Abnormal placentation, angiogenic factors, and the pathogenesis of preeclampsia.
Preeclampsia is a common complication of pregnancy with potentially devastating consequences to both the mother and the baby.It is the leading cause of maternal deaths in developing countries. In developed countries it is the major cause of iatrogenic premature delivery and contributes significantly to increasing health care cost associated with prematurity. There is currently no known treatment for preeclampsia; ultimate treatment involves delivery of the placenta. Although there are several risk factors (such as multiple gestation or chronic hypertension), most patients present with no obvious risk factors. The molecular pathogenesis of preeclampsia is just now being elucidated. It has been proposed that abnormal placentation and an imbalance in angiogenic factors lead to the clinical findings and complications seen in preeclampsia. Preeclampsia is characterized by high levels of circulating antiangiogenic factors such as soluble fms-like tyrosine kinase-1 and soluble endoglin, which induce maternal endothelial dysfunction. These soluble factors are altered not only at the time of clinical disease but also several weeks before the onset of clinical signs and symptoms. Many methods of prediction and surveillance have been proposed to identify women who will develop preeclampsia, but studies have been inconclusive. With the recent discovery of the role of angiogenic factors in preeclampsia, novel methods of prediction and diagnosis are being developed to aid obstetricians and midwives in clinical practice. This article discusses the role of angiogenic factors in the pathogenesis, prediction, diagnosis, and possible treatment of preeclampsia.
Silasi
Michelle
M
Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Kirstein 3182, Boston, MA 02215, USA.
Cohen
Bruce
B
Karumanchi
S Ananth
SA
Rana
Sarosh
S
D042501:Angiogenic Proteins / Q000502:physiology; D005260:Female; D005315:Fetal Diseases / Q000209:etiology; D006801:Humans; D018919:Neovascularization, Physiologic; D010920:Placenta / Q000098:blood supply; D010922:Placenta Diseases / Q000503:physiopathology; D010929:Placentation; D011225:Pre-Eclampsia / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D011247:Pregnancy; D011505:Protein-Tyrosine Kinases; D042461:Vascular Endothelial Growth Factor A
D042501:Angiogenic Proteins; D042461:Vascular Endothelial Growth Factor A; D011505:Protein-Tyrosine Kinases