High efficacy and minor renal effects of indomethacin treatment during individualized fluid intake in premature infants with patent ductus arteriosus.

AIM: To determine the efficacy and the renal side effects of indomethacin treatment for closure of a patent ductus arteriosus (PDA) in premature infants during an individualized fluid regime that avoids hypovolaemia and subsequent prostaglandin-dependent renal perfusion. METHODS: Observational retrospective analysis of the efficacy of indomethacin in premature infants with PDA treated in a single institution from June 1992 to May 2000. The clinical course and renal effects were analysed in the subgroup of infants born from June 1995 to May 2000. The management of infants at risk and the treatment of infants with PDA followed a standardized protocol that included echocardiographic screening for PDA, indomethacin treatment before congestive failure develops (early symptomatic treatment) and an individualized fluid intake. RESULTS: In total, 412 infants with a gestational age < or = 32 wk were identified. Fifty-six infants with a PDA (14%) were treated with indomethacin [mean birthweight 936 (95% confidence interval 866-1006) g; gestational age 27.3 (26.8-27.9) wk]. Indomethacin treatment was successful in 52 infants (93%). The clinical course and renal effects were analysed in 41 infants. Most infants received three indomethacin doses of 0.2 mg kg(-1) every 12 h. Urine output transiently decreased from 5.6 (4.6-6.4) to 4.6 (3.9-5.3) ml kg(-1) (h(-1). Serum creatinine temporarily increased from 0.90 (0.83-0.98) to 1.06 (0.87-1.24)mg dl(-1). Fluid intake was 158 (148-168) ml kg(-1) d(-1) before indomethacin and decreased to 142 (131-154) ml kg(-1) d(-1). CONCLUSION: Indomethacin is very effective for closure of a PDA, even in very premature infants, and is not associated with clinically significant renal side effects.

Effect of preterm formula with and without long-chain polyunsaturated fatty acids on the urinary excretion of F2-isoprostanes and 8-epi-prostaglandin F2alpha.

BACKGROUND: The objective of this study was to evaluate the effect of conventional and long-chain polyunsaturated fatty acids (LCP)-enriched preterm formula on the endogenous formation of F2-isoprostanes and 8-epi-prostaglandin (PG) F2alpha as possible markers of lipid peroxidation in preterm infants during their first weeks of life. METHODS: In a prospective, randomized, double-blind study, infants received either formula enriched with LCP (n = 8), standard preterm formula (n = 7), or (expressed) breast milk (n = 8). Urine was sampled at study entry and after the study period of 3 weeks. The formation of F2-isoprostanes and 8-epi-PGF2alpha was evaluated by measuring the urinary excretion by gas chromatography-mass spectrometry. RESULTS: No differences in the urinary excretion of F2-isoprostanes and 8-epi-PGF2alpha were observed at the end of the study period. CONCLUSIONS: This result suggests that supplementation of a preterm formula with LCP for a period of 3 weeks does not stimulate lipid peroxidation in preterm infants.

Prostanoid formation during feeding of a preterm formula with long-chain polyunsaturated fatty acids in healthy preterm infants during the first weeks of life.

The objective of this study was to evaluate the effect of conventional and long-chain polyunsaturated fatty acids (LCP)-enriched preterm formula on prostanoid formation in preterm infants during their first weeks of life. In a prospective, randomized, double-blind study, healthy infants received either formula enriched with LCP (n = 10), standard preterm formula (n = 10), or (expressed) breast milk (n = 10). Urine was sampled, and anthropometric measurements were taken at study entry and after the study period of 3 wk. In vivo formation of prostaglandin E2, thromboxane A2, and prostacyclin was evaluated by measuring the urinary excretion of the respective index metabolities by gas chromatography-mass spectrometry. There were no significant differences in urinary prostanoid excretion and anthropometric data between the groups at the end of the study period. We conclude that neither conventional formula nor supplementation of a preterm formula with LCP for a period of 3 wk substantially influence prostanoid formation in healthy preterm infants.