Pre-eclampsia pathophysiology: Difference between revisions

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{{Pre-eclampsia}}
{{Pre-eclampsia}}
{{CMG}}; {{AE}} {{Sara.Zand}} {{Ochuko}}
{{CMG}}; {{AE}} {{Sara.Zand}} {{Ochuko}}
==Overview==
[[Preeclampsia]] may be the result of placental factors in maternal circulation leading to [[endothelial dysfunction]], [[hypertension]], and [[proteinuria]]. Increased levels of  an [[angiogenic factor]] named fms-like [[tyrosine kinase]] 1 in the [[placenta]] is correlated  with [[endothelial dysfunction]]. In [[villous trophoblast]] of [[preeclamptic]] women, [[apoptosis]] was considered. Following [[uteroplacental ischemia]], and invasion [[spiral arteries]] by [[trophoblasts]], releasing some [[angiogenic factors]] causes other organ involvement. Incomplete penetration in recessive or dominant genes was noticed in [[pathogenesis]] of [[preeclampsia]].


==Pathophysiology==
==Pathophysiology==
 
* The pathogenesis of [[preeclampsia]] is characterized by the following :<ref name="JohansenRedman1999">{{cite journal|last1=Johansen|first1=M|last2=Redman|first2=C.W.G|last3=Wilkins|first3=T|last4=Sargent|first4=I.L|title=Trophoblast Deportation in Human Pregnancy—its Relevance for Pre-eclampsia|journal=Placenta|volume=20|issue=7|year=1999|pages=531–539|issn=01434004|doi=10.1053/plac.1999.0422}}</ref><ref name="DekkerSibai1998">{{cite journal|last1=Dekker|first1=Gustaaf A.|last2=Sibai|first2=Baha M.|title=Etiology and pathogenesis of preeclampsia: Current concepts|journal=American Journal of Obstetrics and Gynecology|volume=179|issue=5|year=1998|pages=1359–1375|issn=00029378|doi=10.1016/S0002-9378(98)70160-7}}</ref>
 
* The pathogenesis of[[preeclampsia]] is characterized by the following :<ref name="JohansenRedman1999">{{cite journal|last1=Johansen|first1=M|last2=Redman|first2=C.W.G|last3=Wilkins|first3=T|last4=Sargent|first4=I.L|title=Trophoblast Deportation in Human Pregnancy—its Relevance for Pre-eclampsia|journal=Placenta|volume=20|issue=7|year=1999|pages=531–539|issn=01434004|doi=10.1053/plac.1999.0422}}</ref>
 
:* Chronic [[uteroplacental ischemia]]<ref name="Espinoza2012">{{cite journal|last1=Espinoza|first1=J.|title=Uteroplacental ischemia in early- and late-onset pre-eclampsia: a role for the fetus?|journal=Ultrasound in Obstetrics & Gynecology|volume=40|issue=4|year=2012|pages=373–382|issn=09607692|doi=10.1002/uog.12280}}</ref>
:* Chronic [[uteroplacental ischemia]]<ref name="Espinoza2012">{{cite journal|last1=Espinoza|first1=J.|title=Uteroplacental ischemia in early- and late-onset pre-eclampsia: a role for the fetus?|journal=Ultrasound in Obstetrics & Gynecology|volume=40|issue=4|year=2012|pages=373–382|issn=09607692|doi=10.1002/uog.12280}}</ref>
 
:* [[Genetic susceptibility]]
:* [[Genetic imprinting]]
:* [[Very-low-density lipoprotein toxicity]]
:* [[very-low-density lipoprotein toxicity]]
:* Increased trophoblast apoptosis or necrosis<ref name="CrockerCooper2003">{{cite journal|last1=Crocker|first1=Ian P.|last2=Cooper|first2=Suzanne|last3=Ong|first3=Stephen C.|last4=Baker|first4=Philip N.|title=Differences in Apoptotic Susceptibility of Cytotrophoblasts and Syncytiotrophoblasts in Normal Pregnancy to Those Complicated with Preeclampsia and Intrauterine Growth Restriction|journal=The American Journal of Pathology|volume=162|issue=2|year=2003|pages=637–643|issn=00029440|doi=10.1016/S0002-9440(10)63857-6}}</ref>
:* Increased trophoblast apoptosis or necrosis<ref name="CrockerCooper2003">{{cite journal|last1=Crocker|first1=Ian P.|last2=Cooper|first2=Suzanne|last3=Ong|first3=Stephen C.|last4=Baker|first4=Philip N.|title=Differences in Apoptotic Susceptibility of Cytotrophoblasts and Syncytiotrophoblasts in Normal Pregnancy to Those Complicated with Preeclampsia and Intrauterine Growth Restriction|journal=The American Journal of Pathology|volume=162|issue=2|year=2003|pages=637–643|issn=00029440|doi=10.1016/S0002-9440(10)63857-6}}</ref>


:* 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]]
 
*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>
*[[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>
*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]].<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==
{{Reflist|2}}
{{Reflist|2}}


[[Category:Disease]]
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[[Category:Emergency medicine]]
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[[Category:Cardiology]]
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Latest revision as of 14:36, 30 September 2021

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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]

Overview

Preeclampsia may be the result of placental factors in maternal circulation leading to endothelial dysfunction, hypertension, and proteinuria. Increased levels of an angiogenic factor named fms-like tyrosine kinase 1 in the placenta is correlated with endothelial dysfunction. In villous trophoblast of preeclamptic women, apoptosis was considered. Following uteroplacental ischemia, and invasion spiral arteries by trophoblasts, releasing some angiogenic factors causes other organ involvement. Incomplete penetration in recessive or dominant genes was noticed in pathogenesis of preeclampsia.

Pathophysiology

References

  1. ↑ 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.
  2. ↑ Dekker, Gustaaf A.; Sibai, Baha M. (1998). "Etiology and pathogenesis of preeclampsia: Current concepts". American Journal of Obstetrics and Gynecology. 179 (5): 1359–1375. doi:10.1016/S0002-9378(98)70160-7. ISSN 0002-9378.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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.
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