PEDIATRICS Vol. 99 No. 5 May 1997, pp. 672-680
Received Mar 5, 1996; accepted Jul 30, 1996.
,
From the * Beatrix Children's Hospital, Division of
Neonatology, and
Department of Cardiopulmonary Surgery, Division
of Blood Interaction Research, University Hospital Groningen,
University of Groningen, Groningen, The Netherlands.
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 to moderate (n = 18) RDS who were consecutively admitted.
Interventions. PMN and platelet counts and plasma
concentrations of elastase-
1-proteinase inhibitor
(E-
1-PI) and thromboxane B2
(TxB2) were recorded each day during the first 5 days of
life. E-
1-PI-to-PMN and TxB2-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 × 109/L), lower mean
platelet counts (136 vs 230 × 109/L), and more
elastase and thromboxane release, indicated by higher median
E-
1-PI-to-PMN (39.2 vs 13.0 ng/10 PMNs on
day 2) and TxB2-to-platelet (2.61 vs 0.52 pg/10 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.
Key words: neonatal respiratory distress syndrome severity, polymorphonuclear leukocytes, platelets, elastase, thromboxane.
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