Pre-eclampsia causes: Difference between revisions
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==Causes== | ==Causes== | ||
Common cause of [[preeclampsia]] include [[uteroplacental ischemia]] and [[genetic predisposition]] due to the following: | |||
* The formation of [[atheromatous plaques]] and [[fibrinoid necrosis]] of the [[vessel walls]] | |||
* [[Oxidative stress]] in [[trophoblast cells]] | |||
* [[apoptosis]] in [[trophoblast cells]] | |||
* [[Systemic inflammatory response]] | |||
* [[vasospasm]] | |||
*[[Platelet aggreggation]] | |||
* [[thrombin formation]] | |||
*[[ Deposition of the [[fibrin]] in multiple [[organs]] | |||
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In these cases, the arteries undergo a | |||
process of atherosis with very similar results to the formation | |||
of atheromatous plaques, with their lumens invaded by lipidrich | |||
macrophages, perivascular mononuclear inflammatory | |||
infiltrate, and fibrinoid necrosis of the vessel walls, with | |||
consequent uteroplacental ischemia.Then, a vicious circle of | |||
ischemia and reperfusion in the intervillous space is installed, | |||
with the metabolic stress of the endoplasmic reticulum | |||
of the trophoblast cells, which are structures responsible | |||
for cellular homeostasis and, ultimately, for the apoptosis | |||
of the same. This process releases nanomolecules into the | |||
maternal circulation, which is capable of triggering a broad | |||
intravascular inflammatory response, an essential step for the | |||
development of preeclampsia [33], as well as free radicals, | |||
in consequence of the extensive oxidative stress and the | |||
collapse of placental mechanisms and antioxidants enzymes | |||
[36]. It can be said that such a process is immunomediated, | |||
as it involves systemic inflammatory response and maternal | |||
genetic predisposition [34, 36, 37]. | |||
Theaforementioned oxidative stress, aswell as the cellular | |||
apoptosis, would be determinant for an imbalance between | |||
proangiogenic and antiangiogenic factors, with a predominance | |||
of the latter [37]. Increased concentrations of VEGFR-1 | |||
(capable of blocking the angiogenic action of VEGF) and the | |||
soluble form of this vascular endothelial growth factor, sFlt- | |||
1(fms-like tyrosine kinase 1), a potent antagonist of VEGF | |||
action, and decreased synthesis of placental growth factor | |||
(PlGF) are associated with the predominance of antiangiogenic | |||
elements characteristic of preeclampsia [37, 38]. | |||
Finally, the understanding of the pathophysiology of | |||
preeclampsia, even though it is partial, includes the activation | |||
and consequent platelet consumption at levels above those | |||
observed in normal pregnancies, vasospasm, and prostacyclin | |||
deficiency that have a vasodilatory action and inhibit | |||
platelet aggregation. Otherwise, the synthesis of thromboxane | |||
A2 is increased in placentas of women with preeclampsia, | |||
which determines the predominance of vasoconstriction and | |||
increased platelet aggregation [39], as well as thrombin, | |||
which has its maximum expression in disseminated intravascular | |||
coagulation, clinically translated to placental abruption | |||
[40]. Bigger synthesis of thrombin is part of a more vigorous | |||
inflammatory response characteristic of preeclampsia, as | |||
already exposed above, and determines the deposition of | |||
fibrin in multiple organs, which reinforces the systemic | |||
character of the pathological condition. | |||
Revision as of 15:30, 11 October 2020
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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]
Causes
Common cause of preeclampsia include uteroplacental ischemia and genetic predisposition due to the following:
- The formation of atheromatous plaques and fibrinoid necrosis of the vessel walls
- Oxidative stress in trophoblast cells
- apoptosis in trophoblast cells
- Systemic inflammatory response
- vasospasm
- Platelet aggreggation
- thrombin formation
- [[ Deposition of the fibrin in multiple organs
In these cases, the arteries undergo a
process of atherosis with very similar results to the formation
of atheromatous plaques, with their lumens invaded by lipidrich
macrophages, perivascular mononuclear inflammatory
infiltrate, and fibrinoid necrosis of the vessel walls, with
consequent uteroplacental ischemia.Then, a vicious circle of
ischemia and reperfusion in the intervillous space is installed,
with the metabolic stress of the endoplasmic reticulum
of the trophoblast cells, which are structures responsible
for cellular homeostasis and, ultimately, for the apoptosis
of the same. This process releases nanomolecules into the
maternal circulation, which is capable of triggering a broad
intravascular inflammatory response, an essential step for the
development of preeclampsia [33], as well as free radicals,
in consequence of the extensive oxidative stress and the
collapse of placental mechanisms and antioxidants enzymes
[36]. It can be said that such a process is immunomediated,
as it involves systemic inflammatory response and maternal
genetic predisposition [34, 36, 37].
