Preterm infants drug metabolism

Metabolic bone disease in children receiving parenteral nutrition manifests primarily as osteopenia and, on occasion, fractures (5). The etiology is multifactorial calcium and phosphate deficiency play a major role in the preterm infant but the part played by aluminium toxicity in this population is unknown. Lack of reference values of bone histomorphometry in the premature infant, as well as lack of reference data for biochemical markers of bone turnover in these patients, contributes to the uncertainty. Other factors that may play a role in the pathogenesis of bone disease associated with parenteral nutrition include lack of periodic enteral feeding underljdng intestinal disease, including malabsorption and inflammation the presence of neoplasms and drug-induced alterations in calcium and bone metabohsm. However, the true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients are unknown. 

To study the plasma protein binding at least in newborns and infants is recommended, as the protein binding is reduced in the preterm and term infant at birth and in the first weeks of life. Also, the drug elimination is slowed down in this subgroup of children, due to immaturity of both metabolic pathways and renal function. 

The hepatic metabolism of certain drugs has also been fonnd to be different in neonates versus children and adults. The N-methylation of theophylline to caffeine occurs in preterm and full-term infants, whereas in adults theophylline is primarily N-demethylated and C-oxidated to monomethylxanthines and methyluric acid, respectively. 

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