Talk:Placenta - Abnormalities

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Cite this page: Hill, M.A. (2024, March 28) Embryology Placenta - Abnormalities. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Placenta_-_Abnormalities

2012

Prenatal hypoxic-ischemic insult changes the distribution and number of NADPH-diaphorase cells in the cerebellum

PLoS One. 2012;7(4):e35786. Epub 2012 Apr 23.

Savignon T, Costa E, Tenorio F, Manhães AC, Barradas PC. Source Departamento de Farmacologia e Psicobiologia, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract

Astrogliosis, oligodendroglial death and motor deficits have been observed in the offspring of female rats that had their uterine arteries clamped at the 18(th) gestational day. Since nitric oxide has important roles in several inflammatory and developmental events, here we evaluated NADPH-diaphorase (NADPH-d) distribution in the cerebellum of rats submitted to this hypoxia-ischemia (HI) model. At postnatal (P) day 9, Purkinje cells of SHAM and non-manipulated (NM) animals showed NADPH-d+ labeling both in the cell body and dendritic arborization in folia 1 to 8, while HI animals presented a weaker labeling in both cellular structures. NADPH-d+ labeling in the molecular (ML), and in both the external and internal granular layer, was unaffected by HI at this age. At P23, labeling in Purkinje cells was absent in all three groups. Ectopic NADPH-d+ cells in the ML of folia 1 to 4 and folium 10 were present exclusively in HI animals. This labeling pattern was maintained up to P90 in folium 10. In the cerebellar white matter (WM), at P9 and P23, microglial (ED1+) NADPH-d+ cells, were observed in all groups. At P23, only HI animals presented NADPH-d labeling in the cell body and processes of reactive astrocytes (GFAP+). At P9 and P23, the number of NADPH-d+ cells in the WM was higher in HI animals than in SHAM and NM ones. At P45 and at P90 no NADPH-d+ cells were observed in the WM of the three groups. Our results indicate that HI insults lead to long-lasting alterations in nitric oxide synthase expression in the cerebellum. Such alterations in cerebellar differentiation might explain, at least in part, the motor deficits that are commonly observed in this model.

PMID 22540005

The branching pattern of villous capillaries and structural changes of placental terminal villi in type 1 diabetes mellitus

Placenta. 2012 Feb 6. [Epub ahead of print]

Jirkovská M, Kučera T, Kaláb J, Jadrníček M, Niedobová V, Janáček J, Kubínová L, Moravcová M, Zižka Z, Krejčí V. Source Institute of Histology and Embryology, First Faculty of Medicine, Charles University in Prague, Albertov 4, CZ-12801 Prague 2, Czech Republic.

Abstract

Maternal diabetes is associated with changes of the placental structure. These changes include great variability of vascularity manifested by strikingly hypovascular as well as hypervascular terminal villi. In this paper, normal placental terminal villi and pathological villi of type 1 diabetic placentas were compared concerning the structure of villous stroma, spatial arrangement of villous capillary bed and quantitative assessment of capillary branching pattern. Formalin fixed and paraffin embedded specimens of 14 normal and 17 Type 1 diabetic term placentas were used for picrosirius staining, vimentin and desmin immunohistochemistry and confocal microscopy. 3D models of villi and villous capillaries were constructed from stacks of confocal optical sections. Hypervascular as well as hypovascular villi of diabetic placenta displayed changed structure of villous stroma, i.e. the collagen envelope around capillaries looked thinner and the network of collagen fibers seemed less dense. The desmin immunocytochemistry has shown that stromal cells of hypervascular as well as hypovascular villi appeared nearly or completely void of desmin filaments. In comparison with normal villi, capillaries of hypovascular villi had a smaller diameter and displayed a markedly wavy course whereas in hypervascular villi numerous capillaries occurred in reduced stroma and often had a large diameter. The quantitative assessment of capillary branching has shown that villous capillaries are more branched in diabetic placentas. It is concluded that type 1 maternal diabetes enhances the surface area of the capillary wall by elongation, enlargement of diameter and higher branching of villous capillaries and disrupts the stromal structure of terminal villi. Copyright © 2012 Elsevier Ltd. All rights reserved.

