Pre-eclampsia causes
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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
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 J Clinical Endorcinol Metabolism Sept 2007 92(9) 3517-22
- 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.