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1
Arzhanova, Olga N., Yulia M. Paikacheva, Anna V. Ruleva, Roman V. Kapustin, and Natalya G. Nichiporuk. "Causes of patients’ obstetric complications after ART." Journal of obstetrics and women's diseases 66, no. 3 (June 15, 2017): 25–33. http://dx.doi.org/10.17816/jowd66325-33.
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Chronic placental insufficiency remains a major cause of perinatal morbidity and mortality. In this regard, prediction of this pregnancy complications becomes particularly relevant. Currently, the frequency of pregnancy as result of assisted reproductive technology (ART) increases among the population. Pregnancies after ART administration compare to naturally occurred are accompanied by a higher risk of miscarriage as well as the formation of placental insufficiency. Older women with endocrine and physical disorder participate in the ART programs most frequently.
The aim of our study was to investigate the course of pregnancy, after ART administration, selection groups threatened by the development of placental insufficiency. 261 medical records of women with singleton pregnancies after ART have been studied. It was the main group. 167 women had a chronic placental insufficiency. There were allocated two groups of pregnant women: group I – 86 patients with placental insufficiency and preeclampsia, group II – 81 women with placental insufficiency indeed. The comparison group consisted of 30 women without infertility with a normal singleton pregnancy. The development of placental insufficiency in the main group (after ART) depends on a large causes of somatic pathology due to age of pregnant women as well. Therefore, patients after ART have to allocate in the high risk group of developing preeclampsia and placental insufficiency.
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Novitskaya, Ekaterina V., Vyacheslav M. Bolotskikh, Victoria O. Polyakova, and Igor M. Kvetnoy. "Current trends in the treatment of chronic placental insufficiency." Journal of obstetrics and women's diseases 69, no. 1 (April 14, 2020): 45–52. http://dx.doi.org/10.17816/jowd69145-52.
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According to literature, intrauterine growth retardation complicates about 5% of pregnancies and is usually caused by chronic placental insufficiency. This article reviews literature data on modern views on the issue. Special attention is paid to the role of melatonin in chronic placental insufficiency and intrauterine growth. Examples of experimental studies demonstrate successful pregnancy course and functional fetal development in animals with melatonin treatment. The data obtained by other researchers on the effect of melatonin on pregnancy, in particular, on chronic placental insufficiency in women, are analyzed. Also in this review, we suggest that melatonin, which is a powerful antioxidant, can reduce morbidity and mortality associated with intrauterine growth retardation.
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Ain, Rupasri, Lindsey N. Canham, and Michael J. Soares. "Dexamethasone-induced intrauterine growth restriction impacts the placental prolactin family, insulin-like growth factor-II and the Akt signaling pathway." Journal of Endocrinology 185, no. 2 (May 2005): 253–63. http://dx.doi.org/10.1677/joe.1.06039.
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Intrauterine growth restriction (IUGR) is a major cause of perinatal death and neonatal morbidity and mortality. There are numerous causes of IUGR. Glucocorticoid-induced IUGR is highly relevant because administration of synthetic glucocorticoids, principally dexamethasone, to women threatened by premature labor is widely used in clinical practice. Fetal growth is directly related to placental growth and development. In this report, we analyzed the effect of dexamethasone on placental development in the rat. Dexamethasone administered between days 13 and 20 of pregnancy not only induced IUGR but also decreased placental mass by approximately 50%. Impaired placental development was associated with dysregulated placental prolactin (PRL) family and insulin-like growth factor-II (IGF-II) gene expression. Furthermore, there was a significant decrease in the activation of Akt/protein kinase B in the junctional zone of the placenta, as assessed by the phosphorylation status of Akt and the pro-apoptotic protein BAD, a downstream target of the Akt signaling pathway. Such changes are consistent with increases in indices of apoptosis, including increased cleavage of poly(ADP-ribose) polymerase (PARP) in the junctional zone of the placenta of dexamethasone-treated rats. In summary, dexamethasone-induced IUGR is associated with placental insufficiency, including dysregulated placental hormone/cytokine gene expression and down-regulation of the IGF-II/Akt signaling pathway resulting in increases in indices of placental apoptosis.
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Hu, Chengjun, Yunyu Yang, Ming Deng, Linfang Yang, Gang Shu, Qingyan Jiang, Shuo Zhang, et al. "Placentae for Low Birth Weight Piglets Are Vulnerable to Oxidative Stress, Mitochondrial Dysfunction, and Impaired Angiogenesis." Oxidative Medicine and Cellular Longevity 2020 (May 25, 2020): 1–12. http://dx.doi.org/10.1155/2020/8715412.
