CX3CL1/Fractalkine as a biomarker for early pregnancy prediction of preterm premature rupture of membranes.
CX3CL1
PPROM
fractalkine
inflammation
prediction
pregnancy
Journal
Clinical chemistry and laboratory medicine
ISSN: 1437-4331
Titre abrégé: Clin Chem Lab Med
Pays: Germany
ID NLM: 9806306
Informations de publication
Date de publication:
26 Jan 2024
26 Jan 2024
Historique:
received:
25
10
2023
accepted:
13
01
2024
medline:
27
1
2024
pubmed:
27
1
2024
entrez:
26
1
2024
Statut:
aheadofprint
Résumé
The objective of our study was to evaluate serum CX3CL1/Fractalkine, a monocyte/macrophage chemoattractant expressed in cytotrophoblasts and decidual cells, as a predictive biomarker for the occurrence of preterm premature rupture of membranes (PPROM). A case-control study of 438 pregnancies including 82 PPROM cases and 64 preterm labor with intact membranes cases with blood samples collected at first trimester, second trimester and delivery was conducted. The predictive ability of CX3CL1 and maternal risk factors for the occurrence of PPROM was assessed by receiver operating characteristic curve analysis. A second, independent cohort was prospectively constituted to confirm the case-control study results. First trimester CX3CL1 was significantly increased in PPROM cases when compared to matched controls. Multivariate regression analysis highlighted a significant difference for CX3CL1 measured during the first trimester (p<0.001). Alone, CX3CL1 predicts PPROM with a 90 % sensitivity and a specificity around 40 %. The area under the receiver operating characteristic curve for PPROM prediction were 0.64 (95% confidence interval: 0.57-0.71) for first trimester CX3CL1, and 0.61 (95% confidence interval: 0.54-0.68) for maternal risk factors (body mass index<18.5 kg/m CX3CL1 is a promising blood biomarker in the early (first trimester) prediction of PPROM.
Identifiants
pubmed: 38278625
pii: cclm-2023-1202
doi: 10.1515/cclm-2023-1202
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2024 Walter de Gruyter GmbH, Berlin/Boston.
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