Preterm infants with chronic lung disease: Are protein and energy intakes after discharge sufficient for optimal growth?

Aim: To document post‐discharge feeding practices of preterm infants with chronic lung disease (CLD) and determine if sufficient protein and energy is consumed for optimal growth. Method: Protein and energy intakes of preterm infants with CLD were quantified through detailed analysis of measured food and fluid intakes at four corrected age (CA) assessments, post‐discharge. Most of the infants were in hospital for the term assessment. Milk intake from breastfeeding was determined by test weighing. Protein and energy intakes were compared with the Australian and New Zealand Nutrient Reference Values (NRV) for healthy term‐born infants, and CA z‐scores for weight, length and head circumference were calculated using Australian national gestational growth data and Centre for Disease Control 2000 growth data. Results: Ten of the 28 CLD infants who were exclusively receiving expressed breast milk in hospital were transitioned to infant formula within 1 month of discharge. Complementary foods were introduced at a median CA of 3.6 months. Protein intakes almost always exceeded the NRV for healthy term‐born infants, and at each assessment, at least 63% of infants met the energy NRV. Longitudinal growth data are available for 20 infants, four of whom had been small for gestational age. At the 12‐month assessment, 10 of these infants weighed less than the 10th percentile. Conclusion: Preterm infants who develop CLD do not always achieve reference growth in their first year following discharge, despite protein and energy intakes being mostly comparable to those recommended for healthy term‐born infants.     

Exhaled breath measures of inflammation: are they useful in neonatal chronic lung disease?

Neonatal chronic lung disease is a common problem for surviving infants of extreme prematurity. Although the precise pathophysiology is still not known, it is clear that inflammation provides a common link that amplifies the injury to the premature lung. Current invasive measures of pulmonary inflammation include markers in blood and airway effluent, with the cellular composition of tracheal fluid being the "gold standard". In this article available exhaled breath measures, particularly nitric oxide, carbon monoxide, volatile hydrocarbons, and exhaled breath condensate, are reviewed with particular reference to sample collection, analysis, and common pitfalls as they apply to the ventilated premature newborn at risk of chronic lung disease. Although they have great potential, all measures require thorough validation before being used clinically.     

Can polyclonal intravenous immunoglobulin limit cytokine mediated cerebral damage and chronic lung disease in preterm infants?

Recent evidence suggests that inflammatory cytokines may play an important role in cerebral and pulmonary injury, especially in preterm infants. Immunomodulatory agents may help to limit such injury by reducing inflammation. Immunoglobulin has multiple anti-inflammatory properties and can modulate the inflammatory cytokine response. New evidence is required to test the hypotheses that prophylaxis or treatment with intravenous immunoglobulin may limit such inflammatory damage.     

Are the neonatal outcomes similar in large-for-gestational age infants delivered by women with or without gestational diabetes mellitus?

Background

Infants are considered large for gestational age (LGA) if their birth weight is greater than the 90th percentile for gestational age and they have an increased risk for adverse perinatal outcomes. Maternal diabetes is one of the factors affecting birthweight. However there are limited data on the perinatal outcomes of infants of gestational diabetic mothers. The aim of the present study was to compare the neonatal outcomes of LGA infants delivered by women with and without gestational diabetes mellitus.

Methods

This was a retrospective study of LGA infants of ??36 weeks of gestation born at the Gazi University Medical School Hospital during the period of 2006?C2009. Neonatal outcomes included hypoglycemia and polycythemia in the early neonatal period and hospital admissions. The Chi-square and Student??s t test were used for comparing variables.

Results

Seven hundred eligible infant-mother pairs were enrolled in the study. Eighty-seven of them (12.4%) were infants of gestational diabetic mothers and 613 (87.6%) were infants of non-diabetic mothers. The incidence of hypoglycemia at the first hour was higher in infants of diabetic mothers (12.8%) than in infants of non-diabetic mothers (5.3%) (P=0.014). Polycythemia was also more frequently observed in infants of the gestational diabetic mothers (9.3%) than in infants of the non-diabetic mothers (3.0%) (P=0.010). Although overall hospital admission rates were not different between the two groups, infants of diabetic mothers were more likely to be admitted because of resistant hypoglycemia (P=0.045).

Conclusions

The results of this study suggested that LGA infants of mothers with gestational diabetes mellitus were at a greater risk for hypoglycemia and polycythemia in the early neonatal period than LGA infants of nondiabetic mothers.     

What does mucin have to do with lung disease?

Mucin glycoproteins are a major macromolecular component of mucus. Mucins are large, heavily glycosylated glycoproteins that are expressed in two major forms: the membrane-tethered mucins and the secreted mucins. In the airways, MUC1 and MUC4 are the predominant membrane-tethered mucins that are present on epithelial cell surfaces; MUC5AC, MUC5B and MUC2 are the predominant secreted mucins that contribute to the mucus gel. Although the role of MUC1 and MUC4 in the airway is not known, they may function as receptors or receptor ligands and activate intracellular signalling cascades affecting epithelial functions. Several inflammatory mediators increase expression of the secreted mucin genes, MUC5AC and MUC2. Furthermore, overexpression of MUC5AC, MUC5B and MUC2 correlates strongly with secretory cell hyperplasia and metaplasia in human and murine airways. The insights gleaned from the investigations of mucin function and gene regulation should be useful for elucidating the cellular mechanisms leading to airway remodelling and mucus obstruction.     

“New” bronchopulmonary dysplasia and chronic lung disease

Bronchopulmonary dysplasia (BPD) is the major cause of chronic lung disease and morbidity in preterm infants. Since it was first described fifty years ago, the epidemiology, pathogenesis, and treatment for BPD has changed dramatically. This review summarizes these changes and the clinical outcomes for infants diagnosed with BPD.