15. Morphological diagnosis of placental insufficiency

2019 ◽  
pp. 425-434
Keyword(s):  
Placental Insufficiency ◽  
Morphological Diagnosis

Ultrastructural diagnosis of peritoneal malignant mesothelioma

1994 ◽  
Vol 52 ◽  
pp. 234-235
Author(s):  
S. Siew
Keyword(s):  
Malignant Mesothelioma ◽  
Common Type ◽  
Abdominal Discomfort ◽  
The Body ◽  
Metastatic Adenocarcinoma ◽  
Common Site ◽  
Primary Malignancy ◽  
Peritoneal Implant ◽  
Morphological Diagnosis ◽  
Malignant Neoplasia

Mesothelial cells constitute the lining of the three serous sacs of the body i.e. the pleura, pericardium and peritoneum. The more common type of malignant neoplasia of the serous sacs is seeding by metastatic tumors and primary malignancy of the mesothelium is unusual. Of the three sacs, the pleura is the most common site of malignant mesothelioma. Involvement of the peritoneum is extremely rare.We report 3 cases of malignant mesothelioma of the peritoneum. All of them were female. Their ages were 57, 67 and 72 years, respectively. The patients presented with abdominal discomfort and/or ascites. The extent of the tumors ranged from a peritoneal implant to widespread infiltration of the peritoneum and omentum. Histologic examination in Case 1 showed the presence of a diffusely infiltrating papillary mesothelioma without a sarcomatoid component. A mesodermal element was present in the other two cases. In order to establish a morphological diagnosis of malignant mesothelioma, the possibility has to be excluded of a metastatic adenocarcinoma.

NeuN As a Neuronal Nuclear Antigen and Neuron Differentiation Marker

Acta Naturae ◽  
2015 ◽  
Vol 7 (2) ◽  
pp. 42-47 ◽  
Author(s):  
V. V. Gusel’nikova ◽  
D. E. Korzhevskiy
Keyword(s):  
Experimental Data ◽  
Intracellular Localization ◽  
Nuclear Antigen ◽  
Structure And Properties ◽  
Immunocytochemical Detection ◽  
Perinuclear Cytoplasm ◽  
Diagnosis Of Cancer ◽  
Morphological Diagnosis ◽  
The Central Nervous System ◽  
Differentiation Marker

The NeuN protein is localized in nuclei and perinuclear cytoplasm of most of the neurons in the central nervous system of mammals. Monoclonal antibodies to the NeuN protein have been actively used in the immunohistochemical research of neuronal differentiation to assess the functional state of neurons in norm and pathology for more than 20 years. Recently, NeuN antibodies have begun to be applied in the differential morphological diagnosis of cancer. However, the structure of the protein, which can be revealed by antibodies to NeuN, remained unknown until recently, and the functions of the protein are still not fully clear. In the present mini-review, data on NeuN accumulated so far are summarized and analyzed. Data on the structure and properties of the protein, its isoforms, intracellular localization, and hypothesized functions are reported. The application field of immunocytochemical detection of NeuN in scientific and clinical studies, as well as the difficulties in the interpretation of the obtained experimental data and their possible causes, is described in details.

Maternal-Fetal Management in Trombophilia Related and Placenta-Mediated Pregnancy Complications

2018 ◽  
Vol 69 (9) ◽  
pp. 2396-2401
Author(s):  
Costin Berceanu ◽  
Elena Loredana Ciurea ◽  
Monica Mihaela Cirstoiu ◽  
Sabina Berceanu ◽  
Anca Maria Ofiteru ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Pregnancy Complications ◽  
Case Control Study ◽  
Case Control ◽  
Placental Insufficiency ◽  
Management Options ◽  
Specific Therapy ◽  
Pregnancy Morbidity ◽  
The Impact ◽  
Control Study

It is widely accepted that thrombophilia in pregnancy greatly increases the risk of venous thromboembolism. Pregnancy complications arise, at least partly, from placental insufficiency. Any change in the functioning of the gestational transient biological system, such as inherited or acquired thrombophilia, might lead to placental insufficiency. In this research we included 64 pregnant women with trombophilia and 70 cases non-trombophilic pregnant women, with or without PMPC, over a two-year period. The purpose of this multicenter case-control study is to analyze the maternal-fetal management options in obstetric thrombophilia, the impact of this pathology on the placental structure and possible correlations with placenta-mediated pregnancy complications. Maternal-fetal management in obstetric thrombophilia means preconceptional or early diagnosis, prevention of pregnancy morbidity, specific therapy as quickly as possible and fetal systematic surveilance to identify the possible occurrence of placenta-mediated pregnancy complications.

scholarly journals Quantifying Fetal Reprogramming for Biomarker Development in the Era of High-Throughput Sequencing

Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 329
Author(s):  
Fu-Sheng Chou ◽  
Krystel Newton ◽  
Pei-Shan Wang
Keyword(s):  
High Throughput ◽  
High Throughput Sequencing ◽  
Well Being ◽  
Placental Insufficiency ◽  
Definitive Treatment ◽  
Optimal Timing ◽  
Hypertensive Disorders ◽  
Clinical Tools ◽  
Fetal Reprogramming ◽  
Offspring Health

