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Published on: August 2, 2017
Markedly Elevated sFlt-1/PlGF Ratios in Atypical Superimposed Preeclampsia Before 20 Weeks of Gestation: A Three-Case
Chisa Ito1, Manabu Ogoyama1, Akihide Ohkuchi1
1Department of Obstetrics and Gynecology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Atypical superimposed preeclampsia (sPE) developing before 20 weeks of gestation is extremely rare, and its pathophysiology remains unclear. We herein report three women with underlying chronic hypertension or IgA nephropathy who developed severe hypertension, worsening proteinuria, and fetal growth restriction or fetal death before 20 weeks of gestation. All cases showed markedly elevated soluble fms-like tyrosine kinase-1/placental growth factor (sFlt-1/PlGF) ratios (617-1357), and placental pathology demonstrated maternal vascular malperfusion. Maternal clinical manifestations promptly improved after the termination of pregnancy. All three women subsequently achieved successful pregnancies with appropriate management. These results suggest that atypical sPE shares the angiogenic imbalance and placental pathology characteristic of conventional preeclampsia. Although limited by the small number of cases, these results provide additional insights into the pathophysiology of atypical sPE and suggest a role for angiogenic biomarkers in evaluating placental dysfunction.
Atypical superimposed preeclampsia (sPE) developing before 20 weeks of gestation is extremely rare, and its pathophysiology remains unclear. We herein report three women with underlying chronic hypertension or IgA nephropathy who developed severe hypertension, worsening proteinuria, and fetal growth restriction or fetal death before 20 weeks of gestation. All cases showed markedly elevated soluble fms-like tyrosine kinase-1/placental growth factor (sFlt-1/PlGF) ratios (617-1357), and placental pathology demonstrated maternal vascular malperfusion. Maternal clinical manifestations promptly improved after the termination of pregnancy. All three women subsequently achieved successful pregnancies with appropriate management. These results suggest that atypical sPE shares the angiogenic imbalance and placental pathology characteristic of conventional preeclampsia. Although limited by the small number of cases, these results provide additional insights into the pathophysiology of atypical sPE and suggest a role for angiogenic biomarkers in evaluating placental dysfunction.