PMID 22317894

2011

Velamentous cord insertion caused by oblique implantation after in vitro fertilization and embryo transfer

J Obstet Gynaecol Res. 2011 Nov;37(11):1698-701. doi: 10.1111/j.1447-0756.2011.01555.x. Epub 2011 Jun 9.

Hasegawa J, Iwasaki S, Matsuoka R, Ichizuka K, Sekizawa A, Okai T. Source Department of Obstetrics and Gynecology, Showa University School of Medicine, Tokyo, Japan. hasejun@oak.dti.ne.jp

Abstract

We present a case of a 36-year-old pregnant female after intracytoplasmic sperm injection. Ultrasonographic examination at 8 weeks' gestation revealed umbilical cord insertion with a viable fetus located on the septum membrane of dichorionic twin pregnancy near the anterior wall, while the other fetus was observed to have vanished. Next, this umbilical cord was seen to connect to the anterior wall and the placenta developed on the posterior wall later in the pregnancy. As a result, velamentous cord insertion with long membranous umbilical vessels developed at the time of delivery. The present case indicates that the assessment of the cord insertion site during the early gestation period is very important to predict any abnormality of the cord insertion site at the time of delivery. Furthermore, this case is valuable to understand the pathophysiological development of the placenta and velamentous cord insertion. © 2011 The Authors. Journal of Obstetrics and Gynaecology Research © 2011 Japan Society of Obstetrics and Gynecology.

PMID 21651650

http://onlinelibrary.wiley.com/doi/10.1111/j.1447-0756.2011.01555.x/full

2010

Chorioamnionitis: a multiorgan disease of the fetus?

J Perinatol. 2010 Oct;30 Suppl:S21-30. Gantert M, Been JV, Gavilanes AW, Garnier Y, Zimmermann LJ, Kramer BW. Source Department of Obstetrics and Gynecology, Klinikum Osnabrück, Osnabrück, Germany.

Abstract

The bacterial infection of chorion and amnion is a common finding in premature delivery and is referred to as chorioamnionitis. As the mother rarely shows symptoms of a systemic inflammation, the course of chorioamnionitis is frequently asymptomatic and chronic. In contrast, the fetal inflammatory response syndrome represents a separate phenomenon, including umbilical inflammation and increased serum levels of proinflammatory cytokines in the fetus. Ascending maternal infections frequently lead to systemic fetal inflammatory reaction. Clinical studies have shown that antenatal exposure to inflammation puts the extremely immature neonates at a high risk for worsening pulmonary, neurological and other organ development. Interestingly, the presence of chorioamnionitis is associated with a lower rate of neonatal mortality in extremely immature newborns. In the following review, the pathogeneses of inflammation-associated perinatal morbidity are outlined. The concept of fetal multiorganic disease during intrauterine infection is introduced and discussed.

PMID 20877404

Recurrent hydatidiform moles

Eur J Obstet Gynecol Reprod Biol. 2010 May;150(1):3-7. Epub 2010 Feb 19.