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Intrauterine growth restriction (IUGR) is associated with fetal mortality and morbidity. One of the most common causes of IUGR is placental insufficiency, including placental vascular defects, and mitochondrial dysfunction. In addition, a high level of oxidative stress induces placental vascular lesions. Here, we evaluated the oxidative stress status, mitochondrial function, angiogenesis, and nutrient transporters in placentae of piglets with different birth weights: <500 g (L), 500–600 g (LM), 600–700 g (M), and >700 g (H). Results showed that placentae from the L group had higher oxidative damage, lower adenosine triphosphate and citrate synthase levels, and lower vascular density, compared to those from the other groups. Protein expression of angiogenic markers, including vascular endothelial cadherin, vascular endothelial growth factor A, and platelet endothelial cell adhesion molecule-1, was the lowest in the L group placentae compared to the other groups. In addition, the protein levels of glucose transporters GLUT1 and GLUT3 were downregulated in the L group, compared to the other groups. Furthermore, oxidative stress induced by H2O2 inhibited tube formation and migration in porcine vascular endothelial cells. Collectively, placentae for lower birth weight neonates are vulnerable to oxidative damage, mitochondrial dysfunction, and impaired angiogenesis.
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Manna, Samprikta, Cathal McCarthy, and Fergus P. McCarthy. "Placental Ageing in Adverse Pregnancy Outcomes: Telomere Shortening, Cell Senescence, and Mitochondrial Dysfunction." Oxidative Medicine and Cellular Longevity 2019 (May 22, 2019): 1–11. http://dx.doi.org/10.1155/2019/3095383.
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Preeclampsia is a multisystemic pregnancy disorder and a major cause of maternal and neonatal morbidity and mortality worldwide. The exact pathophysiology of preeclampsia remains unclear; however, it is speculated that the various pathologies can be attributed to impaired vascular remodelling and elevated oxidative stress within the placenta. Oxidative stress plays a key role in cell ageing, and the persistent presence of elevated oxidative stress precipitates cellular senescence and mitochondrial dysfunction, resulting in premature ageing of the placenta. Premature ageing of the placenta is associated with placental insufficiency, which reduces the functional capacity of this critical organ and leads to abnormal pregnancy outcomes. The changes brought about by oxidative insults are irreversible and often lead to deleterious modifications in macromolecules such as lipids and proteins, DNA mutations, and alteration of mitochondrial functioning and dynamics. In this review, we have summarized the current knowledge of placental ageing in the aetiology of adverse pregnancy outcomes and discussed the hallmarks of ageing which could be potential markers for preeclampsia and fetal growth restriction.
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Hart, Bethany, Elizabeth Morgan, and Emilyn U. Alejandro. "Nutrient sensor signaling pathways and cellular stress in fetal growth restriction." Journal of Molecular Endocrinology 62, no. 2 (February 2019): R155—R165. http://dx.doi.org/10.1530/jme-18-0059.
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Fetal growth restriction is one of the most common obstetrical complications resulting in significant perinatal morbidity and mortality. The most frequent etiology of human singleton fetal growth restriction is placental insufficiency, which occurs secondary to reduced utero-placental perfusion, abnormal placentation, impaired trophoblast invasion and spiral artery remodeling, resulting in altered nutrient and oxygen transport. Two nutrient-sensing proteins involved in placental development and glucose and amino acid transport are mechanistic target of rapamycin (mTOR) and O-linked N-acetylglucosamine transferase (OGT), which are both regulated by availability of oxygen. Impairment in either of these pathways is associated with fetal growth restriction and accompanied by cellular stress in the forms of hypoxia, oxidative and endoplasmic reticulum (ER) stress, metabolic dysfunction and nutrient starvation in the placenta. Recent evidence has emerged regarding the potential impact of nutrient sensors on fetal stress response, which occurs in a sexual dysmorphic manner, indicating a potential element of genetic gender susceptibility to fetal growth restriction. In this mini review, we focus on the known role of mTOR and OGT in placental development, nutrient regulation and response to cellular stress in human fetal growth restriction with supporting evidence from rodent models.
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Revina, D. B., A. V. Balatskiy, E. B. Larina, N. A. Oleynikova, G. A. Mishurovsky, P. G. Malkov, L. M. Samokhodskaya, O. B. Panina, and V. A. Tkachuk. "Associations between SNPS in the genes encoding urokinase system proteins and the risk of placental insufficiency." Bulletin of Russian State Medical University, no. 2019;6 (2019): 49–56. http://dx.doi.org/10.24075/brsmu.2019.076.
