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Reprod Sci. 2014 Oct;21(10):1215-27. doi: 10.1177/1933719114534535. Epub 2014 May 19.

Synergy and interactions among biological pathways leading to preterm premature rupture of membranes.

Author information

1
Department Obstetrics & Gynecology, University of Washington, Seattle, WA, USA rothbes@uw.edu.
2
Swedish Medical Center, Seattle, WA, USA.
3
Department Obstetrics & Gynecology, University of Washington, Seattle, WA, USA.
4
Department Obstetrics & Gynecology, University of Washington, Seattle, WA, USA Global Alliance to Prevent Prematurity & Stillbirth, Seattle, WA, USA.

Abstract

Preterm premature rupture of membranes (PPROM) occurs in 1% to 2% of births. Impact of PPROM is greatest in low- and middle-income countries where prematurity-related deaths are most common. Recent investigations identify cytokine and matrix metalloproteinase activation, oxidative stress, and apoptosis as primary pathways to PPROM. These biological processes are initiated by heterogeneous etiologies including infection/inflammation, placental bleeding, uterine overdistention, and genetic polymorphisms. We hypothesize that pathways to PPROM overlap and act synergistically to weaken membranes. We focus our discussion on membrane composition and strength, pathways linking risk factors to membrane weakening, and future research directions to reduce the global burden of PPROM.

KEYWORDS:

PPROM; abruption; chorioamnion; chorioamnionitis; fetal membranes; inflammation; intraamniotic infection; oxidative stress; preterm birth; preterm premature rupture of membranes

PMID:
24840939
PMCID:
PMC5933184
DOI:
10.1177/1933719114534535
[Indexed for MEDLINE]
Free PMC Article

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