Williams D, Hodgetts V, Gupta J. Source Department of Clinical Genetics, Birmingham Women's Hospital, Edgbaston, Birmingham B15 2TG, United Kingdom. Abstract Hydatidiform moles (HMs) are abnormal conceptions of excessive trophoblast development resulting in abnormal human pregnancies with no embryo and cystic degeneration of the chorionic villi. Prompt diagnosis, treatment and follow-up of patients using assays for betahCG from centres that specialise in this condition enable early diagnosis of potential malignant change. Hydatidiform moles occur quite frequently and although recurrence is rare, women who have experienced one molar pregnancy should be aware that they are at an increased risk of a further molar pregnancy in comparison to other women in the general population. For some women multiple molar pregnancies occur. In these women the recurrent molar pregnancies may be non-familial, referred to as recurrent molar hydatidiform moles in this article, or may result from an inherited predisposition, which we refer to as familial recurrent hydatidiform moles. We use the term familial biparental hydatidiform moles (FBHMs) for cases in which the parental contribution to the moles has been investigated and found to be biparental. It is important to recognise, however, that in some apparently non-familial cases, the absence of female siblings, or the absence of female siblings who have tried to conceive, may not allow the inherited nature of the molar pregnancies to manifest in more than one woman and be obviously familial. This review considers our current understanding about the aetiology of HMs and explores the mechanisms of both types of recurrent hydatidiform moles. It highlights the role that genetics can play in determining the origin of multiple molar pregnancies, which should be considered essential in providing women with accurate advice about their risk of recurrence, so allowing them to make appropriate reproductive choices. Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.

PMID 20171777

2009

Guidelines for the management of vasa previa

J Obstet Gynaecol Can. 2009 Aug;31(8):748-60.

[Article in English, French] Gagnon R, Morin L, Bly S, Butt K, Cargill YM, Denis N, Hietala-Coyle MA, Lim KI, Ouellet A, Raciot MH, Salem S; Diagnostic Imaging Committee, Hudon L, Basso M, Bos H, Delisle MF, Farine D, Grabowska K, Menticoglou S, Mundle W, Murphy-Kaulbeck L, Pressey T, Roggensack A; Maternal Fetal Medicine Committee. Source The Society of Obstetricians and Gynaecologists of Canada (SOGC), Montreal, QC.

Abstract OBJECTIVES: To describe the etiology of vasa previa and the risk factors and associated condition, to identify the various clinical presentations of vasa previa, to describe the ultrasound tools used in its diagnosis, and to describe the management of vasa previa. OUTCOMES: Reduction of perinatal mortality, short-term neonatal morbidity, long-term infant morbidity, and short-term and long-term maternal morbidity and mortality. EVIDENCE: Published literature on randomized trials, prospective cohort studies, and selected retrospective cohort studies was retrieved through searches of PubMed or Medline, CINAHL, and the Cochrane Library, using appropriate controlled vocabulary (e.g., selected epidemiological studies comparing delivery by Caesarean section with vaginal delivery; studies comparing outcomes when vasa previa is diagnosed antenatally vs. intrapartum) and key words (e.g., vasa previa). Results were restricted to systematic reviews, randomized control trials/controlled clinical trials, and observational studies. Searches were updated on a regular basis and incorporated into the guideline to October 1, 2008. Grey (unpublished) literature was identified through searching the websites of health technology assessment and health technology assessment-related agencies, clinical practice guideline collections, clinical trial registries, and from national and international medical specialty societies. VALUES: The evidence collected was reviewed by the Diagnostic Imaging Committee and the Maternal Fetal Medicine Committee of the Society of Obstetricians and Gynaecologists of Canada (SOGC) and quantified using the evaluation of evidence guidelines developed by the Canadian Task Force on Preventive Health Care. BENEFITS, HARMS, AND COSTS: The benefit expected from this guideline is facilitation of optimal and uniform care for pregnancies complicated by vasa previa. SPONSORS: The Society of Obstetricians and Gynaecologists of Canada. SUMMARY STATEMENT: A comparison of women who were diagnosed antenatally and those who were not shows respective neonatal survival rates of 97% and 44%, and neonatal blood transfusion rates of 3.4% and 58.5%, respectively. Vasa previa can be diagnosed antenatally, using combined abdominal and transvaginal ultrasound and colour flow mapping; however, many cases are not diagnosed, and not making such a diagnosis is still acceptable. Even under the best circumstances the false positive rate is extremely low. (II-2).

