Salafia C M, Ernst L M, Pezzullo J C, Wolf E J, Rosenkrantz T S, Vintzileos A M
Department of Pathology, University of Connecticut School of Medicine, Farmington, USA.
Am J Perinatol. 1995 Mar;12(2):106-10. doi: 10.1055/s-2007-994417.
The placental lesions of the very low birthweight (VLBW) infant were investigated in relation to clinical complications leading to preterm birth and evidence of growth impairment. The 249 singleton gestations yielding infants less than 1500 g were grouped according to the clinical complications leading to preterm birth as premature membrane rupture (116/249, 47%) preterm labor (55/249, 22%), pregnancy-induced hypertension (PIH, 54/249, 22%), and normotensive abruption (ABR, 24/249, 10%). Specifically excluded from this data set were cases with greater than 2 weeks discordance, fetal congenital anomalies, placenta previa, and maternal medical or gestational diseases such as chronic hypertension and diabetes mellitus, and intrauterine growth retardation (IUGR) as a primary indication for delivery. Placental weight and lesions including decidual vasculopathy and related villous lesions, chronic villitis/intervillositis, and decidual plasmacytosis were considered as variables in analyses in which raw birthweight was the dependent variable and gestational age a confounder. Of the 195 VLBW, 79 (41%) infants from normotensive mothers had lesions of decidual vasculopathy or chronic inflammation. In the VLBW infants from hypertensive mothers, growth restriction was related to markers of decidual vasculopathy. In the absence of maternal hypertension the growth restriction was independently associated with chronic villitis. Decidual vasculopathy (characteristic of PIH) and chronic intrauterine inflammation underlie the complications of many normotensive VLBW infants. The placental lesions in VLBW-IUGR depend on the presence or absence of maternal hypertension. In the absence of maternal hypertension, VLBW-IUGR is associated with chronic inflammation and is independent of decidual vasculopathy. In the presence of maternal hypertension, VLBW-IUGR is directly related to decidual vasculopathy.
对极低出生体重（VLBW）婴儿的胎盘病变进行了研究，探讨其与导致早产的临床并发症及生长发育受限证据之间的关系。将249例单胎妊娠且出生体重小于1500g的婴儿，根据导致早产的临床并发症进行分组，包括胎膜早破（116/249，47%）、早产（55/249，22%）、妊娠高血压综合征（PIH，54/249，22%）和血压正常的胎盘早剥（ABR，24/249，10%）。该数据集特别排除了双胎差异大于2周、胎儿先天性异常、前置胎盘以及母亲患有如慢性高血压和糖尿病等内科或妊娠疾病，以及将胎儿宫内生长受限（IUGR）作为分娩主要指征的病例。胎盘重量和病变，包括蜕膜血管病变及相关绒毛病变、慢性绒毛炎/绒毛间炎和蜕膜浆细胞增多症，在分析中被视为变量，其中原始出生体重为因变量，胎龄为混杂因素。在195例极低出生体重儿中，79例（41%）来自血压正常母亲的婴儿有蜕膜血管病变或慢性炎症。在来自高血压母亲的极低出生体重儿中，生长受限与蜕膜血管病变标志物有关。在无母亲高血压的情况下，生长受限与慢性绒毛炎独立相关。蜕膜血管病变（妊娠高血压综合征的特征）和慢性宫内炎症是许多血压正常的极低出生体重儿并发症的基础。极低出生体重儿合并胎儿宫内生长受限的胎盘病变取决于母亲是否患有高血压。在无母亲高血压的情况下，极低出生体重儿合并胎儿宫内生长受限与慢性炎症有关，且与蜕膜血管病变无关。在有母亲高血压的情况下，极低出生体重儿合并胎儿宫内生长受限与蜕膜血管病变直接相关。
