Pre-eclampsia pathophysiology
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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 ofpreeclampsia is characterized by the following :[1]
- Chronic uteroplacental ischemia[2]
- Genetic imprinting
- very-low-density lipoprotein toxicity
- Increased trophoblast apoptosis or necrosis[3]
- Increased Maternal inflammatory response to fetal trophoblast
- Imbalance of angiogenic factors [4]
- Studies suggest that hypoxia resulting from inadequate perfusion upregulates sFlt-1, a VEGF and PlGF antagonist, leading to a damaged maternal endothelium and restriction of placental growth.[5] In addition, endoglin, a TGF-beta antagonist, is elevated in pregnant women who develop preeclampsia.[6]
- Soluble endoglin is likely upregulated by the placenta in response to an upregulation of cell-surface endoglin produced by the maternal immune system, a *sEng is produced by the maternal endothelium.
- Levels of both sFlt-1 and sEng increase as severity of disease
- Increased levels of sEng surpassing levels of sFlt-1 in HELLP syndrome cases.
- Both sFlt-1 and sEng are upregulated in all pregnant women to some extent
- Initial maternal rejection of the placental cytotrophoblasts may be the cause of the inadequately remodeled spiral arteries in preeclampsia associated with shallow implantation, leading to hypoxia and upregulated sFlt-1 and sEng.
- Placental lesion such as hypoxia allows increased fetal material into maternal circulation that leads to an inflammatory response and endothelial damage ultimately resulting in preeclampsia and eclampsia.[7]
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.
- ↑ Maynard S, Min J, Merchan J, Lim K, Li J, Mondal S, Libermann T, Morgan J, Sellke F, Stillman I, Epstein F, Sukhatme V, Karumanchi S (2003). "Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia". J Clin Invest. 111 (5): 649–58. PMID 12618519.
- ↑ Venkatesha, S (2006). "Soluble endoglin contributes to the pathogenesis of preeclampsia". Nat Med. 12 (6): 642–9. PMID 16751767. Unknown parameter
|coauthors=ignored (help) - ↑ Hahn S, Holzgreve W (2002). "Fetal cells and cell-free fetal DNA in maternal blood: new insights into pre-eclampsia". Hum Reprod. 8 (6): 501–8. PMID 12498420.