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Inositol supplementation in respiratory distress syndrome: relationship between serum concentration, renal excretion,
Insights
Inositol supplementation in preterm infants with respiratory distress syndrome increased serum inositol levels and improved surfactant phospholipids. Further research is recommended for its use as a dietary supplement.
Area of Science:
- Neonatal Medicine
- Biochemistry
- Pediatrics
Background:
- Respiratory distress syndrome (RDS) is a common condition in preterm infants.
- Inositol plays a crucial role in surfactant phospholipid synthesis.
- Preterm infants often have lower inositol levels, potentially impacting lung function.
Purpose of the Study:
- To investigate the effect of inositol supplementation on serum inositol concentrations in preterm infants with RDS.
- To assess the impact of inositol on surfactant phospholipids and lung development markers.
Main Methods:
- A randomized controlled trial involving 48 preterm infants with RDS.
- Administration of inositol (40 mg/kg every 6 hours) or placebo.
- Measurement of serum and renal inositol concentrations, and surfactant phospholipids in tracheal aspirates.
Main Results:
- Inositol supplementation significantly increased serum inositol concentrations compared to placebo.
- Infants who developed bronchopulmonary dysplasia had lower serum inositol.
- Inositol increased the saturated phosphatidylcholine/sphingomyelin ratio in tracheal aspirates.
Conclusions:
- Inositol supplementation effectively raises serum inositol levels in preterm infants with RDS.
- Inositol may improve lung surfactant composition, potentially aiding in RDS management.
- Further investigation is warranted for inositol as a dietary supplement in preterm infants, especially those not receiving full human milk feeds.
Abstract:
Inositol or placebo was given to 48 small preterm infants with respiratory distress syndrome (mean birth weight 1365 g, gestational age 30.1 weeks) between 48 hours and 10 days of age. The dose of inositol, 40 mg/kg every 6 hours, was at least as high as amounts received in full preterm human milk feedings. Serum inositol concentration increased between days 2 and 3 from a mean of 566 mumol/L to 823 mumol/L in the infants given supplement and fell from 451 mumol/L to 292 mumol/L in the controls. On day 16, serum inositol values remained higher in the infants given supplement than in those given placebo (mean 334 mumol/L vs 146 mumol/L, P = 0.014). The infants who developed bronchopulmonary dysplasia had significantly higher renal inositol clearance, lower inositol intake, and lower serum inositol concentrations. Inositol supplementation increased the saturated phosphatidylcholine/sphingomyelin ratio in tracheal aspirates. According to these results, supplementation with inositol in preterm infants leads to a rise in serum inositol concentration and improvement in the surfactant phospholipids. Inositol deserves further study as a dietary supplement for immature preterm infants who do not receive full human milk feeds.