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Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/8502
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dc.contributor.authorDekker, G.-
dc.contributor.authorSibai, B.-
dc.date.issued1999-
dc.identifier.citationSeminars in Perinatology, 1999; 23(1):24-33-
dc.identifier.issn0146-0005-
dc.identifier.issn1558-075X-
dc.identifier.urihttp://hdl.handle.net/2440/8502-
dc.description.abstractThe immune maladaptation hypothesis of preeclampsia is concordant with cytokine-mediated oxidative stress, chronology of endothelial activation, lipid changes, adverse effect of changing partners, and the protective effect of sperm exposure. Genetic factors may involve underlying hereditary thrombophilic disorders and hyperhomocysteinemia, essential hypertension and/or obesity, or control of the Th1/Th2 balance and thus affect the maternal response against fetal antigens. Placental ischemia and increased syncytiotrophoblast deportation are probably end-stage disease phenomena.-
dc.description.statementofresponsibilityGustaaf A. Dekker and Baha M. Sibai-
dc.language.isoen-
dc.publisherGrune & Stratton-
dc.source.urihttp://dx.doi.org/10.1016/s0146-0005(99)80057-3-
dc.subjectUterus-
dc.subjectFetus-
dc.subjectPlacenta-
dc.subjectHumans-
dc.subjectPre-Eclampsia-
dc.subjectIschemia-
dc.subjectAntigens-
dc.subjectPregnancy-
dc.subjectVasoconstriction-
dc.subjectFemale-
dc.titleThe immunology of preeclampsia-
dc.typeJournal article-
dc.identifier.doi10.1016/S0146-0005(99)80057-3-
pubs.publication-statusPublished-
dc.identifier.orcidDekker, G. [0000-0002-7362-6683]-
Appears in Collections:Aurora harvest 4
Obstetrics and Gynaecology publications

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