Pre-eclampsia pathophysiology: Difference between revisions
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{{Pre-eclampsia}} | {{Pre-eclampsia}} | ||
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==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 20:47, 20 February 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2]
Pathophysiology
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 theendothelium (lining of blood vessels), alterations in metabolism, and inflammation.
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.[1] In addition, endoglin, a TGF-beta antagonist, is elevated in pregnant women who develop preeclampsia.[2] 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.
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.)
It has been documented that fetal cells such as fetal erythroblasts 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.[3]
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
References
- ↑ 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.