Elevated urinary leukotriene E4 in chronic lung disease of extreme prematurity.
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.[1]References
- Elevated urinary leukotriene E4 in chronic lung disease of extreme prematurity. Davidson, D., Drafta, D., Wilkens, B.A. Am. J. Respir. Crit. Care Med. (1995) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
