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Soluble intercellular cell adhesion molecule-1 and L-selectin plasma concentrations and response to surfactant in
Petra S Koehne1, Mathias H Wagner, Carsten Willam
1Department of Neonatology, Charité Virchow-Hospital, Humboldt University, Berlin, Germany.
Insights
Elevated intercellular cell adhesion molecule (ICAM)-1 at 24 hours indicates a poor response to surfactant in preterm infants. Low L-selectin levels at 24 hours predict the need for prolonged oxygen support.
Area of Science:
- Neonatal Medicine
- Pediatric Pulmonology
- Biomarkers in Neonatal Care
Background:
- Preterm infants often suffer from respiratory distress syndrome (RDS).
- Exogenous surfactant therapy is a standard treatment for RDS.
- Predicting treatment response and long-term outcomes is crucial for optimizing care.
Purpose of the Study:
- To determine if plasma levels of soluble intercellular cell adhesion molecule (ICAM)-1 and L-selectin at 24 hours of life correlate with surfactant response in preterm infants.
- To identify potential biomarkers for predicting treatment outcomes in neonatal respiratory distress.
Main Methods:
- A prospective study was conducted in a Level III neonatal intensive care unit.
- Plasma samples were collected at 24 hours of life from 29 preterm infants with severe RDS and 17 healthy preterm controls.
- Infants with RDS received natural surfactant, and response was defined by a >50% decrease in FiO2 within 6 hours.
Main Results:
- Elevated ICAM-1 concentrations at 24 hours were significantly associated with a poor response to surfactant therapy (p <.001).
- Plasma L-selectin levels were lower in surfactant-treated infants compared to controls (p =.004).
- Reduced L-selectin at 24 hours predicted a prolonged need for supplemental oxygen at 36 weeks gestational age (p =.004).
Conclusions:
- Elevated circulating ICAM-1 at 24 hours of age is a marker of poor surfactant response in preterm infants with respiratory distress.
- Low plasma L-selectin levels at 24 hours of age can predict the need for extended supplemental oxygen support.
- These biomarkers may aid in tailoring respiratory support and predicting outcomes in neonates with RDS.
Objective:
To investigate whether plasma concentrations of soluble intercellular cell adhesion molecule (ICAM)-1 and L-selectin at 24 hrs of life are related to good or poor response to exogenous surfactant in preterm infants.
Design:
Prospective study of markers of inflammation in circulating blood at 24 hrs of life.
Setting:
Level III neonatal intensive care unit.
Patients:
Twenty-nine preterm newborns suffering from severe respiratory distress syndrome (Fio(2) > 0.4) without signs of infection or fetal acidosis, and 17 healthy preterm newborns of similar gestational age serving as controls.
Interventions:
Infants with respiratory distress were treated with natural surfactant at 0.3-5 hrs of life. A response to surfactant, defined as a decrease of Fio(2) >50% within 6 hrs after surfactant, was seen in 21 infants.
Measurements And Main Results:
Soluble ICAM-1 and L-selectin concentrations were determined in plasma samples taken at 24 hrs of age. ICAM-1 was elevated (p <.001) in infants who responded poorly to surfactant (median, 392 ng/mL; range, 58.26-4884.24 ng/mL) compared with good responders (20.52 ng/mL, 2.32-138.58 ng/mL) or controls (21.91 ng/mL, 2.61-65.73 ng/mL), without differences between controls and good responders. L-selectin was lower (p =.004) in surfactant-treated infants (4.45 nmol/L, 2.0-10.4 ng/mL) than in controls (6.0/2.35-10.25 nmol/L) without differences between surfactant good and poor responders. However, infants requiring supplemental oxygen at 36 wks of gestational age had reduced L-selectin at 24 hrs of age (3.2/2.0-3.45 vs. 5.0/2.35-10.4 nmol/L, p =.004), whereas there was no difference in ICAM-1.
Conclusions:
In preterm infants with respiratory distress, a poor response to surfactant within 6 hrs of administration is associated with elevated circulating ICAM-1 concentrations at 24 hrs of age. Low plasma L-selectin at 24 hrs of age predicts prolonged requirement for supplemental oxygen.