细胞应激和危险相关分子模式在未足月胎膜早破的研究进展

未足月胎膜早破(PPROM)易导致母儿感染,诱发自发性早产。 PPROM 发生机制尚不明确, 胎膜细胞的无菌性或细菌性炎症反应导致局部胎膜薄弱、发生破裂是其组织病理学特征。 胎膜细胞应 激引起机体产生具有免疫调节作用的危险相关分子模式(DAMPs),引起炎症免疫应答,在 PPROM 中发 挥重要作用。 在感染、细胞拉伸等作用下,高迁移率族蛋白 B1(HMGB1)、热休克蛋白 70(HSP70)、S100 蛋白、细胞外基质(ECM)分解产物等 DAMPs 分子,激发免疫反应、弱化胎膜结构。 本文对近年来细胞 应激和 DAMPs 在 PPROM 的发生机制进行综述,为 PPROM 的研究提供新思路。     

重视未足月胎膜早破的研究

未足月胎膜早破（preterm premature rupture of the membranes,PPROM）是指妊娠37周内胎膜在临产前发生自发性破裂。孕妇中的PPROM发生率约为3％;30％～40％的早产与PPROM有关,其中25％出现在妊娠26周前。长期以来,PPROM的处理是产科临床中较为棘手的问题,若处理不当,可能并发羊膜腔感染、胎盘早剥、羊水过少、早产、胎儿窘迫和新生儿呼吸窘迫综合征（NRDS）等,     

早产孕妇的阴道代谢组学研究及展望

<正>早产是指妊娠不足37周分娩者，是目前导致新生儿死亡的主要原因，同时会显著增加患儿成年后发生慢性疾病的风险[1],如高血压、1型或2型糖尿病和慢性肾脏疾病等。早产按病因可分为自发性早产和治疗性早产，其中自发性早产约占70%～80%,包括胎膜完整早产和未足月胎膜早破早产(PPROM),胎膜完整的自发性早产是最常见的早产类型。目前关于早产的确切病因尚未明确，其中50%可能与环境、心理、遗传、内分泌等多种因素有关，其余仍可能为特发性，     

未足月胎膜早破对母儿的影响

胎膜在临产前自然破裂称为胎膜早破（premature rupture of membrane，PROM），而妊娠未满37周时胎膜在临产前自然破裂则为未足月胎膜早破（preterm premature rupture of membrane．PPROM）。在所有妊娠中PPROM发生率为1％～2％，早产合并PPROM占30％。PPROM孕妇中只有7．7％～9．7％的胎膜破口能够自然愈合，而持续阴道流液的孕妇60％在7天内启动分娩。     

未足月胎膜早破的封闭疗法

1PPROM概况 未足月胎膜早破（preterm premature rupture of the membranes，PPROM）是指妊娠未满37周胎膜在临产前发生破裂。在所有妊娠中PPROM发生率为2％～3％，早产30％～40％由PPROM引发，PPROM孕妇中只有7．7％～9．7％的胎膜破损能够自然闭合，而60％～80％的孕妇在胎膜破裂7d内分娩，其中位潜伏期为6．6d。     

基质金属蛋白酶降解胞外基质致未足月胎膜早破研究进展

早产是威胁围生儿生命健康的首要病因。据统计,2012年中国早产发生率为8.1%。未足月胎膜早破(preterm premature rupture of membranes,PPROM)占早产的25%~30%,重要诱因为宫内感染。近年研究发现,PPROM的分子机制为胎膜组织中胞外基质过早降解,主要由基质金属蛋白酶(matrix metalloproteinases,MMPs)在胎膜组织中的激活引起。MMPs的激活原因有炎症因子的表达增高,如白细胞介素1(IL-1),IL-6以及肿瘤坏死因子α(TNF-α),但具体机制尚有待研究。MMPs在正常分娩与PPROM发生过程中的激活、分泌及其影响因素仍需探索,其可能作为预测妊娠结局的标记物,为PPROM的预防与治疗提供突破点。     

未足月胎膜早破的处理

<正>未足月胎膜早破(preterm premature rupture of the membranes,PPROM)是指妊娠未满37周胎膜在临产前发生破裂。单胎妊娠PPROM的发生率为2%～4%,双胎妊娠为7%～20%[1]。PPROM导致的早产占早产的1/3,同时可能并发绒毛膜羊膜炎、     

