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==Pathophysiology==
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Although much research into the [[etiology]] and mechanism of pre-eclampsia has taken place, its exact pathogenesis remains uncertain. Most studies support the notion of inadequate blood supply to the placenta making it release particular hormones or chemical agents that, in mothers predisposed to the condition, leads to damage of the[[endothelium]] (lining of blood vessels), alterations in [[metabolism]], and [[inflammation]].<ref name=DrifeMagowan/>
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{{Pre-eclampsia}}
{{CMG}}; {{AE}} {{Sara.Zand}} {{Ochuko}}


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.<!--
==Overview==
  --><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, although there is also the potential that sEng is produced by the maternal endothelium.  Levels of both sFlt-1 and sEng increase as severity of disease increases, with levels of sEng surpassing levels of sFlt-1 in [[HELLP syndrome]] cases.
[[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]].


Both sFlt-1 and sEng are upregulated in all pregnant women to some extent, supporting the idea that hypertensive disease in pregnancy is a normal pregnancy adaptation gone awry. As natural killer cells are intimately involved in placentation and as placentation involves a degree of maternal tolerance for a foreign placenta which requires maternal resources for its support, it is not surprising that the maternal immune system might respond more negatively to the arrival of placentae under certain circumstances, such as a placenta which is more invasive than normal. Initial maternal rejection of the placental cytotrophoblasts may be the cause of the inadequately remodeled spiral arteries in those cases of preeclampsia associated with shallow implantation, leading to downstream hypoxia and the appearance of maternal symptoms in response to upregulated sFlt-1 and sEng. (See [[parent-offspring conflict]].)
==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>
It has been documented that fetal cells such as fetal [[erythroblast]]s as well as cell-free fetal [[DNA]] are increased in the maternal circulation in women who develop preeclampsia. These findings have given rise to the hypothesis that preeclampsia is a disease process by which a 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.<!--
:* 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>
  --><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>
:* [[Genetic susceptibility]]
:* [[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>


Pre-eclampsia may develop at varying times within pregnancy and its progress differs among patients; most cases are diagnosed pre-term. It has no known cure apart from ending the pregnancy (induction of labor or abortion). It may also occur up to six weeks post-partum. Of dangerous pregnancy complications, it is the most common; it may affect both the mother and the fetus.<ref name=DrifeMagowan
:* 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 [[prostacycline]] and [[ thromboxan-A2]]


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
[[Category:Disease]]
[[Category:Obstetrics]]
[[Category:Pregnancy]]
[[Category:Emergency medicine]]
[[Category:Cardiology]]
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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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