Abstract

The cause of pre-eclampsia is unknown. Different postulates have been developed to explain its pathogenesis. The two-stage theory and angiogenic imbalance are two notable postulates of the disease. Together, they propose that there is a lack of cytotrophoblastic invasion of the uterine spiral arteries in pre-eclampsia. The lumen of these arteries remains narrow instead of converting to the wide channels seen in normal pregnancy, and result in poor placental perfusion. Coupled with maternal susceptibility, this process leads to the release of mediators, including an excess of anti-angiogenic factors that result in the clinical manifestations of the disease. Circulating levels of anti-angiogenic factors such as soluble fms-like tyrosine kinase-1 increase, whereas pro-angiogenic factors such as placental growth factor decrease. Assessment of the circulating concentrations of these angiogenic factors, such as the soluble fms-like tyrosine kinase-1/placental growth factor ratio, has diverse clinical relevance in pre-eclampsia. The present review describes the role of angiogenic factors in the pathogenesis and management of pre-eclampsia.

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