未足月胎膜早破的研究进展

未足月胎膜早破(preterm premature rupture of the membranes，PPROM)是指妊娠未满37周胎膜在临产前发生破裂。在所有妊娠中PPROM发生率为1％～2％，早产合并PPROM占30％。PPROM孕妇中只有7．7％～9．7％的胎膜破口能够自然愈合，而持续阴道流液的孕妇，60％在7d内启动分娩。由于羊膜腔处于与外界相通的状态和羊水持续渗漏，PPROM不仅可导致羊水过少，羊膜腔内感染；还可能引起早产，围产儿病死率显著增加。因此，及早诊断和有效治疗PPROM极其重要。     

早产与胎膜早破

早产胎膜早破 (preterm prem ature rupture of mem-branes,PPROM)是指发生在妊娠 2 0～ 37周内的胎膜破裂且最终为早产者。据文献报道〔1 ,2〕,PPROM约占妊娠总数的 2 %～ 3% ,约占整个早产的 1/ 3。其中 70 %～ 80 %的孕妇在一周内分娩。与胎膜完整的妊娠相比 ,PPROM的围产儿死亡比、新生儿发病率及母亲感染率较高 ,围产儿死亡数占整个围产儿死亡数的 2 0 %左右 ,其围产儿死亡比的高低与 PPROM的分娩孕周及其处理有关。因此 ,早产合并胎膜早破应引起产科工作者的高度重视。1　病因与发病机理1.1　感染 :目前多数学者认为 ,下生殖…     

细胞间黏附分子-1在早产胎膜早破中的表达及临床意义

目的:研究细胞间黏附分子-1(ICAM-1)在早产胎膜早破中的表达及临床意义.方法:选取38例早产胎膜早破(PPROM)孕妇为研究组(PPROM组),36例与PPROM组孕周相对应之胎膜完整的自发早产(PTL)孕妇为对照组(PTL组),应用sP法检测各组胎膜ICAM-1的表达,并进行临床病理的相关性分析.结果:PPROM组中有55.26%(21/38)存在绒毛膜羊膜炎,PIL组中为36.11%(13/36),两组比较差异有统计学意义(P<0.05);两组胎膜中均存在不同程度的ICAM-1阳性表达,两组比较差异有统计学意义(P<0.05),PPROM组和PTL组ICAM-1的阳性表达与绒毛膜羊膜炎的相关系数分别为0.90和0.72,且病理结果中炎症越重的患者其胎膜上ICAM-1的阳性表达越明显.结论:ICAM-1的表达与感染相关,异常表达在早产胎膜早破的发病过程中起一定作用.感染越重的患者,ICAM-1的表达越明显,提示妊娠结局的严重化.     

Etiology of preterm premature rupture of membranes.

Numerous factors have been indicted as playing a role in causing preterm premature rupture of membranes (PPROM). After discussing the development of the amnion and chorion, this article focuses primarily on the effects that infection, nutrition, smoking, and cervical incompetence have on the fetal membrane and the subsequent advent of PPROM. However, evidence continues to support a multifactorial etiology for this entity, with numerous factors acting in concert.     

An evidence-based approach to the evaluation and treatment of premature rupture of membranes: Part I

Preterm premature rupture of membranes (PPROM) occurs in 3% of pregnancies and is responsible for one third of all preterm births. PPROM will affect 120,000 women in the United States each year. It is associated with significant maternal, fetal, and neonatal morbidity and mortality resulting from infection, umbilical cord compression, abruptio placentae, and prematurity. The etiology is multifactorial, but the most significant risk factors are previous preterm birth and previous preterm premature rupture of membranes. Accurate diagnosis is extremely important to assure proper treatment. Evaluation is based on patient history and clinical examination. This review presents the available evidence and grades it according to the U.S. Preventative Task Force recommendations. In part I of this review, the definition, pathophysiology, and methods of PPROM diagnosis are presented. In part II, the management, treatment, neonatal outcome, and the maternal and fetal evaluation of women with PPROM in the presence of cerclage and medical complications is reviewed. LEARNING OBJECTIVES: After completion of this article, the reader should be able to define the term: preterm premature rupture of membranes, to list the factors associated with premature rupture of membranes, and to outline the tests available for the diagnosis of intra-amniotic infection.     

