scholarly journals Why Do the Fetal Membranes Rupture Early after Fetoscopy? A Review

2021 ◽  
pp. 1-11
Author(s):  
Benjamin J. Amberg ◽  
Ryan J. Hodges ◽  
Karyn A. Rodgers ◽  
Kelly J. Crossley ◽  
Stuart B. Hooper ◽  
...  
Keyword(s):  
Fetal Surgery ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Preclinical Models ◽  
Premature Rupture ◽  
Domestic Species ◽  
New Therapies ◽  
Preterm Premature Rupture ◽  
Limited Success ◽  
Membrane Physiology

Iatrogenic preterm premature rupture of the fetal membranes (iPPROM) remains the Achilles’ heel of keyhole fetal surgery (fetoscopy) despite significant efforts in preclinical models to develop new therapies. This limited success is partially due to incomplete understanding why the fetal membranes rupture early after fetoscopy and notable differences in membrane physiology between humans and domestic species. In this review, we summarize aspects of fetoscopy that may contribute to iPPROM, the previous efforts to develop new therapies, and limitations of preclinical models commonly used in fetal membrane research.

Visualisation of the insertion of a membrane for the treatment of preterm rupture of fetal membranes using a synthetic model of a pregnant uterus

2018 ◽  
Vol 33 (2) ◽  
pp. 234-244
Author(s):  
Sabiniano Roman ◽  
Christopher Hillary ◽  
Brenda Narice ◽  
Anthony J Bullock ◽  
Dilly OC Anumba ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Amniotic Fluid ◽  
Bilayer Membrane ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Premature Rupture ◽  
Management Options ◽  
Pregnant Uterus ◽  
Fetal Survival ◽  
Preterm Premature Rupture

Preterm premature rupture of fetal membranes is a leading cause of preterm delivery. Preterm labour can compromise fetal survival, and even if a pregnancy affected by preterm premature rupture of fetal membrane continues, major complications associated with leakage of amniotic fluid and risk of infection can affect the normal development and survival of the baby. There are limited management options for preterm premature rupture of fetal membrane other than delivery of the baby if ascending infection (chorioamnionitis) is suspected. We have previously reported the development and characterisation of an implantable membrane with the aim of using it to occlude the internal os of the cervix, in order to prevent amniotic fluid loss, allow fluid reaccumulation and reduce the risk of chorioamnionitis. For this, an electrospun biocompatible and distensible bilayer membrane was designed with mechanical properties similar to the human amniotic membrane. In this study, we consider the effects of sterilization on the membrane, how to insert the membrane and visualise it using routine clinical methods. To do this, we used e-beam sterilisation and examined the ability of the membrane to adhere to ex vivo human cervical tissues. We also studied its insertion into a custom-synthesised model of a 20-week pregnant uterus and imaged the membrane using ultrasound. Sterilisation produced minor effects on physical and mechanical properties, but these did not affect the capacity of the membrane to be sutured or to provide a fluid barrier. We demonstrated that fibrin glue can successfully adhere the bilayer membrane to cervical tissues. Finally, we demonstrated that the membrane can be inserted through the cervix as well as visualized in place using ultrasound imaging and an endoscope. In summary, we suggest this membrane is a candidate for further development in an appropriate animal model, supported by appropriate imaging, to precede possible future human studies if judged to demonstrate satisfactory safety and efficacy profiles.

The role of apoptosis in preterm premature rupture of the human fetal membranes

2013 ◽  
Vol 288 (3) ◽  
pp. 501-505 ◽  
Author(s):  
Aylin Saglam ◽  
Cinar Ozgur ◽  
Iris Derwig ◽  
Bekir Serdar Unlu ◽  
Funda Gode ◽  
...  
Keyword(s):  
Fetal Membranes ◽  
Premature Rupture ◽  
Preterm Premature Rupture

Risk factors for preterm premature rupture of fetal membranes: A multicenter case-control study

1990 ◽  
Vol 163 (1) ◽  
pp. 130-137 ◽  
Author(s):  
James H. Harger ◽  
Ann W. Hsing ◽  
Ruth E. Tuomala ◽  
Ronald S. Gibbs ◽  
Philip B. Mead ◽  
...  
Keyword(s):  
Risk Factors ◽  
Case Control Study ◽  
Case Control ◽  
Fetal Membranes ◽  
Premature Rupture ◽  
Preterm Premature Rupture ◽  
Control Study

scholarly journals Ubiquitin-Proteasome-Collagen (CUP) Pathway in Preterm Premature Rupture of Fetal Membranes

2017 ◽  
Vol 8 ◽  
Author(s):  
Xinliang Zhao ◽  
Xiaoyan Dong ◽  
Xiucui Luo ◽  
Jing Pan ◽  
Weina Ju ◽  
...  
Keyword(s):  
Fetal Membranes ◽  
Premature Rupture ◽  
Preterm Premature Rupture ◽  
Ubiquitin Proteasome

