Mild hyperhomocysteinemia in adults is associated with an increased risk of vascular disease. Although information is available about plasma homocysteine concentrations in childhood, data are entirely lacking for preterm infants despite their known abnormalities of sulfur amino acid metabolism. We measured plasma total homocysteine concentrations of 9 preterm infants (gestational age 23–31 weeks) within 48 h of birth and over the subsequent 14 days of life, and 4 term infants (gestational age 36–39 weeks) on a single occasion within 72 h of birth. As measured within 48 h of birth, average plasma homocysteine and cysteine concentrations of the preterm infants were 3.8 ± 0.3 and 122 ± 8 μM, both significantly less than those of the term infants (6.1 ± 1.3 and 187 ± 39) and of normal adults (8.2 ± 0.5 and 232 ± 6). Plasma homocysteine (but not cysteine) appeared to gradually increase during the first 2 weeks of life (p = 0.053). Our results indicate that hyperhomocysteinemia does not normally occur in preterm infants.

As part of a double-blind clinical trial of antenatal betamethasone, we studied the effects of this drug on urinary ammonia excretion in 28 premature infants. Betamethasone was administered before 34 weeks of gestation according to dosage schedules which have been shown to alter the incidence of respiratory distress syndrome. Although glucocorticoids affect renal ammoniagenesis in adults, the antenatal betamethasone trial did not augment ammonia excretion measured during the first day of postnatal life. We speculate that precocious maturation of renal ammoniagenesis cannot be triggered by glucocorticoids during the gestational period studied.