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Maternal and fetal death due to placenta previa/accreta ina concealed pregnancy - a case report  [PDF]
Jovanovi? Bo?idar,?or?evi? Mom?ilo
Medicinski Pregled , 2006, DOI: 10.2298/mpns0606277j
Abstract: Introduction. This is a case report of maternal and fetal death due to major hemorrhage of a patients with placenta previa/accreta in a concealed pregnancy. Bleeding is the leading cause of maternal mortality in obstetrics. Postpartum hemorrhage is the most important cause of maternal death. Placenta accreta is a severe complication involving an abnormal attachment to the uterine wall so that it cannot be easily separated from the uterus. Case report. Due to the fact that one part of the placenta is partially detached, while the other part has grown into the uterus, postpartum hemorrhage may occur with lethal outcome, unless the mother is hospitalized. Fetal death was caused by severe meconium aspiration. One way to prevent such complications is to support legal abortions. .
Brain iron accumulation in unexplained fetal and infant death victims with smoker mothers-The possible involvement of maternal methemoglobinemia
Anna M Lavezzi, Lucijan Mohorovic, Graziella Alfonsi, Melissa F Corna, Luigi Matturri
BMC Pediatrics , 2011, DOI: 10.1186/1471-2431-11-62
Abstract: Histochemical investigations by Prussian blue reaction were made on brain nonheme ferric iron deposits, gaining detailed data on their localization in the brainstem and cerebellum of victims of sudden death and controls. The Gless and Marsland's modification of Bielschowsky's was used to identify neuronal cell bodies and neurofilaments.Our approach highlighted accumulations of blue granulations, indicative of iron positive reactions, in the brainstem and cerebellum of 33% of victims of sudden death and in none of the control group. The modified Bielschowsky's method confirmed that the cells with iron accumulations were neuronal cells.We propose that the free iron deposition in the brain of sudden fetal and infant death victims could be a catabolic product of maternal methemoglobinemia, a biomarker of oxidative stress likely due to nicotine absorption.In mammals, iron is a vital constituent of the oxygen-carrrier hemoglobin (Hb). Human Hb is a tetramer consisting of a pair of α-like globin chains and a pair of β-like chains. Each chain is bound to a prosthetic heme group, consisting of an iron atom in the ferrous state located at the center of a porphyrin ring; this structure has a high affinity for oxygen. Thus, Hb is best known for its oxygen-carrying capacity, which facilitates the transport of oxygen from the lungs to the tissues [1-3].There are numerous causes of hemoglobin-related diseases. A distinction can be made between genetically inherited diseases, such as thalassemias and sickle cell disease [4-6], and acquired disorders, such as methemoglobinemia [7-9], a rare condition characterized by the presence of a greater concentration than the normal physiological range of 1-2% methemoglobin in erythrocytes.Despite their different causes, these Hb disorders all arise from an oxidative denaturation of Hb. Oxidative injury can give rise to hemolysis with the consequent release into the circulation of Hb denatured products and of ferric iron (Fe3+), that is the ox
MATERNAL AND FETAL OUTCOME
MUHAMMAD ALI
The Professional Medical Journal , 2005,
Abstract: Objective: To find the maternal and fetal morbidity and mortality in elective versus emergencycaesarean section. Design: Prospective Setting: Obstetrics and Gynaecology Unit-III, Nishtar Hospital, Multan.Period: One year. Material and methods: 150 patients who underwent caesarean section were evaluated for maternaland fetal complications. Results: Overall intra-operative complications rate was 8.67%. 12 out of 13 complicationsoccurred in emergency group. Postoperative complication was 34.66% and out of it emergency versus elective were90.38% vs 9.62% respectively. Similarly maternal mortality was 666/100,000 in emergency group. Fetal complicationswere also higher in emergency group in this study i.e. 22.2% vs 10.86% in emergency vs elective group. Similarlyprenatal morbidity was 15.04% in emergency group vs 8.10% in elective group. Fetal outcome was 100% in electivevs 94.69% in emergency caesarean section group. In one year period of study caesarean birth rate turned out as17.56% which is quite comparable to the rate in western countries but the rate does not reflect true caesarean birthin a given population because of the fact that this hospital being a tertiary referral center drains only complicated casesof the wide spread area of south Punjab. Higher incidence of caesarean birth can be reduced without increasing themorbidity and mortality. Furthermore, proper sterilization and prophylactic antibodies can reduce the infectious morbidityafter both emergency and elective caesarean section. Conclusions: Higher incidence of emergency caesarean sectionis a major contribution for increased rate of maternal and fetal morbidity and mortality in caesarean deliveries. This canbe reduced by improving the quality and availability of antenatal care of masses. We can also reduce the incidenceof caesarean birth without increasing perinatal morbidity and mortality.
