Maternal vascular underperfusion: Nosology and reproducibility of placental reaction patterns

Maternal vascular underperfusion: Nosology and reproducibility of placental reaction patterns
复制标题

DOI:
10.1007/s10024-003-8083-2
复制
发表时间:
2004-05-01
影响因子:
1.9
通讯作者:
Waters, BL
Waters, BL
中科院分区:
医学4区
文献类型:
--
作者:
Redline, RW;Boyd, T;Waters, BL

文献摘要

被引文献

相似文献

胎盘检查是明确妊娠期疾病病因、预后和复发风险的有用工具。本研究的目的是测试一组预先确定的胎盘反应模式的可靠性与母体血管灌注不足,希望这可能会提供一个有用的诊断框架执业病理学家。由8名围产期病理学家对研究病例(14例有母体灌注不足的临床和病理证据,6例对照)中11处病变的存在或不存在进行了评价。在分析了初步结果后,对诊断标准进行了改进,并对第二组重叠病例进行了审查。相对于组一致性,II病变的个体评估的集体灵敏度、特异性和效率范围为74-93%(22/33 > 90%)。生殖能力通过未加权的卡帕值来衡量,解释如下:< 0.2差,0.2-0.6一般/中等,> 0.6实质性。影响绒毛和绒毛间隙的病变的Kappa值为增加的合胞体结(任意-0.42,严重-0.50)、绒毛凝集(0.42)、增加的绒毛间纤维蛋白(0.25)和远端绒毛发育不全(0.57)。合胞体结、绒毛间纤维蛋白和远端绒毛发育不全的个体估计受累百分比与胎盘和胎龄胎儿体重相关。绒毛间纤维蛋白增加的程度与胎盘重量(R = -0.64)和胎儿重量(R = -0.45)的相关性最强。影响母体血管和植入部位病变的Kappa值为急性动脉粥样硬化(0.50)、膜小动脉壁肥厚(0.43)、肌化基板动脉(0.48)、胎盘部位巨细胞增加(0.54)和不成熟中间滋养层(0.36)。母体血管和着床部位病变与子痫前期临床诊断的相关性表明,胎盘部位巨细胞过多和不成熟的中间滋养层细胞是更敏感和有效的预测因子,而动脉粥样硬化和肌化的基板动脉更具特异性。脐带过薄可能是胎儿血容量不足的指标,其Kappa值为0.61。考虑到所有上述病变,母体血管灌注不足的总体印象的再现性为中度(kappa 0.54),在纳入额外的病理和临床数据后有所改善(kappa 0.68)。采用这个定义明确、临床相关且病理可重复的术语可以增强临床病理相关性,并为未来的临床研究提供更客观的框架。
Placental examination cart be a useful tool for specifying the etiology, prognosis, and recurrence risk of pregnancy disorders. The purpose of this study was to test the reliability of a predetermined set of placental reaction patterns seen with maternal vascular underperfusion in the hope that this might provide a useful diagnostic framework for practicing pathologists. Study cases (14 with clinical and pathologic evidence of maternal underperfusion plus 6 controls) were evaluated for the presence or absence of 11 lesions by eight perinatal pathologists. After analysis of initial results, diagnostic criteria were refined and a second, overlapping set of cases was reviewed. The collective sensitivity, specificity, and efficiency of individual assessments for the I I lesions relative to the group consensus ranged from 74-93% (22/33 > 90%). Reproducibility was measured by unweighted kappa-values and interpreted as follows: < 0.2 poor, 0.2-0.6 fair/moderate, > 0.6 substantial. Kappa values for lesions affecting villi and the intervillous space were increased syncytial knots (any -0.42, severe -0.50), villous agglutination (0.42), increased intervillous fibrin (0.25), and distal villous hypoplasia (0.57). Individual estimates of percent involvement for syncytial knots, intervillous fibrin, and distal villous hypoplasia were correlated with placental and fetal weight for gestational age. Extent of increased intervillous fibrin showed the strongest correlation with both placental weight (R = -0.64) and fetal weight (R = -0.45). Kappa values for lesions affecting maternal vessels and the implantation site were acute atherosis (0.50), mural hypertrophy of membrane arterioles (0.43), muscularized basal plate arteries (0.48), increased placental site giant cells (0.54), and immature intermediate trophoblast (0.36). Correlation of maternal vessel and implantation site lesions with the clinical diagnosis of preeclampsia showed that excessive placental site giant cells and immature intermediate trophoblast were more sensitive and efficient predictors, whereas atherosis and muscularized basal plate arteries were more specific. Kappa value for a thin umbilical cord, a possible indicator of fetal volume depletion, was 0.61. Reproducibility for a global impression of maternal vascular underperfusion, taking into account all of the above lesions, was moderate (kappa 0.54) and improved after inclusion of additional pathologic and clinical data (kappa 0.68). Adoption of this clearly defined, clinically relevant, and pathologically reproducible terminology could enhance clinicopathologic correlation and provide a more objective framework for future clinical research.