Equation for predicting weight gain in very low-birth-weight infants.

I developed a single equation that simulated previously published growth charts for very low-birth-weight infants, using birth weight as the only variable. The intent of this study was to validate the equation using infants admitted to our neonatal intensive care unit (NICU) and to determine if this equation could be used as a research tool to compare weight gain among populations. All 171 surviving infants with birth weight < or = 1500 g who received care in our NICU were studied retrospectively. The individual daily weights were compared with the predicted daily weights for each infant using the relative error of the prediction. The relative error of the prediction on all days for all infants was 0.45 +/- 0.13% (mean +/- SEM), and the maximum mean daily relative error of 2.73 +/- 0.90% occurred on Day 9. Black infants had a more positive relative error than white infants (p = 0.0001), due to faster weight gain. Twins gained faster than singletons (p = 0.023). Infants with patent ductus arteriosus (PDA) gained more slowly than normal infants (p = 0.001) after an initial rapid weight gain. Infants with lung disease had initial rapid weight gain similar to infants with PDA, but subsequently were similar to infants without lung disease. This equation accurately predicts weight gain in our population of very low-birth-weight infants. The relative error of the prediction is a useful research tool for determining the effect of clinical conditions or interventions on weight gain.

Enteral glutamine supplementation for very low birth weight infants decreases morbidity.

Glutamine, described as a "conditionally essential" amino acid for critically ill patients, has not been routinely added to parenteral amino acid formulations for critically ill neonates and is provided in only small quantities by the enteral route when enteral intake is low. We conducted a blinded, randomized study of enteral glutamine supplementation in 68 very low birth weight neonates randomly assigned to receive glutamine-supplemented premature formula versus premature formula alone between days 3 and 30 of life. Primary end points consisted of hospital-acquired sepsis, tolerance to subsequent enteral feedings (days with no oral intake), and duration of hospital stay. Hospital acquired sepsis was 30% (control group) and 11% (glutamine group). Logistic regression with birth weight as a covariate showed that: (1) feeding group was significant (p = 0.048) in determining the probability of developing proven sepsis over the course of hospitalization and (2) the estimated odds of developing sepsis were 3.8 times higher for infants in the control group than for those treated with glutamine. Glutamine-supplemented infants had better tolerance to enteral feedings as measured by percent of days on which feedings needed to be withheld (mean percentage of 8.8 vs 23.8, p = 0.007). Analysis of T cells demonstrated a blunting of the rise in HLA-DR+ and CD16 subsets in glutamine-supplemented infants. There were no differences in growth; in serum ammonia, urea, liver transaminase, or prealbumin concentrations; or in mean hospital stay. This study provides evidence for decreased morbidity in very-low-birth-weight neonates who receive enteral glutamine supplementation.

Meconium passage in very-low-birth-weight infants.

The timing of the first meconium stool has been considered a marker for proper gastrointestinal functioning in the term infant. There is limited information on the meconium passage patterns of very-low-birth-weight infants of less than 32 weeks' gestation. It is unknown whether feeding practices influence the timing of the first stool in these infants. We retrospectively studied 47 very-low-birth-weight infants with birth weights of 1250 g or less who were previously enrolled in a study of gastrointestinal (GI) priming. Infants whose mothers desired to breast feed (n = 7) were given GI priming with their own mother's milk. The remaining infants had been randomly assigned to receive total parenteral nutrition alone (n = 21) or GI priming with infant formula (n = 19) during the first 14 days of life. We attempted to advance all infants to full enteral nutrition by 21 days of age. There was no statistically significant difference in timing of the first stool among the three groups. The overall median age at first stool was 43 hours, and the 75th percentile was 10 days. The range was 1/2 hour to 27 days. There was no concordance between time of first stool and birth weight within the range studied. There was no concordance between time of first stool and necrotizing enterocolitis, although there was little statistical power to detect this. There was also very little concordance with feeding tolerance. Other than necrotizing enterocolitis, no significant GI disease developed in any of the infants studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Ontogeny of small intestinal glutaminase and glutamine synthetase in the rat: response to dexamethasone.

The ontogeny of small intestinal glutaminase (GA) and glutamine synthetase (GS) was studied with relation to the maternal administration of dexamethasone (DEX). Pregnant Sprague-Dawley rats were administered 0.2 mg/kg of DEX or saline twice daily on days 19 and 20 of gestation. Activity of GA did not increase from the fetus to the 10-day-old rat; however, GS activity increased 7-fold. DEX induced doubling of GA activity and mRNA, but only a slight increase is GS activity and mRNA was observed in the fetus. GA and GS activities appear to be regulated by different mechanisms.

Gastrointestinal priming prior to full enteral nutrition in very low birth weight infants.

Priming of the gastrointestinal (GI) tract with low-volume feedings before giving full enteral feedings to very premature, high-risk infants is a controversial practice. We designed a study of infants weighing less than 1,250 g and receiving total parenteral nutrition to determine whether GI priming would hasten weight gain, improve tolerance of subsequent feedings, enhance nutritional status, and increase serum concentration of gastrin, a hormone trophic for intestinal growth. Infants were randomly assigned to receive total parenteral nutrition (TPN) alone (N = 21) or GI priming plus TPN (N = 19) for 12 days beginning on day 3 of life. Full-strength premature infant formula was used for priming. Both groups received the same total nutrition. Beginning on day 15, feedings in both groups were increased daily to a maximum of 120 kcal/kg/day on day 20, where they were maintained until day 30. After day 30, the feedings were modified according to the infants' condition. The groups did not differ in birth weight, gestational age, or 5-min Apgar scores. GI-primed infants had improved feeding tolerance after day 20 and a faster rise in serum gastrin during the initial phase of the study. There was no significant difference in weight gain. GI priming improves tolerance of feedings, accelerates rate of rise of serum gastrin during the first weeks of life, and does not increase the risk of feeding complications when compared to TPN alone. This may lead to more rapid maturation of the GI tract in primed infants.