scholarly journals Evaluation of Pattern of Immunostaining for Immunoglobulins and Complement Factors in Placentas with Chronic Villitis of Unknown Etiology: A Pilot Study

2018 ◽  
Vol 54 ◽  
pp. 36-36
Keyword(s):  
Pilot Study ◽  
Unknown Etiology ◽  
Complement Factors ◽  
Chronic Villitis

Perinatal prognosis of pregnancies complicated by placental chronic villitis or intervillositis of unknown etiology and combined lesions: About a series of 178 cases

Placenta ◽  
2016 ◽  
Vol 44 ◽  
pp. 104-108 ◽  
Author(s):  
Christel Nowak ◽  
Madeleine Joubert ◽  
Frederique Jossic ◽  
Agathe Masseau ◽  
Mohamed Hamidou ◽  
...  
Keyword(s):  
Unknown Etiology ◽  
Combined Lesions ◽  
Chronic Villitis

Seasonal Variation of Chronic Villitis of Unknown Etiology

2019 ◽  
Vol 23 (4) ◽  
pp. 253-259
Author(s):  
Alexa A Freedman ◽  
Jeffery A Goldstein ◽  
Gregory E Miller ◽  
Ann Borders ◽  
Lauren Keenan-Devlin ◽  
...  
Keyword(s):  
Seasonal Variation ◽  
Inflammatory Lesion ◽  
Unknown Etiology ◽  
Low Grade ◽  
Text Search ◽  
Standardized Protocol ◽  
Prevalence Estimates ◽  
Chronic Villitis ◽  
Pathology Reports ◽  
Estimate Prevalence

Introduction Chronic villitis of unknown etiology (VUE) is a chronic inflammatory lesion of the placenta. VUE is hypothesized to result from an alloimmune response or as response to an unidentified infection. Lack of a seasonal trend is thought to support VUE as an alloimmune response, though data on seasonal VUE trends are limited. Methods Data were obtained from a hospital in Chicago, Illinois, from 2011–2016. Placentas sent to pathology were reviewed using a standardized protocol, and VUE cases were identified based on an automated text search of pathology records. We used monthly VUE prevalence estimates to investigate the annual trend, and we used Poisson regression to evaluate seasonal variation in the number of VUE cases. Results There were 79 825 deliveries within the study period. Pathologists evaluated 12 074 placentas and identified 2873 cases of VUE. Regression results indicate that the risk of VUE is 16% to 17% higher in the fall and winter as compared to the summer (fall relative risk [RR]: 1.17, 95% confidence interval [CI]: 1.06–1.29; winter RR: 1.16, 95% CI: 1.05–1.29). Discussion Our results suggest that there may be seasonal variation in VUE prevalence, particularly for low-grade VUE. Future studies should evaluate seasonal variation in a representative sample rather than relying on pathology reports to estimate prevalence.

Histological Features of Shallow Placental Implantation Unify Early-Onset and Late-Onset Preeclampsia

2018 ◽  
Vol 22 (2) ◽  
pp. 112-122 ◽  
Author(s):  
Jerzy Stanek
Keyword(s):  
Early Onset ◽  
Late Onset ◽  
Unknown Etiology ◽  
Hypertension In Pregnancy ◽  
Pathological Mechanism ◽  
Comparative Group ◽  
Laminar Necrosis ◽  
Chronic Villitis ◽  
Early Onset Preeclampsia ◽  
In Pregnancy