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Placental insufficiency (PI) and its complications are multifactorial conditions that cause perinatal morbidity and mortality. Since the urokinase system is involved in placentation, it should have a role in PI pathogenesis. The aim of this work was to study the associations between single nucleotide polymorphisms (SNPs) of genes coding for protein components of the urokinase system and PI, as well as investigate their effect on the expression of these proteins in the placenta and placental structure. We examined 114 women with uncomplicated pregnancy and delivery, 48 female patients with pre-eclampsia and/or intrauterine growth restriction (IUGR), and 95 newborns, (pre-eclampsia and/or IUGR: n = 60; uncomplicated pregnancy and delivery: n = 35). Maternal and fetal DNAs were genotyped using real-time PCR. Placenta fragments were subjected to morphometry and immunohistochemistry. We discovered the associations between PI and the maternal C allele of rs4065 (PI group: СС-СТ 64.1%, TT 35.9%; controls: СС-СТ 25.6%, TT 74.49%; OR (95%CI): 6.83 (2.63–17.79)), the maternal A allele of rs2302524 (GG-GA 20.5%, AA 79.5% vs. GG-GA 48.1%, AA 51.9%, OR (95%CI): 0.27 (0.1–0.71)), the fetal C allele of rs4065 (СС-СТ 76.4 %, TT 23.6% vs. СС-СТ 69.6%, TT 30.4%, OR (95%CI): 1.37 (0.45–4.17)), and the fetal C allele of rs344781 (TT-TC 69.1%, СС 30.9% vs. TT-TC 95.7%, СС 4.3%, OR (95% CI): 5.02 (1.07–23.6)). The multivariate analysis confirmed the significance of the fetal rs4065 genotype. In patients with PI, uPA expression was lower (ME (95%CI): 116.45 (100.5; 128.74) vs. 126.09 (113.76; 139.19); р < 0.05). No associations were established between SNPs and protein expression. The degree of vascularization depended on the maternal rs4065 genotype (the stroma-to-vessel ratio for the CC genotype was 0.17 (0.15; 0.19); for the CT genotype, 0.18 (0.15; 0.21) and for the TT genotype, 0.23 (0.2; 0.27); p < 0.05). We conclude that high placental uPA and the presence of the fetal TT rs4065 genotype are protective against the risk of PI.
8
Murthi, Padma, Gayathri Rajaraman, Shaun Patrick Brennecke, and Bill Kalionis. "The Role of Placental Homeobox Genes in Human Fetal Growth Restriction." Journal of Pregnancy 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/548171.
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Fetal growth restriction (FGR) is an adverse pregnancy outcome associated with significant perinatal and paediatric morbidity and mortality, and an increased risk of chronic disease later in adult life. One of the key causes of adverse pregnancy outcome is fetal growth restriction (FGR). While a number of maternal, fetal, and environmental factors are known causes of FGR, the majority of FGR cases remain idiopathic. These idiopathic FGR pregnancies are frequently associated with placental insufficiency, possibly as a result of placental maldevelopment. Understanding the molecular mechanisms of abnormal placental development in idiopathic FGR is, therefore, of increasing importance. Here, we review our understanding of transcriptional control of normal placental development and abnormal placental development associated with human idiopathic FGR. We also assess the potential for understanding transcriptional control as a means for revealing new molecular targets for the detection, diagnosis, and clinical management of idiopathic FGR.
9
Moore, Mackenzie, Nandini Avula, Seokwon Jo, Megan Beetch, and Emilyn U. Alejandro. "Disruption of O-Linked N-Acetylglucosamine Signaling in Placenta Induces Insulin Sensitivity in Female Offspring." International Journal of Molecular Sciences 22, no. 13 (June 28, 2021): 6918. http://dx.doi.org/10.3390/ijms22136918.
