In most cases preeclampsia manifests mid-term or later, but according to contemporary theories the disease has two stages: abnormal placentation and maternal reaction to it.
3.1. Normal and abnormal placentation
During normal development of placenta fetal cytotrophoblasts invade maternal spiral arteries. Consequently, these small-caliber resistance vessels transform to high-caliber capacitance vessels. They lose their endothelial lining and muscoloelastic tissue. These changes in architecture allow them to contain increased blood flow. In preeclampsia cytotrophoblasts invasion is shallow. They remain at distance from the arteries, and even if they invade some, they don’t produce sufficient transformation. Thus, placental blood flow increases …show more content…
Most researchers agree that endothelial dysfunction and oxidative stress are key components of systemic reaction and development of clinical symptoms. Endothelial dysfunction occurs due to imbalance of numerous circulating factors. Among these are fibronectin, endothelin, thrombomodulin, endoglin and others[20–24]. Recent studies also indicate, that women with preeclampsia have elevated levels of sFlt-1 (soluble fms like tyrosine kinase-1). This molecule is a protein derived from a splice variant of the vascular endothelial growth factor (VEGF) receptor Flt-1 mRNA. It lacks the transmembrane and cytoplasmic domain of the membrane-bound receptor[25,26]. Placenta secretes sFlt-1 and releases it into maternal bloodstream where it can disrupt endothelial function, provoking hypertension, proteinuria and other systemic manifestations of preeclampsia. It is not clear, what induces the release of sFlt-1, however according to Kulkarni et al. low levels of DHA may be one of the reasons. Authors compared levels of LCPUFA and sFlt-1 in 69 women with preeclampsia and 40 normotensive controls. Pre-eclamptic women had significantly lower levels of placental DHA and omega-3/omega-6 ratios. They also had higher plasma levels of sFlt-1, which were negatively associated with DHA
3.1. Normal and abnormal placentation
During normal development of placenta fetal cytotrophoblasts invade maternal spiral arteries. Consequently, these small-caliber resistance vessels transform to high-caliber capacitance vessels. They lose their endothelial lining and muscoloelastic tissue. These changes in architecture allow them to contain increased blood flow. In preeclampsia cytotrophoblasts invasion is shallow. They remain at distance from the arteries, and even if they invade some, they don’t produce sufficient transformation. Thus, placental blood flow increases …show more content…
Most researchers agree that endothelial dysfunction and oxidative stress are key components of systemic reaction and development of clinical symptoms. Endothelial dysfunction occurs due to imbalance of numerous circulating factors. Among these are fibronectin, endothelin, thrombomodulin, endoglin and others[20–24]. Recent studies also indicate, that women with preeclampsia have elevated levels of sFlt-1 (soluble fms like tyrosine kinase-1). This molecule is a protein derived from a splice variant of the vascular endothelial growth factor (VEGF) receptor Flt-1 mRNA. It lacks the transmembrane and cytoplasmic domain of the membrane-bound receptor[25,26]. Placenta secretes sFlt-1 and releases it into maternal bloodstream where it can disrupt endothelial function, provoking hypertension, proteinuria and other systemic manifestations of preeclampsia. It is not clear, what induces the release of sFlt-1, however according to Kulkarni et al. low levels of DHA may be one of the reasons. Authors compared levels of LCPUFA and sFlt-1 in 69 women with preeclampsia and 40 normotensive controls. Pre-eclamptic women had significantly lower levels of placental DHA and omega-3/omega-6 ratios. They also had higher plasma levels of sFlt-1, which were negatively associated with DHA