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ArtikelAssociation of Preterm Birth With Sustained Postnatal Inflammatory Response  
Oleh: Skogstrand, Kristin ; Hougaard, David M. ; Schendel, Diana E. ; Bent, Norgaard-Pedersen ; Sverke, Claus ; Thorsen, Poul
Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Obstetrics and Gynecology vol. 111 no. 05 (May 2008), page 1118.
Ketersediaan
  • Perpustakaan FK
    • Nomor Panggil: O01.K.2008.02
    • Non-tandon: 1 (dapat dipinjam: 0)
    • Tandon: tidak ada
    Lihat Detail Induk
Isi artikelObjective: 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)-1ß, IL-6, soluble IL-6r, IL-8, matrix metalloproteinase-9, and transforming growth factor-ß1 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-1ß, 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.
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