University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Obstet Gynecol Surv. 2011 Aug;66(8):497-506. doi: 10.1097/OGX.0b013e3182331028.
Preeclampsia is a leading cause of pregnancy-related morbidity and mortality in the United States. In the past 30 years, a large amount of research has been performed to investigate the pathogenesis and pathophysiology of preeclampsia, ways to treat preeclampsia, markers that can be used to predict preeclampsia, and associations with other factors, such as smoking, stroke, and cardiovascular disease. Preeclampsia has been characterized by some investigators into 2 different disease entities: early-onset preeclampsia and late-onset preeclampsia. Early-onset preeclampsia is usually defined as preeclampsia that develops before 34 weeks of gestation, whereas late-onset preeclampsia develops at or after 34 weeks of gestation. Although the presenting features overlap, they are associated with different maternal and fetal outcomes, biochemical markers, heritability, and clinical features. To date, no review has analyzed the data focusing on early- versus late-onset preeclampsia. This review summarizes the relevant research on the similarities and differences between early- and late-onset preeclampsia as it relates to pathogenesis and biomarkers, including differences in vascular endothelial growth factor, placental growth factor, vascular endothelial growth factor receptor-1, epidermal growth factor, transforming growth factor-β, vascular cell adhesion molecule, toll-like receptor, plasma pentraxin 3, soluble endoglin, and lipid peroxidation. Although many articles have been published regarding these 2 entities, more data regarding differences and similarities between the 2 are clearly needed. Such study should permit more effective diagnosis, treatment, and management of patients with preeclampsia.
Obstetricians & Gynecologists and Family Physicians Learning Objectives: After the completing the CME activity, physicians should be better able to evaluate the role of abnormal placentation in preeclampsia. Develop a protocol for researching biomarkers relevant to early-onset and late-onset preeclampsia. To distinguish the biomarkers that are similar and different in early-onset and late-onset preeclampsia.
子痫前期是美国妊娠相关发病率和死亡率的主要原因。在过去的 30 年中，已经进行了大量的研究来探讨子痫前期的发病机制和病理生理学、子痫前期的治疗方法、可用于预测子痫前期的标志物，以及与其他因素（如吸烟、中风和心血管疾病）的关联。一些研究人员将子痫前期分为两种不同的疾病实体：早发型子痫前期和晚发型子痫前期。早发型子痫前期通常定义为在妊娠 34 周前发生的子痫前期，而晚发型子痫前期则在妊娠 34 周或之后发生。尽管临床表现重叠，但它们与不同的母婴结局、生化标志物、遗传性和临床特征相关。迄今为止，尚无综述分析专门针对早发型与晚发型子痫前期的相关数据。本文综述了早发型和晚发型子痫前期在发病机制和生物标志物方面的相似和不同之处，包括血管内皮生长因子、胎盘生长因子、血管内皮生长因子受体-1、表皮生长因子、转化生长因子-β、血管细胞黏附分子、Toll 样受体、血浆 pentraxin 3、可溶性内皮素、脂质过氧化等方面的差异。尽管已经发表了许多关于这两种疾病的文章，但显然需要更多关于这两种疾病之间差异和相似之处的数据。此类研究应能更好地诊断、治疗和管理子痫前期患者。
妇产科医生和家庭医生学习目标：完成 CME 活动后，医生应能更好地评估异常胎盘在子痫前期中的作用。制定研究与早发型和晚发型子痫前期相关的生物标志物的方案。区分早发型和晚发型子痫前期中相似和不同的生物标志物。