The MicroRNAome of Pregnancy: Deciphering miRNA Networks at the Maternal-Fetal Interface  [PDF]
Jocelyn M. Wessels, Andrew K. Edwards, Kasra Khalaj, Rami T. Kridli, Mallikarjun Bidarimath, Chandrakant Tayade
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072264
Abstract: MicroRNAs (miRNAs) post-transcriptionally regulate a vast network of genes by inhibiting mRNA translation. Aberrant miRNA expression profiles have been implicated in pathologies and physiological processes including pregnancy and angiogenesis. Using our established model of implantation failure and spontaneous fetal loss in pigs (Sus scrofa), 236 miRNAs were profiled and compared between 1) non-pregnant and pregnant endometrium, 2) maternal and fetal tissues, and 3) viable and growth-arrested conceptus attachment sites by microarray and Real-Time PCR. Many significant differences in miRNA expression were observed between each of the aforementioned comparisons, and several were validated by PCR. Results indicated which miRNAs were important during pregnancy, which were elevated on the maternal or fetal side of the maternal-fetal interface, and they implicated the maternal expression of miR-10a, 27a, 29c, 323, 331-5p, 339-3p, 374b-5p, and 935 in the spontaneous loss observed in pigs. Several putative mRNA targets of the miRNAs (elevated in endometrium associated with arresting conceptuses) were assessed by quantitative Real-Time PCR and were depressed, supporting their regulation by miRNAs. Finally, targets were clustered by function to obtain ranked lists of gene networks that indicated which pathways/physiological processes might be important in non-pregnant (extracellular matrix factors) versus pregnant endometrium (nuclear transcription factor regulation), maternal (blood vessel development) versus fetal (neuronal differentiation) tissue, and healthy (extracellular matrix factors) versus arresting (GRAM domain) conceptus attachment sites. Overall, we demonstrate the presence of miRNAs on both sides of the maternal-fetal interface, implicate them in spontaneous fetal loss, and present a unique glimpse into the vast microRNAome of pregnancy.
Ecalmpsia: maternal and fetal outcome
TA Jido
African Health Sciences , 2012,
Abstract: Objective: To determine the incidence of eclampsia and examine the maternal and fetal outcome. Methods: A hundred and twenty consecutive admissions with eclampsia managed in Aminu Kano Teaching Hospital, Kano, Nigeria, were prospectively collated and analysed. Maternal and fetal morbidity and mortality were recorded. Results: The incidence of eclampsia was 1.2% of deliveries. Most (69.2%) of the patients had no antenatal care. In 93 (77.5%), the convulsions were controlled with diazepam, and 22.5% magnesium sulphate. Maternal complications rate was 39.2%, and use of Diazepam for control of convulsions increases complications (RR 3.12, 95% CI = 1.23-7.92, p= 0.02). Case fatality rate was 11.7%, diazepam use failed to achieve significant association with maternal death (RR 8.64, 95% CI = 0.53-140.29, p= 0.13). Stillbirth rate was 22.5% with significant association with diazepam use (RR 7.55, 95% CI= 1.07-53.09, p=0.04). Birth asphyxia was recorded in 39.1% and low birth weight in 25.8%. Conclusion: The incidence of eclampsia in our hospital was very high, with corresponding high maternal and perinatal morbidity and mortality. Increased antenatal screening and use of magnesium sulphate to control convulsions will reduce the incidence and associated morbidity and mortality for both mother and fetus.
