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Elevated urinary leukotriene E4 in chronic lung disease of extreme prematurity

D Davidson1, D Drafta, B A Wilkens

  • 1Division of Neonatal-Perinatal Medicine, Schneider Children's Hospital, Long Island Jewish Medical Center, New Hyde Park, New York.

American Journal of Respiratory and Critical Care Medicine
|March 1, 1995
PubMed

Insights

Peptidoleukotriene production is elevated in premature infants with chronic lung disease (CLD). This finding suggests potential new treatments targeting leukotriene pathways for CLD in neonates.

Area of Science:

  • Neonatology
  • Pulmonology
  • Biochemistry

Background:

  • Chronic lung disease of prematurity (CLD) is a significant concern in extremely premature infants.
  • The role of pulmonary peptidoleukotrienes in CLD pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the contribution of pulmonary peptidoleukotrienes to CLD pathogenesis.
  • To measure urinary leukotriene E4 (uLTE4) levels in premature infants with and without CLD.

Main Methods:

  • Urine samples were collected from infants with birth weights < 1000g.
  • Patients were categorized into normal control (n=8) and CLD (n=26) groups.
  • Urinary LTE4 levels were quantified using established assays.

Main Results:

  • Urinary LTE4 levels were significantly higher in CLD infants compared to controls (288 vs. 35 pg/mg creatinine).
  • Ventilator-dependent CLD infants with elevated uLTE4 required higher peak inspiratory pressures.
  • Dexamethasone therapy reduced uLTE4 levels in ventilator-dependent CLD infants.

Conclusions:

  • Peptidoleukotriene production is activated to pathophysiologic levels in infants with CLD.
  • These findings suggest that leukotriene pathways may be therapeutic targets for CLD treatment.
  • Further research on leukotriene inhibitors or antagonists in CLD is warranted.

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