Preeclampsia is distinguishable from other hypertensive conditions of pregnancy by its high rates of decidual arteriopathy, the uterine type of chronic hypoxic placental injury, the occurrence of villous infarctions, and clusters of multinucleate trophoblasts in the maternal floor. To retrospectively study the clinical and placental phenotypes of 230 women with early-onset preeclampsia, 261 women with late-onset preeclampsia, and 5059 women without hypertension in pregnancy (comparative group), 24 clinical and 46 placental phenotypes were statistically compared (analysis of variance, χ2 with Bonferroni correction). The frequency of decidual arteriopathy (both hypertrophic and atherosis), patterns of chronic hypoxic placental injury, villous infarction, membrane laminar necrosis, membrane microscopic chorionic pseudocysts, clusters of maternal floor multinucleated trophoblasts, excessive number of extravillous trophoblasts, and intervillous thrombi was strikingly higher in both late-onset preeclampsia and early-onset preeclampsia than in the comparative group without hypertension in pregnancy. All 3 patterns of chronic hypoxic placental injury were 2- to 3-fold more common in preeclampsia. Although the preuterine pattern was as common in early-onset preeclampsia as it was in late-onset preeclampsia, the postuterine pattern was 2-fold more common in early-onset preeclampsia, and chronic villitis of unknown etiology was more common in late-onset preeclampsia than in the other 2 groups. Features of shallow placental implantation occurred at the same frequency in early-onset preeclampsia as in late-onset preeclampsia, which reflects an underlying common pathological mechanism in both subgroups of preeclampsia, while hypoxic lesions and patterns of placental injury were more common in early-onset preeclampsia than in late-onset preeclampsia, which correlates with more severe clinical outcomes of the former.

Cognitive decline risk stratification in people with late-onset epilepsy of unknown etiology: An electroencephalographic connectivity and graph theory pilot study

2021 ◽  
Vol 429 ◽  
pp. 117686
Author(s):  
Cinzia Costa ◽  
Fabrizio Vecchio ◽  
Michele Romoli ◽  
Francesca Miraglia ◽  
Elena Nardi Cesarini ◽  
...  
Keyword(s):  
Graph Theory ◽  
Pilot Study ◽  
Risk Stratification ◽  
Cognitive Decline ◽  
Late Onset ◽  
Unknown Etiology

Characterization of Inflammation in Syphilitic Villitis and in Villitis of Unknown Etiology

2004 ◽  
Vol 7 (5) ◽  
pp. 453-458 ◽  
Author(s):  
Payal Kapur ◽  
Dinesh Rakheja ◽  
Ana M. Gomez ◽  
Jeanne Sheffield ◽  
Pablo Sanchez ◽  
...  
Keyword(s):  
Relative Number ◽  
Lymphocytic Infiltrate ◽  
Unknown Etiology ◽  
Histologic Diagnosis ◽  
Cd8 Cells ◽  
Y Chromosomes ◽  
Hla Dr ◽  
Chronic Villitis ◽  
Undetermined Etiology ◽  
Infiltrating Lymphocytes

Chronic villitis is a histologic diagnosis that may be either associated with infection, or termed villitis of undetermined etiology (VUE). The lymphocytic infiltrate in VUE has been reported to consist of maternal lymphocytes, but the origin of the lymphocytic infiltrate in infectious villitis has not been identified. The purpose of our study was to compare the maternal vs. fetal origin of the infiltrating lymphocytes in VUE and syphilitic villitis, and to expand the immunophenotypic data provided by previous studies. Paraffin-embedded placentas from four males with VUE and two males with syphilitic vil litis were subjected to fluorescence in situ hybridization (FISH) for the X and Y chromosomes. Serial sections were stained with antibodies to CD3, CD4, CD8, CD68, HLA-DR, and CD20. Quantitation of the relative number of cells marking with each antibody was done for four villi in each slide. CD3 lymphocytes predominated in both VUE and syphilitic villitis, with slightly more CD8 cells compared to CD4 cells. CD68 and HLA-DR positive cells were as frequent as CD3 cells, and B-lymphocytes were rare. Maternal cells were the predominant intravillous population in both VUE and syphilitic villitis, and neutrophils in syphilitic villitis were also maternal. These data indicate that the immune response in both syphilitic villitis and VUE is similar, raising the possibility of a similar immunopathogenetic pathway.

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