Pre-eclampsia pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
[[Preeclampsia]] may be the result of placental factors in maternal circulation leading to [[endothelial dysfunction]] | [[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== | ||
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:* 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 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> | :* 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> | ||
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
- The pathogenesis of preeclampsia is characterized by the following :[1][2]
- Chronic uteroplacental ischemia[3]
- Genetic susceptibility
- Very-low-density lipoprotein toxicity
- Increased trophoblast apoptosis or necrosis[4]
- Increased Maternal inflammatory response to fetal trophoblast
- Imbalance of angiogenic factors [5]
- Imbalance of prostacycline and thromboxan-A2
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.
- ↑ 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.
- ↑ 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.