during the first postnatal weeks were low and increased at 30 wk GA, irrespective of GA at birth, coinciding with initiation of CU growth. Concentrations of IGF-I were positively associated with change in weight SDS during the GR phase, p ϭ 0.001 and CU phase, p ϭ 0.004 -0.027. Protein and energy intake were not associated with change in SDS weight during the GR phase as opposed to the CU phase (p Ͻ 0.001, respectively). Nutritional intake did not correlate to concentrations of IGF-I before 30 wk GA. IGF-I is associated with growth at an earlier postnatal age than nutrient intake and the effect of nutrition on levels of IGF-I may be restricted to the period of established CU growth. T he maximum growth rate of the fetus is reached in the middle of pregnancy, where it is approximately three times higher than at term (1). Fetal growth rate is to a large extent determined by placental capacity of delivering nutrients to the fetus, whereas genetic influence seems to play a less important role. Placental function depends on the maternal nutritional state and the intrauterine endocrine environment. At preterm birth, the fetal-placental interaction is interrupted, which has an impact on continued extrauterine growth capacity. Postnatal growth retardation occurs almost inevitably after preterm birth and has been associated with decreased brain volumes and impaired neurodevelopmental outcome (2,3). Although attempts are made to optimize postnatal nutritional intakes in preterm infants, these are still commonly suboptimal according to intrauterine requirements (4). Increased postnatal nutritional intake has been shown to improve growth rate in very LBW infants (5), although a recent study could not demonstrate any apparent effect of hyperalimentation on subsequent postnatal growth in very preterm infants (6).IGF-I is an important fetal growth factor, which is essential for the developing brain (7). Concentrations of fetal IGF-I are closely related to placental transfer of glucose where fetal glucose increases insulin secretion, which in turn stimulates fetal IGF-I production (8). Fetal levels of IGF-I may also be regulated by an interaction at the feto-maternal placental interface (9). The disruption of placental nutrient supply after birth is followed by a rapid decrease in postnatal levels of IGF-I, suggesting a low endogenous production (10). While term infants restore their IGF-I levels within the first postnatal weeks, very prete...

Protein analyses of the milk before individual fortification provides a new tool for an individualized feeding system of the preterm infant. The bovine whey protein fortifier attained biochemical and growth results similar to those found in infants fed human milk protein exclusively with the corresponding protein intakes.

No abstract

ABSTRACT. In a double-blind, randomized study, 28 healthy, growing very low birth wt, appropriate-for-gestational-age infants were fed human milk, preferably mother's own, fortified daily with human milk protein and/or human milk fat. The infants entered the study when they were stable on complete enteral intakes of 170 mL/kg/d (mean age = 19 d). The study lasted for a mean of 4 wk.Samples from all the milks were collected daily, and intakes of protein, fat, carbohydrates, energy, and electrolytes were calculated weekly during the whole study period.Protein intakes ranged from 1.7 to 3.9 g/kg/d, and energy intakes from 100 to 150 kcal/kg/d. Wt and length gain in the nonprotein-enriched groups were 15.6 + 2.7 g/kg/d (mean + SD) and 0.88 + 0.17 cm/wk; the corresponding figures for the protein-enriched groups were 20.2 + 2.1 g/ kg/d and 1.24 & 0.14 crnlwk. There was a strong correlation between protein intake and growth in wt and length up to an intake of about 3 g/kg/d; more protein did not result in increased growth. The same was true for energy intake, with a maximal growth rate a t an intake of about 120 kcal/ kg/d. A protein intake of more than 3 g/kg/d resulted in a growth rate equal to or higher than the estimated intrauterine growth rate. Some infants fed mature banked human milk alone had a poor growth. Sodium intake was low, ranging from 1.5 to 2.6 mmol/kg/d. No correlation was found between sodium intake and growth rates.

Routines for breastmilk handling differ among the 36 neonatal units in Sweden. New guidelines can standardize the handling of human milk, thereby improving nutrition and minimizing the risk of breastmilk-induced infection in the preterm infant.

Human alpha-lactalbumin (alpha-LA) has been used as a marker for measuring macromolecular absorption. The serum concentration of human alpha-LA after a human milk feed has been studied in 32 healthy very low birthweight infants (VLBW), fed human milk (gestational age 26-32 weeks) and in 56 term, breast-fed infants, age 3-140 days. At 31 weeks of gestation the serum concentration of human alpha-LA was more than 10 times higher (mean value 3,000 and median value 2,101 micrograms/l serum/l human milk/kg body weight, n = 11) than in the term infants aged 3-30 days (mean value 257 and median value 152, n = 29). The serum concentration of alpha-LA decreased with increasing maturity in the VLBW-infants. At a postconceptional age of 37 weeks the values were similar (mean value 200 and median value 99, n = 8) to those found for term infants during the first month. In the term infants a decreasing absorption of alpha-LA was found with increasing postnatal age.

Of 858 pregnant women studied in matched rectal, urethral and urine cultured specimens, 186 (22%) were found to be colonized by group B streptococci (GBS). GBS were detected significantly more often in rectal specimens (159) than in urethral specimens (108) or in urine specimens (64). This is supporting evidence for the gastrointestinal tract as the main habitat of GBS. Of 1786 women whose urine was sampled at delivery, GBS were isolated from 128 (7%), in 22 of whom (1% of the total) GBS were present in quantities greater than or equal to 10(4) colony forming units (cfu)/ml urine. Neonates born to women with greater than or equal to 10(4) cfu GBS/ml urine were apparently at greater risk for neonatal infection, as they were more commonly and more heavily colonized than were the newborns of women with lower quantities of GBS in urine, or if positive urethral or rectal specimens were considered. The incidence of preterm delivery or obstetric infection was not higher among women in whom GBS were isolated in specimens from any of the 3 sites; foetal distress was more common among their children, but not neonatal respiratory or infectious diseases of which the incidence was low and difficult to assess statistically.

Urea concentrations in serum and urine were measured in 28 growing, very low birth weight, appropriate-for-gestational age infants fed varying human milk protein intakes (range 1.7 to 3.9 g/kg/day). We found a high correlation between serum urea values at the end of the study and mean protein intake (rs = 0.85, p less than 0.001) and between urinary urea concentrations in eight-hour urine collections and protein intake (rs = 0.81, p less than 0.001). All serum and urine urea values were below 1.6 and 18 mmol/l, respectively, at protein intakes less than 3 g/kg/day. Higher protein intakes caused higher serum and urinary urea concentrations. We also found a strong correlation between the individual serum and urinary urea values at the end of the study (rs = 0.90, p less than 0.001). The presented data are consistent with the growth data previously reported and indicate that inadequate or excessive protein intakes can be detected by measurement of urea concentrations in serum and/or urine. If urine urea samples alone can be used for estimating optimal protein intake, painful blood sampling procedures could be obviated.