未足月胎膜早破患者剩余羊水量测定与围产儿结局

未足月胎膜早破发生率较高,一旦剩余羊水量过少,常导致围产儿不良结局。文章重点介绍未足月胎膜早破导致的不良围产儿结局及其机制,根据国内外指南阐述未足月胎膜早破所致羊水过少时的处理原则,以引起对此疾病的关注及思考。     

早产胎膜早破95例妊娠结局的临床分析

目的:探讨早产胎膜早破(PPROM)的相关构成因素及不同孕周的妊娠结局。方法:选取我院2013年10月至2016年7月期间收治的95例PPROM的孕妇作为研究对象,分为观察组(孕周2833~(+6)周)和对照组(孕周3436~(+6)周),分析其相关构成因素、分娩方式及妊娠结局。结果:生殖道感染是PPROM的最主要构成因素,占33.68%。观察组的剖宫产率、新生儿窒息率、新生儿感染率及新生儿死亡率均显著高于对照组,差异均有统计学意义(P0.05)。观察组宫内感染率及产褥期感染率高于对照组,但差异无统计学意义(P0.05)。结论:生殖道感染是PPROM最主要的构成因素,对妊娠不足34周的PPROM患者采取积极保胎治疗及预防感染措施,以延长其孕周降低新生儿并发症的发生率,改善妊娠结局。     

Etiology and epidemiology of preterm premature rupture of the membranes

Preterm premature rupture of membranes continues to be a common complication of pregnancy with significant implications for perinatal outcome. Unfortunately, given the multiple risk factors that have been presented, which are reportedly associated with PPROM, attempts to reduce the incidence of this clinical event may seem daunting to the clinician. Despite this, one should attempt to address the potential risk factors that avail themselves to change. Unfortunately, although many risk factors have been identified, there are few randomized intervention trials for PPROM prevention. Examples of interventions documented to be beneficial include smoking cessation and screening for and treatment of chlamydial infections. These seem to be reasonable and logical interventions to consider in general, and may potentially have an effect on various causal agents of PPROM.     

Preterm premature rupture of the membranes and antioxidants: the free radical connection

AIM: To discuss the role of oxidant stress in preterm, premature rupture of the membranes (PPROM). RESULTS: There is evidence to suggest that preterm, premature rupture of the membranes occurs secondary to focal collagen damage in the fetal membranes. CONCLUSION: Oxidant stress caused by increased ROS formation and/or antioxidant depletion may disrupt collagen and cause premature membrane rupture. We propose that supplementation with vitamins C and E may synergistically protect the fetal membranes, and decrease the risks of PPROM.     

不同类型早产所致围生儿存活及发病情况研究

目的:探讨不同类型早产是否与围生儿的存活及发病情况有关。方法:回顾分析489例活胎妊娠孕妇(孕28~36+6周)及其分娩的550例新生儿(活产儿539个,死产儿11个),按早产类型将其分为自发性早产(SPB)、胎膜早破性早产(PPROM)、医源性早产(IPD)3组。对3组孕妇和新生儿的临床特征,围产儿的存活和发病情况进行了比较分析。结果:(1)IPD单胎围生儿存活率低于SPB和PPROM(P<0.01)。多胎围生儿存活率无统计学差异;(2)围生儿主要并发症的发病率在3组早产中无统计学差异(P>0.05)。(3)非条件Logistic回归多因素分析结果显示:Apgar 5m in评分,孕周,剖宫产与围生儿的存活成正相关。医源性早产,小于胎龄儿与围生儿存活成负相关。Apgar 5m in评分,孕周与围生儿的发病成负相关。结论:IPD与围生儿的存活呈负相关,IPD单胎围生儿存活率低于SPB和PPROM(P<0.01)。     

Surfactant maturation and preterm premature membrane rupture: a case study

Preterm premature membrane rupture (PPROM) is known to accelerate fetal lung surfactant maturation. The mechanism for this is unclear. We report a case of prolonged PPROM, where the maturation of fetal surfactant was studied in detail by the serial analysis of surfactant phospholipids in the drained liquor.     

Prevention of PPROM: Current and future strategies

Our understanding of the pathophysiologic processes leading to preterm premature rupture of membranes (PPROM) has grown tremendously in recent years. Evidence suggests that there may be a genetic susceptibility to PPROM and that genetic and environmental elements are important cofactors in its development. A number of risk-based protocols have been proposed in an attempt to identify those women at highest risk for PPROM. While we have made advances in the area of predicting PPROM, treatments based on current risk-based systems have failed to distinguish a specific, effective preventive therapy for PPROM. The concept that genetic factors increase susceptibility or decrease resistance to disease has stimulated new work in the field of PPROM. Several maternal and fetal gene polymorphisms have been identified that are associated with an increased risk for PPROM. Patients with ‘susceptible’ genotypes may also have clinical risk factors for PPROM resulting in a synergistic increase in the risk for PPROM, a so-called gene–environment interaction. The concept that these gene–environment interactions represent new targets for our efforts to prevent PPROM is explored.