Preterm premature rupture of the fetal membranes: current concepts.

Department of Obstetrics and Gynecology, University of Pennsylvania, Philadelphia, PA, USA.
Minerva ginecologica 09/2005; 57(4):389-96.
Source: PubMed

ABSTRACT Preterm birth and preterm premature rupture of membranes (PPROM) are common causes of perinatal morbidity and mortality. Fetal membrane integrity is regulated partially by collagenases and inhibitors. A number of genetic polymorphisms with genes related to infection, inflammation and collagen degradation have been identified and studies as risk factors for PPROM. This manuscript reviews the state of the science on the pathophysiology of PPROM and possible genetic influences.

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    ABSTRACT: This study was conducted to examine the frequency and clinical significance of a positive Amnisure test in patients with preterm labor and intact membranes by sterile speculum exam. A retrospective cohort study was performed including 90 patients with preterm labor and intact membranes who underwent Amnisure tests prior to amniocentesis (< 72 h); most patients (n=64) also underwent fetal fibronectin (fFN) tests. Amniotic fluid (AF) was cultured for aerobic/anaerobic bacteria and genital mycoplasmas and assayed for matrix metalloproteinase-8. (1) the prevalence of a positive Amnisure test was 19% (17/90); (2) patients with a positive Amnisure test had significantly higher rates of adverse pregnancy and neonatal outcomes (e.g., impending preterm delivery, intra-amniotic infection/inflammation, and neonatal morbidity) than those with a negative Amnisure test; (3) a positive test was associated with significantly increased risk of intra-amniotic infection and/or inflammation, delivery within 7, 14, or 28 days and spontaneous preterm birth (< 35 weeks) among patients with a negative fFN test. A positive Amnisure test in patients with preterm labor and intact membranes is a risk factor for adverse pregnancy outcome, particularly in patients with a negative fFN test. A positive Amnisure test in patients without symptoms or signs of ROM should not be taken as an indicator that membranes have ruptured.
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    ABSTRACT: Preterm birth (PTB) is a live birth delivered before 37 weeks of gestation (GW). About one-third of PTBs result from the preterm premature rupture of membranes (PPROM). Up to the present, the pathogenic mechanisms underlying PPROM are not clearly understood. Here, we investigated the differential expression of long chain non-coding RNAs (lncRNAs) in placentas of PTBs with PPROM, and their possible involvement in the pathogenic pathways leading to PPROM. A total number of 1954, 776, and 1050 lncRNAs were identified with a microarray from placentas of PPROM (group A), which were compared to full-term birth (FTB) (group B), PTB (group C), and premature rupture of membrane (PROM) (group D) at full-term, respectively. Instead of investigating the individual pathogenic role of each lncRNA involved in the molecular mechanism underlying PPROM, we have focused on investigating the metabolic pathways and their functions to explore what is the likely association and how they are possibly involved in the development of PPROM. Six groups, including up-regulation and down-regulation in the comparisons of A vs. B, A vs. C, and A vs. D, of pathways were analyzed. Our results showed that 22 pathways were characterized as up-regulated 7 down-regulated in A vs. C, 18 up-regulated and 15 down-regulated in A vs. D, and 33 up-regulated and 7 down-regulated in A vs. B. Functional analysis showed pathways of infection and inflammatory response, ECM-receptor interactions, apoptosis, actin cytoskeleton, and smooth muscle contraction are the major pathogenic mechanisms involved in the development of PPROM. Characterization of these pathways through identification of lncRNAs opened new avenues for further investigating the epigenomic mechanisms of lncRNAs in PPROM as well as PTB.
    PLoS ONE 11/2013; 8(11):e79897. · 3.53 Impact Factor
    This article is viewable in ResearchGate's enriched format
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    ABSTRACT: The chronically catheterized fetal sheep is a widely used model for fetal physiologic and pathophysiologic investigations. Catheterization involves opening the amniochorion to gain access to the fetus. In the current study, we explored the role of the amnion and amniochorion in maintaining normal amniotic fluid volume (AFV) and composition and fetal blood-gas status after surgery. Fetal sheep were catheterized at 119.6 ± 0.3 (mean ± SE, n = 25) d gestation (term, approximately 147 d). An opening equal to approximately 5% of total membrane surface area was created by resecting a portion of the amnion or amniochorion during surgery. The uterine wall was closed in all animals. Compared with control sheep (AFV = 992 ± 153 mL, n = 11), resection of the amnion had no significant effect on AFV (745 ± 156 mL, n = 7) measured 5 d after surgery, whereas resection of the amniochorion resulted in extensive loss of amniotic fluid (AFV = 131 ± 38 mL, n = 7). This loss resulted from extensive entry of amniotic fluid into the space between the chorion and uterine wall. Amniotic fluid, fetal plasma, and urinary solute concentrations; arterial pH; oxygen tension; and carbon dioxide tension were unchanged. A small opening in the amnion has minimal effects on ovine AFV, whereas a small opening in the amniochorion results in oligohydramnios. In addition, the amnion appears to be the primary site that limits the rate of amniotic fluid absorption by the chorionic vasculature.
    Journal of the American Association for Laboratory Animal Science: JAALAS 01/2011; 50(6):939-42. · 0.73 Impact Factor