Theaforementioned oxidative stress, aswell as the cellular
apoptosis, would be determinant for an imbalance between
proangiogenic and antiangiogenic factors, with a predominance
of the latter [37]. Increased concentrations of VEGFR-1
(capable of blocking the angiogenic action of VEGF) and the
soluble form of this vascular endothelial growth factor, sFlt-
1(fms-like tyrosine kinase 1), a potent antagonist of VEGF
action, and decreased synthesis of placental growth factor
(PlGF) are associated with the predominance of antiangiogenic
elements characteristic of preeclampsia [37, 38].
Finally, the understanding of the pathophysiology of
preeclampsia, even though it is partial, includes the activation
and consequent platelet consumption at levels above those
observed in normal pregnancies, vasospasm, and prostacyclin
deficiency that have a vasodilatory action and inhibit
platelet aggregation. Otherwise, the synthesis of thromboxane
A2 is increased in placentas of women with preeclampsia,
which determines the predominance of vasoconstriction and
increased platelet aggregation [39], as well as thrombin,
which has its maximum expression in disseminated intravascular
coagulation, clinically translated to placental abruption
[40]. Bigger synthesis of thrombin is part of a more vigorous
inflammatory response characteristic of preeclampsia, as
already exposed above, and determines the deposition of
fibrin in multiple organs, which reinforces the systemic
character of the pathological condition.
The pre-eclampsia syndrome is thought in some cases to be caused by a shallowly implanted placenta which becomes hypoxic, leading to upregulated inflammatory mediators secreted by the placenta and acting on the vascular endothelium. The shallow implantation is thought to stem from the maternal system's response to the placenta. But in some cases of preeclampsia, the placenta appears to have implanted normally. Possibly women with higher baseline levels of inflammation stemming from underlying conditions such as chronic hypertension may have normally implanted placentae, but less tolerance for the inflammatory burden of pregnancy.
If severe, preeclampsia progresses to fulminant pre-eclampsia, with headaches, visual disturbances, and epigastric pain, and further to HELLP syndrome andeclampsia. Placental abruption is associated with hypertensive pregnancies. These are life-threatening conditions for both the developing baby and the mother.
Many theories have attempted to explain why the pre-eclampsia syndrome arises in some pregnancies:
- Vitamin D deficiency
- Endothelial cell injury
- Rejection phenomenon
- Compromised placental perfusion
- Altered vascular reactivity
- Imbalance between prostacyclin and thromboxane
- Decreased glomerular filtration rate with retention of salt and water
- Decreased intravascular volume
- Increased central nervous system irritability
- Disseminated intravascular coagulation
- Uterine muscle stretch (ischemia)
- Dietary factors
- Genetic factors[1]
The current understanding of the disease is as a two-stage process, with a variable first stage which predisposes the placenta to hypoxia, followed by the release of soluble factors which result in many of the other observed phenomena. Many of the older theories can be subsumed under this umbrella, as the soluble factors have been shown to cause, for example, endothelial cell injury, altered vascular reactivity, the classic lesion of glomerular endotheliosis, decreased intravascular volume, etc. Underlying maternal susceptibility to the damage is likely implicated as well.
References
- ↑ Courtney Reynolds, MD, William C. Mabie, MD, & Baha M. Sibai, MD (2006). "Preeclampsia". Pregancy - Hypertensive Disorders. Armenian Medical Network. Retrieved 2006-11-23.