Am. J. Respir. Crit. Care Med., Vol 151, No. 3, 03 1995, 841-845.
Elevated urinary leukotriene E4 in chronic lung disease of extreme prematurity
D Davidson, D Drafta and BA Wilkens
Division of Neonatal-Perinatal Medicine, Schneider Children's Hospital, Long Island Jewish Medical Center, New Hyde Park, New York.
We determined if pulmonary peptidoleukotrienes contribute to the
pathogenesis of chronic lung disease of extreme prematurity (CLD) by
measuring urinary leukotriene E4 (uLTE4). Study patients had a birth weight
< 1000 g and were about 28 d old when they were classified as normal
control subjects (n = 8) or as having CLD (n = 26, abnormal chest X-ray,
supplemental O2 requirement +/- ventilator). Urinary LTE4 levels were
significantly elevated in CLD compared with the control group (288 +/- 92
versus 35 +/- 10 pg/mg creatinine, mean +/- SE, p < 0.05).
Ventilator-dependent CLD patients, who required dexamethasone and had
demonstrated uLTE4 levels above the normal range, needed significantly
higher peak inspiratory pressures (20 +/- 1 cm H2O versus 15 +/- 1 cm H2O)
than similar patients with uLTE4 in the normal range, and the former group
had a significant reduction in uLTE4 in the first 5 d of dexamethasone
therapy (626 +/- 198 to 451 +/- 176 pg/mg Cr) as ventilatory support was
reduced. We conclude that peptidoleukotriene production is activated in
patients with CLD (and no other detectable organ dysfunction) to
pathophysiologic levels described in adults with acute asthma. Prospective
studies focused on infants dependent on high levels of ventilatory support
may provide insights into the role of leukotriene synthesis inhibitors or
receptor antagonists in the treatment of CLD.