Mild Diabetes Models and Their Maternal-Fetal Repercussions  [PDF]
D. C. Damasceno,Y. K. Sinzato,A. Bueno,A. O. Netto,B. Dallaqua,F. Q. Gallego,I. L. Iessi,S. B. Corvino,R. G. Serrano,G. Marini,F. Piculo,I. M. P. Calderon,M. V. C. Rudge
Journal of Diabetes Research , 2013, DOI: 10.1155/2013/473575
Abstract: The presence of diabetes in pregnancy leads to hormonal and metabolic changes making inappropriate intrauterine environment, favoring the onset of maternal and fetal complications. Human studies that explore mechanisms responsible for changes caused by diabetes are limited not only for ethical reasons but also by the many uncontrollable variables. Thus, there is a need to develop appropriate experimental models. The diabetes induced in laboratory animals can be performed by different methods depending on dose, route of administration, and the strain and age of animal used. Many of these studies are carried out in neonatal period or during pregnancy, but the results presented are controversial. So this paper, addresses the review about the different models of mild diabetes induction using streptozotocin in pregnant rats and their repercussions on the maternal and fetal organisms to propose an adequate model for each approached issue. 1. Introduction Diabetes mellitus (DM) is considered a chronic disease characterized by hyperglycemia resulting from insulin resistance and/or insulin secondary deficiency caused by failure in beta cells (β) pancreatic [1]. DM1 is an autoimmune disease in which there are deficiency of insulin and loss of control of blood glucose, caused by the destruction of pancreatic β cells mediated by T cells [2]. DM2 is characterized by β-cell dysfunction and decreased insulin action in some tissues [3]. Another classification is the gestational DM, which occurs by glucose intolerance with variable magnitude. It is first diagnosed during pregnancy and may or may not persist after delivery [4]. Human studies that explore mechanisms responsible for changes caused by diabetes are limited not only for ethical reasons but also by the many uncontrollable variables (diet, socioeconomic factors, nutrition, and genetic factors) that can alter the intrauterine environment and increase congenital malformations. So there is a need to develop a suitable experimental model [5]. The use of animal models provides an essential tool for investigating the molecular mechanisms that control cell growth. The maternal-fetal interface is no exception. Although there are some differences in the organization of rodent versus primate maternal-fetal interface, there are many similarities in the functions and in cell lines that compose it. The induction of experimental diabetes by cytotoxic drugs such as beta-streptozotocin (STZ) is well characterized [6]. Depending on the animal strain used, dose, route of drug administration, and the life period in which STZ is
Expression of Bcl-2 and p53 at the fetal-maternal interface of rhesus monkey
Peng Wei, Xuan Jin, Xue-Sen Zhang, Zhao-Yuan Hu, Chun-Sheng Han, Yi-Xun Liu
Reproductive Biology and Endocrinology , 2005, DOI: 10.1186/1477-7827-3-4
Abstract: Apoptosis plays important roles in placentation and embryonic development [1]. The cells undergoing apoptosis have characteristic structural changes in the nucleus and cytoplasm. The nuclear disintegration involves DNA cleavage into oligonucleosomal length DNA fragments [2-4], and the DNA fragments can be detected by terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end-labelling (TUNEL) technique. Expressions of apoptotic regulatory molecules, such as Fas, Fas ligand, P53, and the proteins of Bcl-2 family, have been reported in human placenta [5-8]. Bcl-2 and P53 are two of the key players in the apoptotic signaling cascades. Bcl-2, a proto-oncogene first discovered in human follicular lymphoma [9], is involved in the inhibition of apoptosis and the survival of a variety of cell types [10]. Bcl-2 protein is located in the membranes of endoplasmic reticulum, nuclear envelope, and mitochondria. Over-expression of Bcl-2 suppresses apoptosis by preventing the activation of caspases that carry out the process. P53 is well known as a tumor suppressor. It is a transcription factor that induces apoptosis mainly through inducing the expression of a batch of redox-related genes [11] and the down-regulating Bcl-2 [12].The expression of Bcl-2 and P53 human placenta has been studied [1,13]. However, their cellular distribution in the implantation site at early stage of pregnancy has not been reported. Because the monkey and the human share a very similar implantation process in terms of timing, morphological changes, and cell types involved [14], we aimed, in the present study, to investigate the expression, localization of Bcl-2 and P53 in the implantation site of the rhesus monkey, in order to gain some insights to the mechanism of time-dependent apoptosis occurring at the fetal-maternal interface.Healthy adult male and female rhesus monkeys (Macaca mulatta) were purchased from the monkey colony of the Primate Research Center (PRC), Ku
Cyclosporine A Enhances Th2 Bias at the Maternal-Fetal Interface in Early Human Pregnancy with Aid of the Interaction between Maternal and Fetal Cells  [PDF]
Hai-Lan Piao, Song-Cun Wang, Yu Tao, Rui Zhu, Chan Sun, Qiang Fu, Mei-Rong Du, Da-Jin Li
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0045275
Abstract: Our previous study has demonstrated that cyclosporine A (CsA) administration in vivo induces Th2 bias at the maternal-fetal interface, leading to improved murine pregnancy outcomes. Here, we investigated how CsA treatment in vitro induced Th2 bias at the human maternal-fetal interface in early pregnancy. The cell co-culture in vitro in different combination of component cells at the maternal-fetal interface was established to investigate the regulation of CsA on cytokine production from the interaction of these cells. It was found that interferon (IFN)-γ was produced only by decidual immune cells (DICs), and not by trophoblasts or decidual stromal cells (DSCs); all these cells secreted interleukin (IL)-4, IL-10, and tumor necrosis factor (TNF)-α. Treatment with CsA completely blocked IFN-γ production in DICs and inhibited TNF-α production in all examined cells. CsA increased IL-10 and IL-4 production in trophoblasts co-cultured with DSCs and DICs although CsA treatment did not affect IL-10 or IL-4 production in any of the cells when cultured alone. These results suggest that CsA promotes Th2 bias at the maternal-fetal interface by increasing Th2-type cytokine production in trophoblasts with the aid of DSCs and DICs, while inhibiting Th1-type cytokine production in DICs and TNF-α production in all investigated cells. Our study might be useful in clinical therapeutics for spontaneous pregnancy wastage and other pregnancy complications.