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Placental dysfunction can lead to fetal growth restriction which is associated with perinatal morbidity and mortality. Fetal growth restriction increases the risk of obesity and diabetes later in life. Placental O-GlcNAc transferase (OGT) has been identified as a marker and a mediator of placental insufficiency in the setting of prenatal stress, however, its role in the fetal programming of metabolism and glucose homeostasis remains unknown. We aim to determine the long-term metabolic outcomes of offspring with a reduction in placental OGT. Mice with a partial reduction and a full knockout of placenta-specific OGT were generated utilizing the Cre-Lox system. Glucose homeostasis and metabolic parameters were assessed on a normal chow and a high-fat diet in both male and female adult offspring. A reduction in placental OGT did not demonstrate differences in the metabolic parameters or glucose homeostasis compared to the controls on a standard chow. The high-fat diet provided a metabolic challenge that revealed a decrease in body weight gain (p = 0.02) and an improved insulin tolerance (p = 0.03) for offspring with a partially reduced placental OGT but not when OGT was fully knocked out. Changes in body weight were not associated with changes in energy homeostasis. Offspring with a partial reduction in placental OGT demonstrated increased hepatic Akt phosphorylation in response to insulin treatment (p = 0.02). A partial reduction in placental OGT was protective from weight gain and insulin intolerance when faced with the metabolic challenge of a high-fat diet. This appears to be, in part, due to increased hepatic insulin signaling. The findings of this study contribute to the greater understanding of fetal metabolic programming and the effect of placental OGT on peripheral insulin sensitivity and provides a target for future investigation and clinical applications.
10
Hornbuckle, Janet, and James G. Thornton. "The fetal circulatory response to chronic placental insufficiency and relation to pregnancy outcome." Fetal and Maternal Medicine Review 10, no. 3 (August 1998): 137–52. http://dx.doi.org/10.1017/s0965539598000321.
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Chronic fetal growth restriction is associated with both increased perinatal mortality and impaired neurodevelopment. Although it is a much more important cause of fetal neurological damage than intrapartum birth asphyxia, it is more difficult to treat, since the main intervention, timed delivery, carries its own risks. Since it is associated with a range of circulatory changes, which may also cause fetal damage, understanding these may improve management. In this article we review these fetal circulatory changes and assess their significance for predicting perinatal and long term neurodevelopmental outcome. We describe the Doppler assessment techniques, their clinical role in prediction of adverse outcome and the pathogenesis of brain injury in the preterm growth restricted fetus.
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Cosmi, Erich, Tiziana Fanelli, Silvia Visentin, Daniele Trevisanuto, and Vincenzo Zanardo. "Consequences in Infants That Were Intrauterine Growth Restricted." Journal of Pregnancy 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/364381.
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Intrauterine growth restriction is a condition fetus does not reach its growth potential and associated with perinatal mobility and mortality. Intrauterine growth restriction is caused by placental insufficiency, which determines cardiovascular abnormalities in the fetus. This condition, moreover, should prompt intensive antenatal surveillance of the fetus as well as follow-up of infants that had intrauterine growth restriction as short and long-term sequele should be considered.
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Choudhary, Rana A., Khyati Patrawala, Kavita Desai, and Kedar Ganla. "Sildenafil citrate therapy in absent end diastolic flow in umbilical artery in an early onset fetal growth restriction (FGR) fetus." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 12 (November 26, 2018): 5173. http://dx.doi.org/10.18203/2320-1770.ijrcog20184988.
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Fetal growth restriction (FGR), a pregnancy complication still poses as a challenge for obstetricians worldwide. This is because of its association with severe morbidity and mortality outcomes. Obstetrical management becomes a dilemma in determining the optimal time of delivery and weighing the risks of prematurity against the risks of a potentially hostile intrauterine environment. There may be placental insufficiency characterized by insufficient blood flow in the umbilical artery. This is termed as abnormal umbilical artery flow with absent or reversed end diastolic flow on Doppler USG. Worsening of this condition demands an earlier delivery of the fetus. Authors report a case of structurally normal foetus showing severe early onset FGR with absent end diastolic flow in umbilical artery on Doppler, which was managed using vaginal Sildenafil citrate. Sildenafil citrate led to improvement in uterine artery and umbilical artery Doppler parameters; thereby improving the utero-placental blood flow with a favorable fetal outcome at delivery. The gestation was prolonged by 51 days. Thus, Sildenafil citrate can be used as promising agent in early onset FGR in selected cases.
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Kapustin, R. V., E. V. Kopteeva, E. N. Alexeenkova, E. M. Tsybuk, and O. N. Arzhanova. "Analysis of Risk Factors and Perinatal Mortality Structure in Pregnant Patients with Diabetes Mellitus." Doctor.Ru 20, no. 6 (2021): 46–52. http://dx.doi.org/10.31550/1727-2378-2021-20-6-46-52.
