Synergy and interactions among biological pathways leading to preterm premature rupture of membranes.
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.
Department Obstetrics & Gynecology, University of Washington, Seattle, WA, USA rothbes@uw.edu.
Sophia M R
SM
Lannon
Swedish Medical Center, Seattle, WA, USA.
Jeroen P
JP
Vanderhoeven
Department Obstetrics & Gynecology, University of Washington, Seattle, WA, USA.
David A
DA
Eschenbach
Department Obstetrics & Gynecology, University of Washington, Seattle, WA, USA Global Alliance to Prevent Prematurity & Stillbirth, Seattle, WA, USA.
Michael G
MG
Gravett
Department Obstetrics & Gynecology, University of Washington, Seattle, WA, USA.
Kristina M
KM
Adams Waldorf
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000175:diagnosis* / Q000378:metabolism*; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*; D011247:Pregnancy; D015398:Signal Transduction / Q000502:physiology*
PPROM; abruption; chorioamnion; chorioamnionitis; fetal membranes; inflammation; intraamniotic infection; oxidative stress; preterm birth; preterm premature rupture of membranes