Pre-eclampsia pathophysiology: Difference between revisions
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:* Increased [[Maternal]] [[inflammatory]] response to [[fetal]] [[trophoblast]] | :* Increased [[Maternal]] [[inflammatory]] response to [[fetal]] [[trophoblast]] | ||
:* Imbalance of angiogenic factors <ref name="LevineMaynard2004">{{cite journal|last1=Levine|first1=Richard J.|last2=Maynard|first2=Sharon E.|last3=Qian|first3=Cong|last4=Lim|first4=Kee-Hak|last5=England|first5=Lucinda J.|last6=Yu|first6=Kai F.|last7=Schisterman|first7=Enrique F.|last8=Thadhani|first8=Ravi|last9=Sachs|first9=Benjamin P.|last10=Epstein|first10=Franklin H.|last11=Sibai|first11=Baha M.|last12=Sukhatme|first12=Vikas P.|last13=Karumanchi|first13=S. Ananth|title=Circulating Angiogenic Factors and the Risk of Preeclampsia|journal=New England Journal of Medicine|volume=350|issue=7|year=2004|pages=672–683|issn=0028-4793|doi=10.1056/NEJMoa031884}}</ref> | :* Imbalance of angiogenic factors <ref name="LevineMaynard2004">{{cite journal|last1=Levine|first1=Richard J.|last2=Maynard|first2=Sharon E.|last3=Qian|first3=Cong|last4=Lim|first4=Kee-Hak|last5=England|first5=Lucinda J.|last6=Yu|first6=Kai F.|last7=Schisterman|first7=Enrique F.|last8=Thadhani|first8=Ravi|last9=Sachs|first9=Benjamin P.|last10=Epstein|first10=Franklin H.|last11=Sibai|first11=Baha M.|last12=Sukhatme|first12=Vikas P.|last13=Karumanchi|first13=S. Ananth|title=Circulating Angiogenic Factors and the Risk of Preeclampsia|journal=New England Journal of Medicine|volume=350|issue=7|year=2004|pages=672–683|issn=0028-4793|doi=10.1056/NEJMoa031884}}</ref> | ||
:* Imbalance of [[prostacycline]] and [[ thromboxan-A2]] | |||
==References== | ==References== |
Revision as of 06:50, 16 October 2020
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Pre-eclampsia Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Ogheneochuko Ajari, MB.BS, MS [3]
Pathophysiology
- The pathogenesis of preeclampsia is characterized by the following :[1]
- Chronic uteroplacental ischemia[2]
- Genetic susceptibility
- very-low-density lipoprotein toxicity
- Increased trophoblast apoptosis or necrosis[3]
- Increased Maternal inflammatory response to fetal trophoblast
- Imbalance of angiogenic factors [4]
- Imbalance of prostacycline and thromboxan-A2
References
- ↑ Johansen, M; Redman, C.W.G; Wilkins, T; Sargent, I.L (1999). "Trophoblast Deportation in Human Pregnancy—its Relevance for Pre-eclampsia". Placenta. 20 (7): 531–539. doi:10.1053/plac.1999.0422. ISSN 0143-4004.
- ↑ Espinoza, J. (2012). "Uteroplacental ischemia in early- and late-onset pre-eclampsia: a role for the fetus?". Ultrasound in Obstetrics & Gynecology. 40 (4): 373–382. doi:10.1002/uog.12280. ISSN 0960-7692.
- ↑ Crocker, Ian P.; Cooper, Suzanne; Ong, Stephen C.; Baker, Philip N. (2003). "Differences in Apoptotic Susceptibility of Cytotrophoblasts and Syncytiotrophoblasts in Normal Pregnancy to Those Complicated with Preeclampsia and Intrauterine Growth Restriction". The American Journal of Pathology. 162 (2): 637–643. doi:10.1016/S0002-9440(10)63857-6. ISSN 0002-9440.
- ↑ Levine, Richard J.; Maynard, Sharon E.; Qian, Cong; Lim, Kee-Hak; England, Lucinda J.; Yu, Kai F.; Schisterman, Enrique F.; Thadhani, Ravi; Sachs, Benjamin P.; Epstein, Franklin H.; Sibai, Baha M.; Sukhatme, Vikas P.; Karumanchi, S. Ananth (2004). "Circulating Angiogenic Factors and the Risk of Preeclampsia". New England Journal of Medicine. 350 (7): 672–683. doi:10.1056/NEJMoa031884. ISSN 0028-4793.