RECOMMENDATIONS:

1. If the placenta is found to be low lying at the routine second trimester ultrasound examination, further evaluation for placental cord insertion should be performed. (II-2B) 2. Transvaginal ultrasound may be considered for all women at high risk for vasa previa, including those with low or velamentous insertion of the cord, bilobate or succenturiate placenta, or for those having vaginal bleeding, in order to evaluate the internal cervical os. (II-2B) 3. If vasa previa is suspected, transvaginal ultrasound colour Doppler may be used to facilitate the diagnosis. Even with the use of transvaginal ultrasound colour Doppler, vasa previa may be missed. (II-2B) 4. When vasa previa is diagnosed antenatally, an elective Caesarean section should be offered prior to the onset of labour. (II-1A) 5. In cases of vasa previa, premature delivery is most likely; therefore, consideration should be given to administration of corticosteroids at 28 to 32 weeks to promote fetal lung maturation and to hospitalization at about 30 to 32 weeks. (II-2B) 6. In a woman with an antenatal diagnosis of vasa previa, when there has been bleeding or premature rupture of membranes, the woman should be offered delivery in a birthing unit with continuous electronic fetal heart rate monitoring and, if time permits, a rapid biochemical test for fetal hemoglobin, to be done as soon as possible; if any of the above tests are abnormal, an urgent Caesarean section should be performed. (III-B) 7. Women admitted with diagnosed vasa previa should ideally be transferred for delivery in a tertiary facility where a pediatrician and blood for neonatal transfusion are immediately available in case aggressive resuscitation of the neonate is necessary. (II-3B) 8. Women admitted to a tertiary care unit with a diagnosis of vasa previa should have this diagnosis clearly identified on the chart, and all health care providers should be made aware of the potential need for immediate delivery by Caesarean section if vaginal bleeding occurs. (III-B). Republished in Int J Gynaecol Obstet. 2010 Jan;108(1):85-9.

PMID 19772710

2008

Chorioamnionitis and increased galectin-1 expression in PPROM --an anti-inflammatory response in the fetal membranes?

Am J Reprod Immunol. 2008 Oct;60(4):298-311.

Than NG, Kim SS, Abbas A, Han YM, Hotra J, Tarca AL, Erez O, Wildman DE, Kusanovic JP, Pineles B, Montenegro D, Edwin SS, Mazaki-Tovi S, Gotsch F, Espinoza J, Hassan SS, Papp Z, Romero R. Source Perinatology Research Branch, NICHD/NIH/DHHS, Wayne State University/Hutzel Women's Hospital, 3990 John R, Box 4, Detroit, MI 48201, USA. nthan@med.wayne.edu Abstract PROBLEM: Galectin-1 can regulate immune responses upon infection and inflammation. We determined galectin-1 expression in the chorioamniotic membranes and its changes during histological chorioamnionitis. METHOD OF STUDY: Chorioamniotic membranes were obtained from women with normal pregnancy (n = 5) and from patients with pre-term pre-labor rupture of the membranes (PPROM) with (n = 8) and without histological chorioamnionitis (n = 8). Galectin-1 mRNA and protein were localized by in situ hybridization and immunohistochemistry. Galectin-1 mRNA expression was also determined by quantitative reverse transcriptase polymerase chain reaction. RESULTS: Galectin-1 mRNA and protein were detected in the amniotic epithelium, chorioamniotic fibroblasts/myofibroblasts and macrophages, chorionic trophoblasts, and decidual stromal cells. In patients with PPROM, galectin-1 mRNA expression in the fetal membranes was higher (2.07-fold, P = 0.002) in those with chorioamnionitis than in those without. Moreover, chorioamionitis was associated with a strong galectin-1 immunostaining in amniotic epithelium, chorioamniotic mesodermal cells, and apoptotic bodies. CONCLUSION: Chorioamnionitis is associated with an increased galectin-1 mRNA expression and strong immunoreactivity of the chorioamniotic membranes; thus, galectin-1 may be involved in the regulation of the inflammatory responses to chorioamniotic infection.

