HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Skogstrand, K. Articles by Thorsen, P. PubMed PubMed Citation Articles by Skogstrand, K. Articles by Thorsen, P. Related Collections Preterm labor

Association of Preterm Birth With Sustained Postnatal Inflammatory Response

From the ¹Department of Clinical Biochemistry, Statens Serum Institut, Copenhagen, Denmark; ²NANEA at Department of Epidemiology, Institute of Public Health, University of Aarhus, Aarhus, Denmark; the ³National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, Atlanta, Georgia; and the ⁴Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia.

Objective: To investigate fetal or neonatal inflammatory patterns based on 25 inflammatory markers in neonatal dried blood spots samples from infants born preterm and term, collected several days after birth.

Methods: Dried blood spots samples from 160 neonates were analyzed for 25 inflammatory markers using multiplex technology: 26 neonates born very preterm (before 32 weeks of gestation), drawn at a mean 6 days (95% confidence interval [CI], 5–7 days) after birth; 52 born preterm (32–36 weeks of gestation), drawn at mean 5 days (95% CI, 5–6 days) after birth; and 82 born at term (at or after 37 weeks of gestation), drawn at mean 5 days (95% CI, 5–5 days) after birth. Markers statistically significantly associated with preterm birth were analyzed in a multivariable model together with maternal and neonatal risk factors for preterm birth.

Results: Elevated levels of interleukin (IL)-1β, IL-6, soluble IL-6r, IL-8, matrix metalloproteinase-9, and transforming growth factor-β1 and decreased levels of IL-18, brain-derived neurotrophic factor, and C-reactive protein were associated with preterm birth. Maternal risk factors could explain only an increase of IL-1β, whereas neonatal factors could explain several of the elevated and decreased inflammatory markers in the dried blood spots samples from the infants born preterm compared with the infants born at term.

Conclusion: The differences in levels of inflammatory markers in dried blood spots samples from infants born preterm compared with infants born at term supports the hypothesis that inflammation of fetal origin might be a cause of preterm birth.

LEVEL OF EVIDENCE: II