PE is defined as hypertension and proteinuria during pregnancy and is associated with major maternal, neonatal and fetal morbidity and mortality. PE is primarily caused by pathological trophoblast invasion and a consequent reduced blood flow in the intervillous region that causes placental hypoxia. These processes cause the release of sFlt-1, an indicator for endothelial dysfunction and other so called biomarkers (BH) (1). The clinical consequences are maternal hypertension; the fetal consequences can be intrauterine growth restriction due to placental insufficiency. Different reasons are discussed that are responsible for the pathological development in the early phase of pregnancy including thrombosis, vascular and endothelial inflammation, or an imbalance of angiogenic and antiangiogenic placental factors (KMP). To date, there is no reliable preventive or therapeutic treatment available. First studies that were published recently show a possible treatment approach both prophylactically and therapeutically (2), however, more clinical research is urgently needed. The aim of this proposal is to identify possible treatment strategies, to both prevent and treat the onset of preeclampsia and its complications during pregnancy.
1. Mantovani A, Sica A, Sozzani S, Allavena P, Vecchi A, Locati M. The chemokine system in diverse forms of macrophage activation and polarization. Trends Immunol. 2004;25:677–686. doi: 10.1016/j.it.2004.09.015.
2. Chelli D, Hamdi A, Saoudi S,Jenayah AA, Zagre A, Jguerim H, Bedis C, Sfar E.. Clinical Assessment of Soluble FMS-Like Tyrosine Kinase-1/Placental Growth Factor Ratio for the Diagnostic and the Prognosis of Preeclampsia in the Second Trimester. Clin Lab. 2016;62(10):1927-193. doi: 10.7754/Clin.Lab.2016.151004.