Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12188/30585
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dc.contributor.authorSamardjiski, Igoren_US
dc.contributor.authorSimeonova Krstevska, Slagjanaen_US
dc.contributor.authorLivrinova, Vesnaen_US
dc.contributor.authorTodorovska, Irenaen_US
dc.contributor.authorPaneva, I.en_US
dc.contributor.authorJoksimovich, Marijaen_US
dc.contributor.authorAtanasova Boshku, Aleksandraen_US
dc.date.accessioned2024-06-14T08:16:17Z-
dc.date.available2024-06-14T08:16:17Z-
dc.date.issued2024-02-
dc.identifier.urihttp://hdl.handle.net/20.500.12188/30585-
dc.description.abstractPreeclampsia (PE) is a multisystem disorder in pregnancy with a specific collection of signs and symptoms as a result of serious dysfunction of multiple organs. Abnormal placentation in the first trimester, most likely triggers the disbalance of the placental anti-angiogenic factor soluble fms-like tyrosine kinase-1(sFlt-1) and pro-angiogenic placental growth factor (PlGF), which result in systemic endothelial dysfunction (injury) to progressive end-organ damage. According the PROGNOSIS study, the cut-off value of the sFlt-1/PlGF ratio over 85 confirms the suspected PE and proved to be useful in preeclampsia diagnosis. A severely elevated sFlt-1/PlGF ratio is associated closely with the need to deliver within 48hours.en_US
dc.language.isoenen_US
dc.publisherElsevier BVen_US
dc.relation.ispartofEuropean Journal of Obstetrics & Gynecology and Reproductive Biologyen_US
dc.titlePostpartum decline in sflt-1/plgf ratio confirms placental source of angiogenic imbalance and endothelial dysfunction in preeclampsiaen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.ejogrb.2023.08.029-
dc.identifier.urlhttps://api.elsevier.com/content/article/PII:S0301211523003354?httpAccept=text/xml-
dc.identifier.urlhttps://api.elsevier.com/content/article/PII:S0301211523003354?httpAccept=text/plain-
dc.identifier.volume293-
dc.identifier.fpage5-
item.grantfulltextnone-
item.fulltextNo Fulltext-
crisitem.author.deptFaculty of Medicine-
crisitem.author.deptFaculty of Medicine-
crisitem.author.deptFaculty of Medicine-
Appears in Collections:Faculty of Medicine: Journal Articles
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