Poster Session 2
Category: Prematurity
Poster Session 2
Claudia Rueda, MD
Hospital Clínic Barcelona
BARCELONA, Catalonia, Spain
Clara Murillo Bravo *, MD, PhD (she/her/hers)
Post-Doctoral Researcher
Hospital Clínic Barcelona
HOSPITAL CLINIC BARCELONA / BARCELONA, Catalonia, Spain
Sílvia Ferrero, MD, PhD
Senior Obstetrician
BCNatal – Barcelona Center for Maternal Fetal and Neonatal Medicine Hospital Sant Joan de Déu and Hospital Clínic, University of Barcelona
BARCELONA, Catalonia, Spain
Ana Paula Dantas, PhD
IDIBAPS
Barcelona, Catalonia, Spain
Eduard Gratacós, MD, PhD
Hospital Clínic Barcelona
BARCELONA, Catalonia, Spain
Francesc Figueras, MD, PhD (he/him/his)
Head of Department
BCNatal – Barcelona Center for Maternal Fetal and Neonatal Medicine Hospital Sant Joan de Déu and Hospital Clínic, University of Barcelona
Barcelona, Catalonia, Spain
Laia Grau, MD
Hospital Sant Joan de Deu
BARCELONA, Catalonia, Spain
David Boada, MD
Pre-Doctoral Researcher
Hospital Clínic Barcelona
BARCELONA, Catalonia, Spain
ANA HERRANZ, MD, PhD
Hospital Clínic de Barcelona
BARCELONA, Catalonia, Spain
Montse Palacio *, MD, PhD (she/her/hers)
Senior Consultant
Hospital Clínic Barcelona
BARCELONA, Catalonia, Spain
Teresa Cobo, MD, PhD (she/her/hers)
Senior Researcher
Hospital Clínic de Barcelona
Hospital Clinic (Barcelona), Catalonia, Spain
To characterize placental expression of genes involved in apoptosis and senescence, along with biomarkers related to angiogenesis, inflammation, tissue remodeling, and telomere length, in pregnancies complicated by preterm premature rupture of membranes (PPROM) compared to term asymptomatic pregnancies.
Study Design:
A prospective cohort study including 54 singleton pregnancies: 25 presenting with PPROM between 23+6 and 34+0 weeks of gestation and 29 term pregnancies. Placental tissue samples were analyzed for protein concentrations related to angiogenesis, inflammation, and tissue remodeling via immunoassays. Gene expression of apoptosis and senescence markers, and relative telomere length (TR ratio), were assessed by quantitative PCR. Fold change was used to evaluate group differences. Group comparisons were performed using non-parametric tests.
Results:
Baseline maternal characteristics were similar between groups, with expected differences in clinical outcomes: lower gestational age at delivery, higher rates of labor induction, antenatal corticosteroid exposure, and increased neonatal morbidity in the PPROM group.
Placentas from PPROM pregnancies showed significantly higher levels of IL-8, IL-1β, MCP-1, and G-CSF, indicating an enhanced inflammatory response. Markers related to angiogenesis and tissue remodeling — VEGF, VEGFR1, TIE-2, and FGF-1 — were also significantly increased in PPROM cases.
Of the apoptosis and senescence-related genes evaluated, only SIRT6 showed significantly higher expression in the PPROM group.
No significant differences were found in relative telomere length (TR ratio) between the two groups.
Conclusion:
PPROM is associated with a distinct placental profile characterized by heightened inflammatory and angiogenic activity. Changes in the expression of apoptosis and senescence markers were limited, and no significant differences in telomere length were observed between groups. These findings emphasize the importance of characterizing the underlying physiopathology of PPROM, with inflammation and angiogenic dysfunction emerging as key features in these patients.