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[早产新生儿的绒毛膜羊膜炎与炎症性疾病]

[Chorioamnionitis and inflammatory disease in the premature newborn infant].

作者信息

Vedovato S, Zanardo V

机构信息

Dipartimento di Pediatria, Università degli Studi di Padova, Italy.

出版信息

Minerva Pediatr. 2010 Jun;62(3 Suppl 1):155-6.

Abstract

Preterm births occurs in 6-12% of all pregnancies, accounts for 75% of neonatal death and causes significant neonatal morbidity. A large number of preterm birth is associated with infection (30%), because of the release of many cytokines. In fact acute chorioamnionitis represents the inflammatory response to extracellular microorganisms that gain access to the gestational sac. Clinical signs of infection compare in the 12% of cases, while the prevalence of positive amniotic fluid cultures is approximately 50% in patients with preterm PROM. Despite the recent studies about the dosage of inflammatory biomarkers in the amniotic fluid or in fetal and maternal blood, placenta histology remains the gold standard for the diagnosis of chorioamnionitis. Histological chorioamnionitis describes the progression of the inflammatory process. Organisms first colonise the chorioamnionic surface. Then, the neutrophils migrates to the chorion (chorionitis) and to the amnion (chorioamnionitis) and, in the last stage, amnionic epithelial cells undergo necrosis (necrotising chorioamnionitis). It represents the mother inflammatory response and it differs from the fetal inflammatory response (funisitis). Funisitis first appears in vessels of the chorionic plate (chorionic vasculitis) or in the umbilical vein (umbilical phlebitis), then in the umbilical artery (umbilical arteritis), and in the Wharton's jelly (umbilical perivasculitis). The fetal inflammatory response has been associated with inflammatory diseases of preterm infants, increasing the risk of neonatal sepsis and meningitis, bronchopulmonary dysplasia and cerebral palsy. We present our experience on the relationship between histological chorioamnionitis, preterm birth and inflammatory diseases of VLBW infants.

摘要

早产发生率占所有妊娠的6% - 12%,占新生儿死亡的75%,并导致显著的新生儿发病。大量早产与感染有关(30%),这是由于多种细胞因子的释放。事实上,急性绒毛膜羊膜炎代表了对进入妊娠囊的细胞外微生物的炎症反应。12%的病例有感染的临床体征,而早产胎膜早破患者羊水培养阳性率约为50%。尽管最近有关于羊水或胎儿及母体血液中炎症生物标志物剂量的研究,但胎盘组织学仍然是绒毛膜羊膜炎诊断的金标准。组织学绒毛膜羊膜炎描述了炎症过程的进展。病原体首先在绒毛膜羊膜表面定植。然后,中性粒细胞迁移至绒毛膜(绒毛膜炎)和羊膜(绒毛膜羊膜炎),在最后阶段,羊膜上皮细胞发生坏死(坏死性绒毛膜羊膜炎)。它代表母体的炎症反应,与胎儿的炎症反应(脐带炎)不同。脐带炎首先出现在绒毛膜板血管(绒毛膜血管炎)或脐静脉(脐静脉炎),然后出现在脐动脉(脐动脉炎)和华通胶(脐周血管炎)。胎儿的炎症反应与早产儿的炎症性疾病有关,增加了新生儿败血症和脑膜炎、支气管肺发育不良和脑瘫的风险。我们介绍我们关于组织学绒毛膜羊膜炎、早产与极低出生体重儿炎症性疾病之间关系的经验。

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