A clinical case of pregnancy with suspected trophoblastic disease in 3 trimester

2014 ◽  
Vol 63 (3) ◽  
pp. 66-70
Author(s):  
Yevgeniy Sergeyevich Mikhaylin ◽  
Lada Anatolyevna Ivanova ◽  
Alla Sergeyevna Lisyanskaya ◽  
Aleksey Gennadyevich Savitskiy ◽  
Anna Gennadyevna Minina ◽  
...  
Keyword(s):  
Clinical Case ◽  
Hydatidiform Mole ◽  
Intrauterine Infection ◽  
Fetal Membranes ◽  
Premature Rupture ◽  
Trophoblastic Disease ◽  
Preterm Premature Rupture ◽  
Placental Blood ◽  
Β Hcg ◽  
Placental Blood Flow

Cases of trophoblastic disease in the presence of the living fetus during 2-3 trimesters of pregnancy is a rare phenomenon. The description of the clinical case of suspected trophoblastic disease at term of 26 weeks is provided in article. The decision of pregnancy prolongation under control β- HCG was made. Therapy of gestosis, improvement of maternal-placental blood flow, anticoagulant therapy was carried out. Cesarean section was made at 30 weeks of pregnancy (preterm premature rupture of fetal membranes). In the postpartum period, a decrease of b-HCG to zero was within 1,5 months. In the postoperative period we did not receive convincing pathomorphological data for the presence of trophoblastic disease, so the question of whether there was in this case partial hydatidiform mole in combination with alive fetus, or received changes in the placenta and anomalously high values of b-HCG were the result of primary placental insufficiency with the intrauterine infection, remains open.

Serum concentrations of soluble B7-H4 in early pregnancy are elevated in women with preterm premature rupture of fetal membranes

2016 ◽  
Vol 76 (2) ◽  
pp. 149-154 ◽  
Author(s):  
Pawel Mach ◽  
Angela Köninger ◽  
Lukasz Wicherek ◽  
Rainer Kimmig ◽  
Sabine Kasimir-Bauer ◽  
...  
Keyword(s):  
Early Pregnancy ◽  
Fetal Membranes ◽  
Serum Concentrations ◽  
Premature Rupture ◽  
Preterm Premature Rupture

The Chorion Layer of Fetal Membranes Is Prematurely Destroyed in Women With Preterm Premature Rupture of the Membranes

2013 ◽  
Vol 20 (10) ◽  
pp. 1246-1254 ◽  
Author(s):  
Bernard J. Canzoneri ◽  
Liping Feng ◽  
Chad A. Grotegut ◽  
Rex C. Bentley ◽  
R. Phillips Heine ◽  
...  
Keyword(s):  
Fetal Membranes ◽  
Premature Rupture ◽  
Preterm Premature Rupture

scholarly journals A mouse model of spontaneous preterm birth based on the genetic ablation of biglycan and decorin

Reproduction ◽  
2011 ◽  
Vol 142 (1) ◽  
pp. 183-194 ◽  
Author(s):  
Megan L Calmus ◽  
Elyse E Macksoud ◽  
Richard Tucker ◽  
Renato V Iozzo ◽  
Beatrice E Lechner
Keyword(s):  
Preterm Birth ◽  
Fetal Membranes ◽  
Dependent Manner ◽  
Null Mutant ◽  
Wild Type ◽  
Premature Rupture Of Membranes ◽  
Premature Rupture ◽  
Ehlers Danlos Syndrome ◽  
Genetic Ablation ◽  
Preterm Premature Rupture

Preterm premature rupture of membranes is responsible for one-third of preterm births. Ehlers–Danlos syndrome (EDS) is associated with preterm premature rupture of membranes in humans. In particular, an EDS variant is caused by a genetic mutation resulting in abnormal secretion of biglycan and decorin, two small leucine-rich proteoglycans highly expressed in reproductive tissues. Because biglycan/decorin null mutant (Bgn−/−Dcn−/−) mice demonstrate phenotypic changes similar to EDS, we used this model to test whether either biglycan or decorin or both play a role in the attainment of successful term gestation. Wild-type biglycan null mutant, decorin null mutant, and biglycan/decorin null mutant pregnancies were assessed for the length of gestation, pup and placenta weight, and litter size. Quantitative real-time PCR was performed to measure biglycan and decorin gene expression, and immunohistochemistry was performed to assess protein expression in placenta and fetal membranes at embryonic days E12, E15, and E18.Bgn−/−Dcn−/−dams displayed preterm birth, whereas the possession of at least two biglycan or decorin wild-type alleles was protective of preterm birth. The number ofBgn−/−Dcn−/−pups was decreased at postnatal day P1 but not at E18. Biglycan and decorin were upregulated in the placenta in the absence of each other and were developmentally regulated in fetal membranes, suggesting that these two proteoglycans demonstrate genetic complementation and contribute to gestational success in a dose-dependent manner. Thus, the biglycan/decorin null mutant mouse is a model of genetically induced preterm birth and perinatal loss. This model presents novel targets for preventive or therapeutic manipulation of preterm birth.

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