The International Federation of Gynecology and Obstetrics (FIGO) initiative on pre-eclampsia: A pragmatic guide for first-trimester screening and prevention
The International Federation of Gynecology and Obstetrics (FIGO) initiative on pre-eclampsia: A pragmatic guide for first-trimester screening and prevention
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DOI：
10.1002/ijgo.12802
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发表时间：
2019-05-01
影响因子：
3.8
通讯作者：
Hod, Moshe
中科院分区：
文献类型：
--
作者：
Poon, Liona C.;Shennan, Andrew;Hod, Moshe
先兆子痫（PE）是一种多系统疾病，通常影响2%-5%的孕妇，是孕产妇和围产期发病率和死亡率的主要原因之一，特别是当病情早期发作时。全球每年有76 000名妇女和500 000名婴儿死于这种疾病。此外，与高资源国家的妇女相比，低资源国家的妇女患PE的风险更高。虽然对PE的发病机制的完整理解仍不清楚，但目前的理论认为PE的发病过程分为两个阶段。第一阶段是由滋养层的浅侵入导致螺旋动脉重塑不足引起的。这被推测为导致第二阶段，其涉及母体对内皮功能障碍的反应以及血管生成和抗血管生成因子之间的失衡，从而导致该疾病的临床特征。我们仍然无法作出准确的预测和统一的预防。寻求有效地预测在怀孕的前三个月PE是由希望识别谁是在发展PE的高风险的妇女，以便可以尽早启动必要的措施，以改善胎盘，从而防止或至少减少其发生的频率。此外，确定一个“风险”群体将允许有针对性的产前监测，以预测和识别临床综合征的发作，并及时加以管理。PE以前被定义为妊娠20周后高血压发作伴明显蛋白尿。最近，PE的定义已经扩大。目前国际上公认的PE定义是国际妊娠高血压研究学会（ISSHP）提出的定义。根据ISSHP，PE定义为在先前血压正常的女性中至少两次测量的收缩压≥140 mmHg和/或舒张压≥90 mmHg，间隔4小时，并伴有≥1种以下新发疾病：妊娠20周或之后的蛋白尿（即，≥30 mg/mol蛋白质：肌酐比值; ≥300 mg/24 hr;或≥2+试纸）;其他母体器官功能障碍的证据，包括：急性肾损伤（肌酐≥ 90 umol/L; 1 mg/dL）、肝脏受累（转氨酶升高，例如，丙氨酸氨基转移酶或天冬氨酸氨基转移酶>40 IU/L）伴或不伴右上腹或上腹部疼痛，神经系统并发症（例如，子痫、精神状态改变、失明、中风、阵挛、严重头痛和持续性视觉暗点），或血液学并发症（血小板减少-血小板计数<150 000/μL、弥散性血管内凝血、溶血）;或子宫胎盘功能障碍（如胎儿生长受限、异常脐动脉多普勒波形分析或死胎）。众所周知，一系列母体风险因素与PE的发生相关：高龄产妇、未产、既往PE史、妊娠间隔时间短和长、使用辅助生殖技术、PE家族史、肥胖、非洲-加勒比和南亚人种、合并症（包括妊娠期高血糖症）、既存慢性高血压、肾脏疾病，自身免疫性疾病，如系统性红斑狼疮和抗磷脂综合征。这些风险因素已被描述的各种专业组织的妇女在PE的风险识别，然而，这种方法来筛选是不足以有效预测PE。PE可细分为：早发性PE（妊娠<34+0周时分娩）;早产PE（妊娠<34+0周时分娩）。
Preeclampsia (PE) is a multisystem disorder that typically affects 2%−5% of pregnant women and is one of the leading causes of maternal and perinatal morbidity and mortality, especially when the condition is of early onset. Globally, 76,000 women and 500,000 babies die each year from this disorder. Furthermore, women in low-resource countries are at a higher risk of developing PE compared to those in high-resource countries. Although a complete understanding of the pathogenesis of PE remains unclear, the current theory suggests a 2-stage process. The first stage is caused by shallow invasion of the trophoblast resulting in inadequate remodelling of the spiral arteries. This is presumed to lead to the second stage, which involves the maternal response to endothelial dysfunction and imbalance between angiogenic and anti-angiogenic factors, resulting in the clinical features of the disorder. Accurate prediction and uniform prevention continue to elude us. The quest to effectively predict PE in the first trimester of pregnancy is fuelled by the desire to identify women who are at high risk of developing PE, so that necessary measures can be initiated early enough to improve placentation and thus prevent or at least reduce the frequency of its occurrence. Also, identification of an ‘at risk’ group will allow tailored antenatal surveillance to anticipate and recognize the onset of the clinical syndrome and manage it promptly. PE has been previously defined as the onset of hypertension accompanied by significant proteinuria after 20 weeks’ gestation. Recently, the definition of PE has been broadened. Now the internationally agreed definition of PE is the one proposed by the International Society for the Study of Hypertension in Pregnancy (ISSHP). According to the ISSHP, PE is defined as systolic blood pressure at ≥140 mmHg and/or the diastolic blood pressure at ≥90 mmHg on at least two occasions measured four hours apart in previously normotensive women and is accompanied by ≥1 of the following new-onset conditions at or after 20 weeks’ gestation: proteinuria (i.e., ≥30 mg/mol protein:creatinine ratio; ≥300 mg/24hr; or ≥2+ dipstick); evidence of other maternal organ dysfunction, including: acute kidney injury (creatinine ≥90umol/L; 1 mg/dL), liver involvement (elevated transaminases, e.g., alanine aminotransferase or aspartate aminotransferase >40 IU/L) with or without right upper quadrant or epigastric abdominal pain, neurological complications (e.g., eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, and persistent visual scotomata), or hematological complications (thrombocytopenia–platelet count <150 000/μL, disseminated intravascular coagulation, hemolysis); or uteroplacental dysfunction (such as fetal growth restriction, abnormal umbilical artery Doppler wave form analysis, or stillbirth). It is well established that a series of maternal risk factors are associated with the development of PE: advanced maternal age, nulliparity, previous history of PE, short and long inter-pregnancy intervals, use assisted reproductive technologies, family history of PE, obesity, Afro-Caribbean and South Asian racial origin, co-morbid medical conditions including hyperglycemia in pregnancy, pre-existing chronic hypertension, renal disease, autoimmune diseases, such as systemic lupus erythematosus and anti-phospholipid syndrome. These risk factors have been described by various professional organisations for the identification of women at risk of PE, however, this approach to screening is inadequate for effective prediction of PE. PE can be sub-classified into: Early-onset PE (with delivery at <34+0 week’s gestation); Preterm PE (with …