Sequential disruptions to inflammatory and angiogenic pathways and risk of spontaneous preterm birth in Malawian women

If you need an accessible version of this item, please submit a remediation request.
Date
2023-05-19
Language
American English
Embargo Lift Date
Committee Members
Degree
Degree Year
Department
Grantor
Journal Title
Journal ISSN
Volume Title
Found At
Elsevier
Abstract

Preterm birth is a leading cause of death in children under five years of age. We hypothesized that sequential disruptions to inflammatory and angiogenic pathways during pregnancy increase the risk of placental insufficiency and spontaneous preterm labor and delivery. We conducted a secondary analysis of inflammatory and angiogenic analytes measured in plasma samples collected across pregnancy from 1462 Malawian women. Women with concentrations of the inflammatory markers sTNFR2, CHI3L1, and IL18BP in the highest quartile before 24 weeks gestation and women with anti-angiogenic factors sEndoglin and sFlt-1/PlGF ratio in the highest quartile at 28-33 weeks gestation had an increased relative risk of preterm birth. Mediation analysis further supported a potential causal link between early inflammation, subsequent angiogenic dysregulation detrimental to placental vascular development, and earlier gestational age at delivery. Interventions designed to reduce the burden of preterm birth may need to be implemented before 24 weeks of gestation.

Description
item.page.description.tableofcontents
item.page.relation.haspart
Cite As
Weckman AM, Elphinstone RE, Ssenkusu JM, et al. Sequential disruptions to inflammatory and angiogenic pathways and risk of spontaneous preterm birth in Malawian women. iScience. 2023;26(6):106912. Published 2023 May 19. doi:10.1016/j.isci.2023.106912
ISSN
Publisher
Series/Report
Sponsorship
Major
Extent
Identifier
Relation
Journal
iScience
Source
PMC
Alternative Title
Type
Article
Number
Volume
Conference Dates
Conference Host
Conference Location
Conference Name
Conference Panel
Conference Secretariat Location
Version
Final published version
Full Text Available at
This item is under embargo {{howLong}}