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Study Objective: To analyse risk factors and perinatal mortality structure in patients with various types of diabetes mellitus (DM) over the last 30 years in specialised settings. Study Design: retrospective single-site cohort study. Materials and Methods. We have studied 42 medical records containing cases of perinatal death of foetus or newborn in 1988–2018 in patients with DM1 (n = 20), DM2 (n = 10), gestational DM (n = 12). Study Results. The most common complication in pregnancy was preeclampsia combined with chronic placental insufficiency (47.6%). The most common risk factors of perinatal death were inadequate glycemic control in 1st trimester (69.0%), absence of preconception preparations (66.7%), preconception overweight and obesity (42.8%), and chronic arterial hypertension (28.6%). There were 38.1% antenatal deaths, 16.7% intranatal deaths, and 45.2% cases of postnatal mortality. The major causes of perinatal foetal mortality in 26.2% cases were placental disorders, 16.7% were associated with foetus growth retardation, diabetic fetopathy and respiratory distress syndrome. Conclusion. DM during pregnancy was associated with a higher risk of perinatal death. Timely preconception preparation, BMI normalization and a consolidated approach to term and mode of delivery can reduce the risk of perinatal mortality in women with various types of DM. Keywords: diabetes mellitus, gestational diabetes mellitus, perinatal mortality, stillbirth, obesity, preeclampsia
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Kumar, Ajay, Anuj Singh, and V. B. Tripathi. "Previous caesarean scar rupture: mortality averted a case report." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 9, no. 11 (October 27, 2020): 4719. http://dx.doi.org/10.18203/2320-1770.ijrcog20204842.
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Uterine rupture at the site of a previous cesarean section scar is an uncommon but catastrophic complication of pregnancy by associated with significant foetal and maternal mortality and morbidity. A 31-year old woman, G6P3A2L1 with previous lower segment cesarian section (LSCS), booked case was admitted at 37 week of gestation with complaint of leaking per vaginal (P/V) in our tertiary care centre. Patient had spontaneous labor pain, which subsided after few contractions and sustained hemorrhagic shock with utero placental insufficiency due to previous LSCS scar rupture. Due diligence and expeditious caesarean management strategy needs to be adopted in parturient with previous caesarean patients owing due to risk of scar rupture. Ultrasonography is a useful tool which can be used to assess women with previous cesarean section to carry out risk stratification for subsequent pregnancies.
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Hu and Zhang. "MicroRNAs in Uteroplacental Vascular Dysfunction." Cells 8, no. 11 (October 29, 2019): 1344. http://dx.doi.org/10.3390/cells8111344.
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Pregnancy complications of preeclampsia and intrauterine growth restriction (IUGR) are major causes of maternal and perinatal/neonatal morbidity and mortality. Although their etiologies remain elusive, it is generally accepted that they are secondary to placental insufficiency conferred by both failure in spiral artery remodeling and uteroplacental vascular malfunction. MicroRNAs (miRNAs) are small no-coding RNA molecules that regulate gene expression at the post-transcriptional level. Increasing evidence suggests that miRNAs participate in virtually all biological processes and are involved in numerous human diseases. Differentially expressed miRNAs in the placenta are typical features of both preeclampsia and IUGR. Dysregulated miRNAs target genes of various signaling pathways in uteroplacental tissues, contributing to the development of both complications. In this review, we provide an overview of how aberrant miRNA expression in preeclampsia and IUGR impacts the expression of genes involved in trophoblast invasion and uteroplacental vascular adaptation.
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Alves de Alencar Rocha, Anna Karynna, Beth J. Allison, Tamara Yawno, Graeme R. Polglase, Amy E. Sutherland, Atul Malhotra, Graham Jenkin, Margie Castillo-Melendez, and Suzanne L. Miller. "Early- versus Late-Onset Fetal Growth Restriction Differentially Affects the Development of the Fetal Sheep Brain." Developmental Neuroscience 39, no. 1-4 (2017): 141–55. http://dx.doi.org/10.1159/000456542.