Gestational hypertensive disorders continue to threaten the well-being of pregnant women and their offspring. The only current definitive treatment for gestational hypertensive disorders is delivery of the fetus. The optimal timing of delivery remains controversial. Currently, the available clinical tools do not allow for assessment of fetal stress in its early stages. Placental insufficiency and fetal growth restriction secondary to gestational hypertensive disorders have been shown to have long-term impacts on offspring health even into their adulthood, becoming one of the major focuses of research in the field of developmental origins of health and disease. Fetal reprogramming was introduced to describe the long-lasting effects of the toxic intrauterine environment on the growing fetus. With the advent of high-throughput sequencing, there have been major advances in research attempting to quantify fetal reprogramming. Moreover, genes that are found to be differentially expressed as a result of fetal reprogramming show promise in the development of transcriptional biomarkers for clinical use in detecting fetal response to placental insufficiency. In this review, we will review key pathophysiology in the development of placental insufficiency, existing literature on high-throughput sequencing in the study of fetal reprogramming, and considerations regarding research design from our own experience.

scholarly journals Intrauterine Growth Restriction: Cytokine Profiles of Trophoblast Antigen-Stimulated Maternal Lymphocytes

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Raj Raghupathy ◽  
Majedah Al-Azemi ◽  
Fawaz Azizieh
Keyword(s):  
Inflammatory Cytokines ◽  
Peripheral Blood ◽  
Intrauterine Growth Restriction ◽  
Mononuclear Cells ◽  
Normal Pregnancy ◽  
Placental Insufficiency ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Anti Inflammatory ◽  
Ifnγ And Tnfα

Intrauterine growth restriction (IUGR) is an important perinatal syndrome that poses several serious short- and long-term effects. We studied cytokine production by maternal peripheral blood lymphocytes stimulated by trophoblast antigens. 36 women with a diagnosis of IUGR and 22 healthy women with normal fetal growth were inducted. Peripheral blood mononuclear cells were stimulated with trophoblast antigens and levels of the proinflammatory cytokines IL-6, IL-8, IL-12, IL-23, IFNγ, and TNFα and the anti-inflammatory cytokines IL-4, IL-10, and IL-13 were measured in culture supernatants by ELISA. IL-8 was produced at higher levels by blood cells of the IUGR group than normal pregnant women, while IL-13 was produced at lower levels. IL-8, IFNγ, and TNFα were higher in IUGR with placental insufficiency than in normal pregnancy. IL-12 levels were higher and IL-10 levels were lower in IUGR with placental insufficiency than in IUGR without placental insufficiency. We suggest that a stronger pro-inflammatory bias exists in IUGR as compared to normal pregnancy and in IUGR with placental insufficiency when compared to IUGR without placental insufficiency. Several ratios of proinflammatory to anti-inflammatory cytokines also support the existence of an inflammatory bias in IUGR.

scholarly journals Elevated Circulating and Placental SPINT2 Is Associated with Placental Dysfunction

2021 ◽  
Vol 22 (14) ◽  
pp. 7467
Author(s):  
Ciara N. Murphy ◽  
Susan P. Walker ◽  
Teresa M. MacDonald ◽  
Emerson Keenan ◽  
Natalie J. Hannan ◽  
...  
Keyword(s):  
Stem Cells ◽  
First Trimester ◽  
Placental Insufficiency ◽  
Human Trophoblast ◽  
Trophoblast Stem Cells ◽  
Placental Dysfunction ◽  
Foetal Growth Restriction ◽  
Term Delivery ◽  
Placental Disease ◽  
Prospective Cohorts

Biomarkers for placental dysfunction are currently lacking. We recently identified SPINT1 as a novel biomarker; SPINT2 is a functionally related placental protease inhibitor. This study aimed to characterise SPINT2 expression in placental insufficiency. Circulating SPINT2 was assessed in three prospective cohorts, collected at the following: (1) term delivery (n = 227), (2) 36 weeks (n = 364), and (3) 24–34 weeks’ (n = 294) gestation. SPINT2 was also measured in the plasma and placentas of women with established placental disease at preterm (<34 weeks) delivery. Using first-trimester human trophoblast stem cells, SPINT2 expression was assessed in hypoxia/normoxia (1% vs. 8% O2), and following inflammatory cytokine treatment (TNFa, IL-6). Placental SPINT2 mRNA was measured in a rat model of late-gestational foetal growth restriction. At 36 weeks, circulating SPINT2 was elevated in patients who later developed preeclampsia (p = 0.028; median = 2233 pg/mL vs. controls, median = 1644 pg/mL), or delivered a small-for-gestational-age infant (p = 0.002; median = 2109 pg/mL vs. controls, median = 1614 pg/mL). SPINT2 was elevated in the placentas of patients who required delivery for preterm preeclampsia (p = 0.025). Though inflammatory cytokines had no effect, hypoxia increased SPINT2 in cytotrophoblast stem cells, and its expression was elevated in the placental labyrinth of growth-restricted rats. These findings suggest elevated SPINT2 is associated with placental insufficiency.

