Number and activation of circulating polymorphonuclear leukocytes and platelets are associated with neonatal respiratory distress syndrome severity

Objective. To determine whether number and activation of circulating polymorphonuclear leukocytes (PMNs) and platelets are associated with disease severity in neonatal respiratory distress syndrome (RDS).Design. Prospective study.Setting. Tertiary neonatal intensive care unit.Patients. Preterm infants with, severe (n = 18) or mild tee moderate (n = 18) RDS who were consecutively admitted.Interventions. FMN and platelet counts and plasma concentrations of elastase-alpha(1)-proteinase inhibitor (E-alpha(1)-PI) and thromboxane B-2 (TxB(2)) were recorded each day during the first 5 days of life. E-alpha(1)-PI-to PMN and TxB(2)-to-platelet ratios were calculated to correct for the influence of the PMN and platelet count on elastase and thromboxane release.Results. From day 2, the severe RDS group had lower median PMN counts (1.5 vs 4.5 x 10(9)/L), lower mean platelet counts (136 vs 230 x 10(9)/L), and more elastase and thromboxane release, indicated by higher median E-alpha(1)-PI-to-PMN (39.2 vs 13.0 ng/10(6) PMNs on day 2) and TxB(2)-to-platelet (2.61 vs 0.52 pg/10(6) platelets on day 3) ratios than the mild-to-moderate group. Lower PMN and platelet counts and higher elastase and thromboxane release were correlated with birth asphyxia (lower 5-minute Apgar scores and umbilical arterial PH values), higher respiratory requirements (fraction of inspired oxygen and peak inspiratory pressure), and decreased values for continuous measures of RDS severity (ventilatory efficiency index and PaO2-to-alveolar oxygen tension ratio).Conclusion. Decreased PMN and platelet counts and increased elastase and thromboxane release are correlated with increased RDS severity. Birth asphyxia (hypoxia and acidosis) and tissue injury caused by high-pressure ventilation and hyperoxia may promote this activation process.