Pre-eclampsia pathophysiology: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
|||
| Line 24: | Line 24: | ||
*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> In addition, [[endoglin]], a TGF-beta antagonist, is elevated in pregnant women who develop 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> | |||
*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. | |||
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.<!-- | *Both sFlt-1 and sEng are upregulated in all pregnant women to some extent | ||
--><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> In addition, [[endoglin]], a TGF-beta antagonist, is elevated in pregnant women who develop 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> | *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]].<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> | |||
Both sFlt-1 and sEng are upregulated in all pregnant women to some extent | |||
==References== | ==References== | ||
Revision as of 14:12, 10 October 2020
| https://https://www.youtube.com/watch?v=RB5s85xDshA%7C350}} |
|
Pre-eclampsia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Pre-eclampsia pathophysiology On the Web |
|
American Roentgen Ray Society Images of Pre-eclampsia pathophysiology |
|
Risk calculators and risk factors for Pre-eclampsia pathophysiology |
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.