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dc.contributor.author Alasztics Bálint
dc.contributor.author Kukor Zoltán
dc.contributor.author Pánczél Zita
dc.contributor.author Valent Sándor
dc.date.accessioned 2014-12-22T08:39:42Z
dc.date.available 2014-12-22T08:39:42Z
dc.date.issued 2012
dc.identifier 84864491414
dc.identifier.citation pagination=1167-1176; journalVolume=153; journalIssueNumber=30; journalTitle=ORVOSI HETILAP;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/830
dc.identifier.uri doi:10.1556/OH.2012.29415
dc.description.abstract Preeclampsia is a common and severe disease in pregnancy, a major cause of maternal and fetal morbidity and mortality. The main features of the disease are de novo hypertension after the 20th gestational week and proteinuria, and it is frequently accompanied by edema and other subjective symptoms. The origin of the disease is the placenta, but its sequelae affect multiple organ systems. According to the two-stage model of preeclampsia, the abnormal and hypoperfused placenta (stage 1) releases factors to the bloodstream, which are responsible for the maternal symptoms (stage 2). Oxidative stress, impaired function of nitric-oxide synthase, cellular and humoral immunological factors play an important role in the pathophysiology of the placenta. Endothelial dysfunction is the common denominator of the clinical symptoms. The theory explains the origins of hypertension, proteinuria, edema and other symptoms as well.
dc.relation.ispartof urn:issn:0030-6002
dc.title A praeeclampsia kórélettana a kétlépcsős modell tükrében [The pathophysiology of preeclampsia in view of the two-stage mode]
dc.type Journal Article
dc.date.updated 2014-12-18T09:23:19Z
dc.language.rfc3066 hu
dc.identifier.mtmt 2046480
dc.identifier.pubmed 22835633
dc.contributor.department SE/ÁOK/I/Orvosi Vegytani, Molekuláris Biológiai és Patobiokémiai Intézet
dc.contributor.department SE/ÁOK/K/II. Sz. Szülészeti és Nőgyógyászati Klinika
dc.contributor.institution Semmelweis Egyetem


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