PMID 18691335

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784815/

2007

The Black-White disparity in pregnancy-related mortality from 5 conditions: differences in prevalence and case-fatality rates

Tucker MJ, Berg CJ, Callaghan WM, Hsia J.

Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, Ga 30341-3724, USA. Comment in:

Am J Public Health. 2007 Sep;97(9):1541; author reply 1541. Abstract OBJECTIVES: We sought to determine whether differences in the prevalences of 5 specific pregnancy complications or differences in case fatality rates for those complications explained the disproportionate risk of pregnancy-related mortality for Black women compared with White women in the United States. METHODS: We used national data sets to calculate prevalence and case-fatality rates among Black and White women for preeclampsia, eclampsia, abruptio placentae, placenta previa, and postpartum hemorrhage for the years 1988 to 1999. RESULTS: Black women did not have significantly greater prevalence rates than White women. However, Black women with these conditions were 2 to 3 times more likely to die from them than were White women. CONCLUSIONS: Higher pregnancy-related mortality among Black women from preeclampsia, eclampsia, abruptio placentae, placenta previa, and postpartum hemorrhage is largely attributable to higher case-fatality rates. Reductions in case-fatality rates may be made by defining more precisely the mechanisms that affect complication severity and risk of death, including complex interactions of biology and health services, and then applying this knowledge in designing interventions that improve pregnancy-related outcomes.


Placenta- umbilical cord torsion.jpg


J Clin Pathol. 2004 Aug;57(8):785-92.

Best practice no 178. Examination of the human placenta

J Clin Pathol. 2004 Aug;57(8):785-92.

Hargitai B, Marton T, Cox PM. Source No 1 Department of Obstetrics and Gynecology, Semmelweis University Budapest, Baross u. 27, 1088 Budapest, Hungary.

Abstract

The human placenta is an underexamined organ. The clinical indications for placental examination have no gold standards. There is also inconsistency in the histological reports and the quality is variable. There is great interobserver variability concerning the different entities. Although there are still grey areas in clinicopathological associations, a few mainstream observations have now been clarified. The histopathological examination and diagnosis of the placenta may provide crucial information. It is possible to highlight treatable maternal conditions and identify placental or fetal conditions that can be recurrent or inherited. To achieve optimal benefit from placental reports, it is essential to standardise the method of placenta examination. This article summarises the clinical indications for placenta referral and the most common acknowledged clinicopathological correlations.

PMID 15280396


Fetal environment

Indian J Radiol Imaging. 2008 Nov;18(4):326-44.

Kinare A.

Department of Ultrasound, K.E.M. Hospital, Jehangir Hospital, Pune, India. Abstract The intrauterine environment has a strong influence on pregnancy outcome. The placenta and the umbilical cord together form the main supply line of the fetus. Amniotic fluid also serves important functions. These three main components decide whether there will be an uneventful pregnancy and the successful birth of a healthy baby. An insult to the intrauterine environment has an impact on the programming of the fetus, which can become evident in later life, mainly in the form of cardiovascular diseases, diabetes, and certain learning disabilities. The past two decades have witnessed major contributions from researchers in this field, who have included ultrasonologists, epidemiologists, neonatologists, and pediatricians. Besides being responsible for these delayed postnatal effects, abnormalities of the placenta, umbilical cord, and amniotic fluid also have associations with structural and chromosomal disorders. Population and race also influence pregnancy outcomes to some extent in certain situations. USG is the most sensitive imaging tool currently available for evaluation of these factors and can offer considerable information in this area. This article aims at reviewing the USG-related developments in this area and the anatomy, physiology, and various pathologies of the placenta, umbilical cord, and the amniotic fluid.

PMID: 19774194 http://www.ncbi.nlm.nih.gov/pubmed/19774194

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747450/?tool=pubmed

(good placental abnormalities ultrasound images)