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https://hdl.handle.net/2440/39257
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DC Field | Value | Language |
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dc.contributor.author | Dekker, G. | - |
dc.contributor.author | Sukcharoen, N. | - |
dc.date.issued | 2004 | - |
dc.identifier.citation | Journal of the Medical Association of Thailand = Chotmaihet thangphaet, 2004; 87(Suppl 3):S96-S103 | - |
dc.identifier.issn | 0125-2208 | - |
dc.identifier.uri | http://hdl.handle.net/2440/39257 | - |
dc.description.abstract | Preeclampsia still ranks as one of obstetrics major problems. Clinicians typically encounter preeclampsia as maternal disease with variable degrees of fetal involvement. More and more the unique immunogenetic maternal - paternal relationship is appreciated, and as such also the specific ‘genetic conflict’ that is characteristic of haemochorial placentation. Factors influencing the unique maternal-fetal (paternal) interaction probably include the length and type of sexual relationship, the maternal (decidual natural killer cells) acceptation of the invading cytotrophoblast (paternal HLA-C), and seminal levels of transforming growth factor-b and probably other cytokines. The magnitude of the maternal response would be determined by factors including a maternal set of genes determining her characteristic inflammatory responsiveness, age, quality of her endothelium, obesity/ insulin resistance and probably a whole series of susceptibility genes amongst which the thrombophilias received a lot of attention in recent years. | - |
dc.description.uri | http://www.ncbi.nlm.nih.gov/pubmed/21213501 | - |
dc.language.iso | en | - |
dc.publisher | Medical Association of Thailand | - |
dc.rights | © Medical Association of Thailand | - |
dc.subject | Etiology | - |
dc.subject | Preeclampsia | - |
dc.title | Etiology of preeclampsia: an update | - |
dc.type | Journal article | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Dekker, G. [0000-0002-7362-6683] | - |
Appears in Collections: | Aurora harvest Obstetrics and Gynaecology publications |
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