전자간증과 기관지폐 형성 이상 = Maternal Preeclampsia and Bronchopulmonary Dysplasia

다국어 초록 (Multilingual Abstract)

Preeclampsia is one of the most common complications of pregnancy that is prevalent worldwide, resulting in substantial maternal and neonatal morbidity and mortality. Although the cause remains unclear, preeclampsia may be initiated by abnormal placentation and reduced placental perfusion, followed by an imbalance of angiogenic and antiangiogenic factors and subsequent systemic endothelial dysfunction. High level of antiangiogenic factors, such as soluble vascular endothelial growth factor (VEGF) receptor 1 (sVEGFR-1, also known as sFlt-1) and soluble endoglin, and low levels of angiogenic factors, such as free maternal VEGF and placental growth factor (PlGF), are associated with preeclampsia. Angiogenic and antiangiogenic factors also play an important role during lung angiogenesis, and an imbalance between the two types of factors triggered by inflammation disrupts angiogenesis in bronchopulmonary dysplasia (BPD). Because preeclampsia represents an antiangiogenic state, preterm infants born to mothers with preeclampsia would be at increased risk of developing BPD due to impaired lung development. Recently, preeclampsia has been shown to be independently associated with a high risk for BPD. I have reviewed recent progress in research concerning the correlation between preeclampsia and BPD in aspect of pathophysiology and epidemiology.