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Fetal growth restriction (FGR) is a common complication of pregnancy, principally caused by suboptimal placental function, and is associated with high rates of perinatal mortality and morbidity. Clinical studies suggest that the time of onset of placental insufficiency is an important contributor towards the neurodevelopmental impairments that are evident in children who had FGR. It is however currently unknown how early-onset and late-onset FGR differentially affect brain development. The aim of this study was to examine neuropathology in early-onset and late-onset FGR fetal sheep and to determine whether they differentially alter brain development. We induced placental insufficiency and FGR via single umbilical artery ligation at either 88 days (early-onset) or 105 days (late-onset) of fetal sheep gestation (term is approx. 147 days), reflecting a period of rapid white matter brain development. Fetal blood samples were collected for the first 10 days after surgery, and all fetuses were sacrificed at 125 days' gestation for brain collection and subsequent histopathology. Our results show that early-onset FGR fetuses became progressively hypoxic over the first 10 days after onset of placental insufficiency, whereas late-onset FGR fetuses were significantly hypoxic compared to controls from day 1 after onset of placental insufficiency (SaO2 46.7 ± 7.4 vs. 65.7 ± 3.9%, respectively, p = 0.03). Compared to control brains, early-onset FGR brains showed widespread white matter injury, with a reduction in both CNPase-positive and MBP-positive density of staining in the periventricular white matter (PVWM), subcortical white matter, intragyral white matter (IGWM), subventricular zone (SVZ), and external capsule (p < 0.05 for all). Total oligodendrocyte lineage cell counts (Olig-2-positive) did not differ across groups, but mature oligodendrocytes (MBP-positive) were reduced, and neuroinflammation was evident in early-onset FGR brains with reactive astrogliosis (GFAP-positive) in the IGWM and cortex (p < 0.05), together with an increased number of Iba-1-positive activated microglia in the PVWM, SVZ, and cortex (p < 0.05). Late-onset FGR was associated with a widespread reduction of CNPase-positive myelin expression (p < 0.05) and a reduced number of mature oligodendrocytes in all white matter regions examined (p < 0.05). NeuN-positive neuronal cell counts in the cortex were not different across groups; however, the morphology of neuronal cells was different in response to placental insufficiency, most notable in the early-onset FGR fetuses, but it was late-onset FGR that induced caspase-3-positive apoptosis within the cortex. This study demonstrates that early-onset FGR is associated with more widespread white matter injury and neuroinflammation; however, both early- and late-onset FGR are associated with complex patterns of white and grey matter injury. These results indicate that it is the timing of the onset of fetal compromise relative to brain development that principally mediates altered brain development associated with FGR.
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Zefirova, T. P., E. Yu Yupatov, and R. R. Mukhametova. "Iron deficiency anemia in obstetrics." Russian Journal of Woman and Child Health 4, no. 1 (2021): 53–58. http://dx.doi.org/10.32364/2618-8430-2021-4-1-53-58.
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This paper discusses the anemia of pregnancy that is a global issue affecting tens of millions of women. The prevalence of anemia increases as pregnancy progresses and is maximum in the third trimester having a negative impact on pregnancy course. Major causes of unfavorable perinatal outcomes related to anemia are addressed. The authors highlight that anemia of pregnancy increases the rate of stillbirths, premature birth, and intrauterine growth restriction. The mechanisms accounting for placental insufficiency (e.g., circulatory hypoxia, abnormal blood rheology, microcirculatory abnormalities) are described. Current data on the increased risk of maternal death in anemia are discussed. Its major causes are hemorrhages, infectious septic complications, and thromboses. Diagnostic and therapeutic modalities for anemia are emphasized. Personalized management strategy and rational choice of iron products require an understanding of iron metabolism and the knowing of the role of hepcidin-mediated inhibition of the mechanism of iron metabolism. KEYWORDS: iron deficiency anemia, pregnancy, maternal mortality, placental insufficiency, hep-cidin, pre-pregnancy preparation, hemodilution. FOR CITATION: Zefirova T.P., Yupatov E.Yu., Mukhametova R.R. Iron deficiency anemia in obstetrics. Russian Journal of Woman and Child Health. 2021;4(1):53–58. DOI: 10.32364/2618-8430-2021-4-1-53-58.
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Maeda, Kenji J., Kurt C. Showmaker, Ashley C. Johnson, Michael R. Garrett, and Jennifer M. Sasser. "Spontaneous superimposed preeclampsia: chronology and expression unveiled by temporal transcriptomic analysis." Physiological Genomics 51, no. 8 (August 1, 2019): 342–55. http://dx.doi.org/10.1152/physiolgenomics.00020.2019.
