期刊
PLACENTA
卷 89, 期 -, 页码 99-106出版社
W B SAUNDERS CO LTD
DOI: 10.1016/j.placenta.2019.12.007
关键词
Preterm birth; Uteroplacental lesion; Inflammation
资金
- Richard King Mellon Foundation
- Magee Obstetrical Maternal & Infant (MOMI) Databank
- Commonwealth of Pennsylvania Department of Health, Maternal Lipids and Placental Function [RFA-67-16]
- [P30CA047904]
Introduction: Preterm birth is a heterogeneous phenotype, with placental abnormalities underlying many cases. The etiology of preterm births that occur in the absence of placental abnormalities, however, remain enigmatic and we considered that early pregnancy biomarkers may provide clues. Methods: Women from a hospital-based cohort (2008-2012, n = 397) were randomly selected within 6 strata of term and preterm birth with and without placental decidual vasculopathy (arteriopathy), intrauterine inflammation/infection (acute chorioamnionitis), or no lesions. Lipids and inflammatory markers were analyzed in first trimester samples (12.5 +/- 0.6 weeks) and related to outcome groups (referent, term births with no lesions). Factor analysis then clustered analytes and related these to preterm birth groups, adjusted for covariates and stratified by pre-pregnancy obesity. Results: Three biomarker patterns were identified. Immune activation cytokines (33% of the variance) were associated with preterm birth with no lesions (aOR 1.5, 95%CI 1.1-2.1), particularly among obese women. In contrast, inflammatory chemokines (9% of variance) were associated with term and preterm vasculopathy among non-obese women (aOR 2.6 [1.3, 4.7] and 2.0 [1.1, 3.0], respectively). Discussion: The early pregnancy maternal immune profile is related to preterm births classified according to placental lesions, and these associations vary according to obesity status.
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