Menon Ramkumar, Fortunato Stephen J
Perinatal Research Center of the Women's Health Research and Education Foundation, Centennial Medical Center, 2300 Patterson Street, Nashville, TN, USA.
Best Pract Res Clin Obstet Gynaecol. 2007 Jun;21(3):467-78. doi: 10.1016/j.bpobgyn.2007.01.008. Epub 2007 Apr 19.
Spontaneous preterm birth, caused by preterm labor (contractions before 37 weeks' gestation) or preterm premature rupture of the membranes (pPROM) (membrane rupture before the onset of labor) or both account for approximately 80% of preterm deliveries. pPROM is associated with 30-40% of preterm deliveries and the incidence of pPROM has increased in the past decade. The question we address here is why some women experience pPROM and some experience preterm labor with no rupture of membranes (ROM) when the etiologic factors associated with both these pathologic complications are the same. To date, studies had evaluated the markers that are commonly elevated in both preterm labor and pPROM. A better understanding of the similarities and differences between the biomolecular pathways leading to each of these conditions may open new avenues for research and intervention. In this chapter we review the role of inflammatory mediators (cytokines and matrix metalloproteinases), and programmed cell death (apoptosis) in preterm labor with no ROM and preterm labor with pPROM to delineate the differences in pathways between the two conditions.
自发性早产由早产(妊娠37周前出现宫缩)或胎膜早破(临产前胎膜破裂)或两者共同导致,约占早产分娩的80%。胎膜早破与30% - 40%的早产分娩相关,且在过去十年中胎膜早破的发生率有所上升。我们在此探讨的问题是,当与这两种病理并发症相关的病因相同时,为什么有些女性会发生胎膜早破,而有些女性会出现未破膜的早产宫缩。迄今为止,已有研究评估了在早产宫缩和胎膜早破中通常都会升高的标志物。更好地理解导致这两种情况的生物分子途径之间的异同,可能会为研究和干预开辟新途径。在本章中,我们回顾炎症介质(细胞因子和基质金属蛋白酶)以及程序性细胞死亡(凋亡)在未破膜早产宫缩和胎膜早破早产宫缩中的作用,以阐明这两种情况之间途径的差异。