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Preeclampsia (PE), a multifactorial pregnancy-specific syndrome accounting for up to 8% of pregnancy complications, is a leading cause of maternal and fetal morbidity and mortality. PE is also associated with long-term risk of hypertension and stroke for both mother and fetus. Currently, the only “cure” is delivery of the baby and placenta, largely because the pathogenesis of PE is not yet fully understood. PE is associated with impaired vascular remodeling at the maternal-fetal interface and placental insufficiency; however, specific factors contributing to this impairment have not been identified. To identify molecular pathways involved in PE, we examined temporal transcriptomic changes occurring within the uterus, uterine implantation sites, and placentae from the Dahl salt-sensitive (Dahl S) rat model of superimposed PE compared with Sprague Dawley (SD) rats. We hypothesized that targeted gene analysis and whole transcriptome analysis would identify genetic factors that contribute to development of the preeclamptic phenotype in the Dahl S rat and unveil novel biomarkers, therapeutic targets, and mechanistic pathways in PE. Quantitative real-time PCR (qRT-PCR) and whole genome microarray analysis were performed on isolated total RNA from uterus ( day 0), uterine implantation sites ( days 7 and 10), and placenta ( days 14 and 20). We found 624, 332, 185, and 366 genes to be differentially expressed between Dahl S (PE) and SD (normal pregnancy) on days 0, 7, 10, and 14, respectively. Our data revealed numerous pathways that may play a role in the pathophysiology of spontaneous superimposed PE and allow for further investigation of novel therapeutic targets and biomarker development.
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Sukharev, A. B., T. V. Kopytsia, and V. I. Boyko. "FEATURES OF THE COURSE OF MULTIPLE PREGNANCY AGAINST THE BACKGROUND OF FETAL GROWTH RETARDATION." Eastern Ukrainian Medical Journal 8, no. 4 (2020): 433–38. http://dx.doi.org/10.21272/eumj.2020;8(4):433-438.
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In most European countries in recent years, the frequency of multiple births ranges from 11 to 14 per 1000. These pregnancies have a high number of complications. Perinatal mortality in multiple births is more than 6 times higher than in singleton pregnancies. Severe neurological abnormalities under the age of 1 year have from 10% to 25% of twins. According to most researchers, the main cause of perinatal losses in multiple births is deep prematurity and severe fetal growth delay. It has now been proven that placental insufficiency is the main reason of developmental delay, discordant fetal growth, antenatal death of one of the fetuses. A fetus that develops and is born in conditions of chronic placental insufficiency is more vulnerable and at high risk of developing perinatal pathology. The purpose of the research was to study the frequency and structure of complications of the pregnancy and labor of women with multiple pregnancies, complicated uteroplacental insufficiency and fetal discordance. The study was carried out at the city clinical maternity house during 2013–2019. The information was gathered from literature and by interviewing pregnant women with twins. 20 pregnant women (group I) with dichorionic, diamnionic twins with the presence of placental insufficiency and fetal discordance of more than 20%. Group II consisted of 20 pregnant women with twins but fetal discordance did not exceed 20%. However, the control group ІІІ consisted of 30 women without complications and ended in physiological labor. The general, somatic, obstetric and gynecological anamnesis, especially the course of pregnancy, childbirth, the state of the cervix by vaginal and ultrasound examination were studied. The results of the study show that in the anamnesis of pregnant women with fetal discordance, take place in vitro fertilization and infections of the respiratory and urinary tract. Multiple pregnancies which were accompanied by fetal discordance exceeding 20% is accompanied by impaired uteroplacental circulation. Labor with twins complicated by impaired uteroplacental circulation occurs in a large number of complications. The results can be applied to the using various medications for the correction of disorders of the uteroplacental circulation.
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Procenko, Ekaterina A., Margarita M. Gurova, Elena V. Podsvirova, Svetlana V. Volobueva, Tatiana A. Romanova, Valentina S. Popova, and Yuliya V. Burtseva. "Regional features of early neonatal mortality (data on the Belgorod region for the period 2012-2015)." Pediatrician (St. Petersburg) 9, no. 1 (March 15, 2018): 61–67. http://dx.doi.org/10.17816/ped9161-67.