Massive Perivillous Fibrin Deposition and Chronic Histiocytic Intervillositis a Complication of SARS-CoV-2 Infection

2021 ◽  
pp. 109352662110207
Author(s):  
T Marton ◽  
B Hargitai ◽  
K Hunter ◽  
M Pugh ◽  
P Murray
Keyword(s):  
Placental Insufficiency ◽  
Intrauterine Death ◽  
Fibrin Deposition ◽  
Fetal Demise ◽  
Trophoblastic Cells ◽  
Stage Disease ◽  
Villous Trophoblast ◽  
Fetal Movements ◽  
Active Viral Replication ◽  
End Stage

An emerging complication of COVID-19 (SARS-CoV-2) infection is reported. A 23-year-old patient presented with high temperature and reduced fetal movements at 25 + 5/40 weeks of gestation. RT-PCR proved maternal COVID-19 infection. Ultrasound examination confirmed intrauterine death. Placenta histology showed necrosis of the villous trophoblast, associated with Chronic Histiocytic Intervillositis (CHI) and Massive Perivillous Fibrin Deposition (MPFD) with up to 90% - of the intervillous spaces being involved. Immunohistochemistry showed CD68 positive histiocytes in the intervillous spaces and the villous trophoblast was positive for the COVID-19 spike protein. RNA scope signal was indicative of the presence of the viral genome and active viral replication in the villous trophoblastic cells, respectively. MPFD is a gradually developing end-stage disease with various etiology, including autoimmune and alloimmune maternal response to antigens expressed at the feto-maternal interface and frequently accompanies chronic alloimmune villitis or histiocytic intervillositis. Covid-19 infection is associated with similar pattern of histological changes of the placenta leading to placental insufficiency and fetal death. This case report supports maternal- fetal vertical transmission of SARS-CoV-2 virus leading to placental insufficiency and fetal demise. MPFD and CHI appear to be the typical placental histology for SARS-CoV-2 virus infection associated fetal demise.

scholarly journals 180 The role of social constructs in placental insufficiency outcomes: an unsupervised machine learning approach

2021 ◽  
Vol 224 (2) ◽  
pp. S121-S122
Author(s):  
Ramamurthy Siripuram ◽  
Nathan R. Blue ◽  
Robert M. Silver ◽  
William A. Grobman ◽  
Uma M. Reddy ◽  
...  
Keyword(s):  
Machine Learning ◽  
Placental Insufficiency ◽  
Learning Approach ◽  
Social Constructs ◽  
Unsupervised Machine Learning ◽  
Machine Learning Approach

scholarly journals Genomic imbalances in the placenta are associated with poor fetal growth

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Giulia F. Del Gobbo ◽  
Yue Yin ◽  
Sanaa Choufani ◽  
Emma A. Butcher ◽  
John Wei ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Sex Chromosome ◽  
Copy Number Variants ◽  
Placental Insufficiency ◽  
Potential Contribution ◽  
Genomic Imbalances ◽  
Significant Difference ◽  
Underlying Causes ◽  
Risk Of Disease ◽  
The Impact

Abstract Background Fetal growth restriction (FGR) is associated with increased risks for complications before, during, and after birth, in addition to risk of disease through to adulthood. Although placental insufficiency, failure to supply the fetus with adequate nutrients, underlies most cases of FGR, its causes are diverse and not fully understood. One of the few diagnosable causes of placental insufficiency in ongoing pregnancies is the presence of large chromosomal imbalances such as trisomy confined to the placenta; however, the impact of smaller copy number variants (CNVs) has not yet been adequately addressed. In this study, we confirm the importance of placental aneuploidy, and assess the potential contribution of CNVs to fetal growth. Methods We used molecular-cytogenetic approaches to identify aneuploidy in placentas from 101 infants born small-for-gestational age (SGA), typically used as a surrogate for FGR, and from 173 non-SGA controls from uncomplicated pregnancies. We confirmed aneuploidies and assessed mosaicism by microsatellite genotyping. We then profiled CNVs using high-resolution microarrays in a subset of 53 SGA and 61 control euploid placentas, and compared the load, impact, gene enrichment and clinical relevance of CNVs between groups. Candidate CNVs were confirmed using quantitative PCR. Results Aneuploidy was over tenfold more frequent in SGA-associated placentas compared to controls (11.9% vs. 1.1%; p = 0.0002, OR = 11.4, 95% CI 2.5–107.4), was confined to the placenta, and typically involved autosomes, whereas only sex chromosome abnormalities were observed in controls. We found no significant difference in CNV load or number of placental-expressed or imprinted genes in CNVs between SGA and controls, however, a rare and likely clinically-relevant germline CNV was identified in 5.7% of SGA cases. These CNVs involved candidate genes INHBB, HSD11B2, CTCF, and CSMD3. Conclusions We conclude that placental genomic imbalances at the cytogenetic and submicroscopic level may underlie up to ~ 18% of SGA cases in our population. This work contributes to the understanding of the underlying causes of placental insufficiency and FGR, which is important for counselling and prediction of long term outcomes for affected cases.

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