Park J S, Park C W, Lockwood C J, Norwitz E R
Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Korea.
Minerva Ginecol. 2005 Aug;57(4):349-66.
Preterm birth (defined as delivery prior to 37 weeks' gestation) complicates 5-10% of all births. It is a major cause of perinatal mortality and morbidity. Approximately 20% of all preterm births are iatrogenic resulting from obstetric intervention for maternal and/or fetal indications. Of the remainder, 2/3 are spontaneous preterm labor with or without preterm premature rupture of the membranes (pPROM). Preterm labor is a syndrome rather than a diagnosis since the etiologies are varied. Risk factors include, among others, pPROM, cervical insufficiency, pathologic uterine distention (polyhydramnios, multiple gestation), uterine anomalies, intrauterine infection/inflammation, and social factors (stress, smoking, heavy work). The final common pathway appears to be activation of the inflammatory cascade. Bacterial colonization and/or inflammation of the choriodecidual interface induces production of pro-inflammatory cytokines that, in turn, lead to neutrophil activation and the synthesis and release of uterotonins such as prostaglandins (which cause uterine contractions) and metalloproteinases (that weaken fetal membranes and remodel cervical collagen). This monograph reviews the role of cytokines in the pathophysiology of preterm labor and delivery.
早产（定义为妊娠37周前分娩）在所有分娩中占比5%-10%，是围产期死亡和发病的主要原因。所有早产中约20%是医源性的，由针对母体和/或胎儿指征的产科干预导致。其余的早产中，2/3是自发性早产，伴有或不伴有胎膜早破（pPROM）。早产是一种综合征而非诊断，因为其病因多种多样。风险因素包括pPROM、宫颈机能不全、病理性子宫扩张（羊水过多、多胎妊娠）、子宫异常、宫内感染/炎症以及社会因素（压力、吸烟、繁重工作）等。最终的共同途径似乎是炎症级联反应的激活。绒毛膜蜕膜界面的细菌定植和/或炎症会诱导促炎细胞因子的产生，进而导致中性粒细胞激活以及子宫收缩素如前列腺素（引起子宫收缩）和金属蛋白酶（削弱胎膜并重塑宫颈胶原蛋白）的合成与释放。本专著综述了细胞因子在早产和分娩病理生理学中的作用。