Muerte fetal inexplicada Unexplained fetal death  [cached]
Janer Sepúlveda,Eliana Maribel Quintero
Revista Colombiana de Obstetricia y Ginecología , 2004,
Abstract: El porcentaje de muertes fetales inexplicadas oscila entre un 21% a 50%; se define como la muerte que ocurre en fetos con edad gestacional mayor de 20 semanas o peso superior a 500 g, en la cual ni la autopsia ni el examen histológico del cordón umbilical, placenta y membranas, se logra identificar la causa. Los factores asociados con muerte fetal inexplicada son edad materna mayor de 35 a os, sobrepeso, nivel educativo menor de 10 a os, cigarrillo y bajo nivel socioeconómico, entre otros. La muerte fetal se relaciona con enfermedades maternas, trombofilia, accidentes del cordón, alteraciones citogenéticas, metabólicas e infecciones congénitas, principalmente. Se realizó una revisión de muerte fetal inexplicada. Reports in the literature demonstrate that the percentage of unexplained fetal death occurs from 21 to 50%. Unexplained fetal death is defined as the demise of the fetus occurring at gestational age beyond 20 weeks or fetal weight of more than 500 g, with a thorough autopsy of the fetus and histology examination of the umbilical cord, placenta, and membranes, fails to demonstrate the cause of death. The following factors are associated with unexplained fetal death, maternal age beyond 35 years, overweight, ten years or less in a school, smoking, low socioeconomic status class and others. Fetal deaths are related to maternal medical disease, thrombophilia, umbilical cord accidents, cytogenetics, metabolic and congenital infections. The following is a review of the main aspects of unexplained fetal death.
Fetal-Maternal Interactions in the Synepitheliochorial Placenta Using the eGFP Cloned Cattle Model  [PDF]
Flavia Thomaz Verechia Pereira, Lilian J. Oliveira, Rodrigo da Silva Nunes Barreto, Andrea Mess, Felipe Perecin, Fabiana Fernandes Bressan, Ligia Garcia Mesquita, Maria Angelica Miglino, José RodrigoValim Pimentel, Paulo Fantinato Neto, Flávio Vieira Meirelles
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0064399
Abstract: Background To investigate mechanisms of fetal-maternal cell interactions in the bovine placenta, we developed a model of transgenic enhanced Green Fluorescent Protein (t-eGFP) expressing bovine embryos produced by nuclear transfer (NT) to assess the distribution of fetal-derived products in the bovine placenta. In addition, we searched for male specific DNA in the blood of females carrying in vitro produced male embryos. Our hypothesis is that the bovine placenta is more permeable to fetal-derived products than described elsewhere. Methodology/Principal Findings Samples of placentomes, chorion, endometrium, maternal peripheral blood leukocytes and blood plasma were collected during early gestation and processed for nested-PCR for eGFP and testis-specific Y-encoded protein (TSPY), western blotting and immunohistochemistry for eGFP detection, as well as transmission electron microscopy to verify the level of interaction between maternal and fetal cells. TSPY and eGFP DNA were present in the blood of cows carrying male pregnancies at day 60 of pregnancy. Protein and mRNA of eGFP were observed in the trophoblast and uterine tissues. In the placentomes, the protein expression was weak in the syncytial regions, but intense in neighboring cells on both sides of the fetal-maternal interface. Ultrastructurally, our samples from t-eGFP expressing NT pregnancies showed to be normal, such as the presence of interdigitating structures between fetal and maternal cells. In addition, channels-like structures were present in the trophoblast cells. Conclusions/Significance Data suggested that there is a delivery of fetal contents to the maternal system on both systemic and local levels that involved nuclear acids and proteins. It not clear the mechanisms involved in the transfer of fetal-derived molecules to the maternal system. This delivery may occur through nonclassical protein secretion; throughout transtrophoblastic-like channels and/or by apoptotic processes previously described. In conclusion, the bovine synepitheliochorial placenta displays an intimate fetal-maternal interaction, similar to other placental types for instance human and mouse.
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