Pre-eclampsia pathophysiology: Difference between revisions
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*Studies suggest that [[Hypoxia (medical)|hypoxia]] resulting from inadequate perfusion upregulates [[sFlt-1]], a [[VEGF]] and PlGF antagonist, leading to a damaged maternal endothelium and restriction of placental growth.<!-- | *Studies suggest that [[Hypoxia (medical)|hypoxia]] resulting from inadequate perfusion upregulates [[sFlt-1]], a [[VEGF]] and PlGF antagonist, leading to a damaged maternal endothelium and restriction of placental growth.<!-- | ||
--><ref name="JClinInvest2003-Maynard">{{cite journal | author=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 | title=Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. | journal=J Clin Invest | volume=111 | issue=5 | pages=649-58 | year=2003 | id=PMID 12618519 | url=http://www.jci.org/cgi/content/full/111/5/649}}</ref> | --><ref name="JClinInvest2003-Maynard">{{cite journal | author=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 | title=Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. | journal=J Clin Invest | volume=111 | issue=5 | pages=649-58 | year=2003 | id=PMID 12618519 | url=http://www.jci.org/cgi/content/full/111/5/649}}</ref> | ||
*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. | *[[Endoglin]], a TGF-beta antagonist, is elevated in [[preeclampsia]].<ref name="PreE">{{cite journal | first = S | last = Venkatesha |coauthors = Toporsian M, Lam C, Hanai J, Mammoto T, Kim YM, Bdolah Y, Lim KH, Yuan HT, Libermann TA, Stillman IE, Roberts D, D'Amore PA, Epstein FH, Sellke FW, Romero R, Sukhatme VP, Letarte M, Karumanchi SA. | year = 2006 | month = | title = Soluble endoglin contributes to the pathogenesis of preeclampsia| journal = Nat Med | volume = 12 |issue =6 | pages = 642-9 | id = PMID 16751767 }}</ref> | ||
*Levels of both sFlt-1 and sEng increase as severity of disease | *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. | *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 | *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]] | *Initial [[maternal]] rejection of the placental cytotrophoblasts may be the cause of the inadequately remodeled [[spiral arteries]] in [[preeclampsia]] 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]].<ref name="Holzgreve2002">{{cite journal | author=Hahn S, Holzgreve W | title= Fetal cells and cell-free fetal DNA in maternal blood: new insights into pre-eclampsia |journal=Hum Reprod | volume=8 | issue=6 | pages=501-8 | year=2002 | id=PMID 12498420 }}</ref> | *[[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]].<ref name="Holzgreve2002">{{cite journal | author=Hahn S, Holzgreve W | title= Fetal cells and cell-free fetal DNA in maternal blood: new insights into pre-eclampsia |journal=Hum Reprod | volume=8 | issue=6 | pages=501-8 | year=2002 | id=PMID 12498420 }}</ref> | ||
==References== | ==References== | ||
Revision as of 14:16, 10 October 2020
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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]
- Endoglin, a TGF-beta antagonist, is elevated in 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 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.