Extrauterine Lesions of Intermediate Trophoblast

2003 ◽  
Vol 22 (4) ◽  
pp. 362-367 ◽  
Author(s):  
Rebecca N. Baergen ◽  
Joanne Rutgers ◽  
Robert H. Young
1995 ◽  
Vol 26 (6) ◽  
pp. 594-600 ◽  
Author(s):  
Raymond W Redline ◽  
Patricia Patterson

1999 ◽  
Vol 30 (6) ◽  
pp. 687-694 ◽  
Author(s):  
Ie-ming Shih ◽  
Jeffrey D Seidman ◽  
Robert J Kurman

Placenta ◽  
2016 ◽  
Vol 48 ◽  
pp. 13-19 ◽  
Author(s):  
Yongzhong Gu ◽  
Yuehong Bian ◽  
Xiaofei Xu ◽  
Xietong Wang ◽  
Changting Zuo ◽  
...  

1987 ◽  
Vol 11 (9) ◽  
pp. 693-694 ◽  
Author(s):  
J arlos Manivel ◽  
Gloria Niehans ◽  
Mark R. Wick ◽  
Louis P. Dehner

2007 ◽  
Vol 10 (4) ◽  
pp. 266-273 ◽  
Author(s):  
Jerzy Stanek ◽  
Zarius Drummond

Placenta creta (accreta, increta, or percreta) is a clinically symptomatic condition, usually diagnosed histologically on hysterectomy specimens. At a minimum, focal absence of decidua is the histological finding for this condition; however, excessive amounts of extravillous trophoblasts were recently documented on hysterectomy specimens. The histological finding of basal plate myometrial fibers (BPMF) without intervening decidua in spontaneously delivered placentas, which we term occult placenta accreta (OPA), is not infrequent, even in clinically asymptomatic cases. To prove that OPA is a missing link between normal placental implantation and clinical placenta accreta, CD146 immunohistochemical stains were performed on 25 sections of OPA (study group) and 25 placental sections without BPMF (control group). Implantation-site intermediate trophoblast (ISIT) cell number, thickness, and density were compared between the study and control groups. The ISIT micrometry thickness and cell number at BPMF sites were statistically significantly higher in OPA than in control group and same OPA placentas away from BPMF. There were no statistically significant differences in ISIT density. Therefore, although asymptomatic, OPA features the same histopathology as clinical placenta accreta and may share same pathogenesis, which may include decidual deficiency, abnormal trophoblast/ decidua interaction, and/or hypoxia.


2004 ◽  
Vol 7 (3) ◽  
pp. 237-249 ◽  
Author(s):  
Raymond W. Redline ◽  
Theonia Boyd ◽  
Valarie Campbell ◽  
Scott Hyde ◽  
Cynthia Kaplan ◽  
...  

Placental examination can 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 11 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.


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