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Early neonatal mortality occupies one of the leading places in the structure of infant mortality, which determines the medical and social significance of this problem. The aim of the study was to study regional features of the structure and causes of early neonatal mortality. The study was carried out on the basis of data from the Department of Pediatric Pathology of the Belgorod Regional Pathoanatomical Bureau for the period from January 2012 to December 2015. It was found that early neonatal mortality decreased from 2.9‰ in 2012 to 2.5‰ in 2015. It was shown the presence of the two main peaks of mortality occurring on the first and third days of a child's life. It was established that the main proportion of children with early neonatal death was children with extremely low body weight (34.7%). These children were born in the result of premature birth – in 60% of cases in 2012 with the growth of the indicator to 71.4% in 2015. The main causes of early neonatal mortality were: 1) respiratory disorders – respiratory distress syndrome of newborns, pneumonia, and aspiration of meconium – 51%; 2) congenital anomalies – multiple congenital malformations and congenital heart defects – 12.5%; 3) non-traumatic intraventricular hemorrhages – 13.5%. 61.2% of pregnant women had pathological conditions during pregnancy. Among the pathological conditions of pregnant women, most often identified chronic feto-placental insufficiency and intrauterine infections with infection of the placenta (moderate and severe) in 78% of cases. Among the pathogens of intrauterine infections dominated chlamydia (more than a third of cases), fungi of the genus Candida, ureaplasma and mycoplasma.
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Kezic, Aleksandra, Radmila Sparic, Biljana Stojimirovic, and Vera Milenkovic. "Multiorgan dysfunction in a gravid woman with placental abruption and disseminated intravascular coagulation." Srpski arhiv za celokupno lekarstvo 135, no. 7-8 (2007): 465–67. http://dx.doi.org/10.2298/sarh0708465k.
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The most frequent obstetrical cause of coagulation disorders as disseminated intravascular coagulation is placental abruption, which can be found in women without any apparent clinical disturbances or in the state of established preeclampsia. Hypertension occurs in 5-8% of all pregnancies and may be complicated by preeclampsia. Preeclampsia is a complex clinical syndrome with insufficiently clear pathophysiology based on the damage of the vascular endothelium. As a result of this, generalized endothelial disruption in preeclampsia, a multiorgan dysfunction, can develop, most frequently reflected in the clinical presentation with hematological and renal disturbances and with a disordered function of the liver and central nervous system. We are presenting a case of a gravid woman with poorly regulated hypertension that resulted from development of preeclampsia, later complicated by placental abruption and disseminated intravascular coagulation (DIC) with multi-organ dysfunction. The importance of rapid recognition of coagulation disorder and the attempt at surgical treatment aiming at removal of the triggering mechanisms of DIC was shown, suggesting all the symptomatic therapeutic measures would be ineffective. Although our patient was surgically treated in the phase of generalized disorder characterized by development of coma, acute respiratory distress syndrome and renal insufficiency when mortality was 70%, the recovery of functions of all involved organs was achieved, except for the renal function that required chronic haemodialysis treatment.
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Matar, Emadeldin. "Study of Maternal and Fetal Doppler Velocimetry, Histopathology of Placental Bed in Diabetic Pregnancy and Its Correlation to Fetal Outcome." Women Health Care and Issues 4, no. 3 (May 12, 2021): 01–10. http://dx.doi.org/10.31579/2642-9756/059.
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Diabetes mellitus still represents an important medical problem during pregnancy, causing perinatal morbidity and mortality. Despite improved outcome reflected by a steep decline in perinatal mortality over the past few decades, controversy still exists regarding the care of the pregnant woman with both pre-existing and gestational Diabetes Mellitus. Doppler ultrasound is especially valuable during pregnancy because fetal maternal and placental circulations can be studied. The aim of this work was to study the vascular changes in the uteroplacental and fetoplacental circulations, and to correlate these findings with histopathology of the placenta and placental bed, which may occur in association with diabetic pregnancies. The study was carried out on 100 pregnant women of comparable age and parity. They were divided into 2 groups. The control group comprising 20 normal non-diabetic pregnant women and the normotensive diabetic group comprising 80 pregnant diabetic women. All were singleton pregnancies of 34 weeks or more and were delivered by C.S the control and the study cases were subjected to history taking and thorough physical examination. They were also subjected to ultrasonographic examination for fetal biometric parameters and for Doppler examination. Doppler examination included umbilical artery, uterine arteries fetal middle cerebral artery. At the time of C.S the placenta and placental bed biopsy was obtained. After delivery, the Apgar score of the newborn was assessed at 1 and 5 minutes, the body weight was measured, and the fetus was followed up for any complications. Result: There was a positive correlation between the umbilical artery PI and the mean blood glucose levels indicating that poor diabetic control is probably associated with increased umbilical artery PI. However, there was no significant difference between the mean value of the umbilical artery PI in the diabetic and control groups. The uterine arteries Doppler indices showed no significant findings between the diabetic and the control groups. Neither did the uterine arteries Doppler indices show a correlation with the mean blood glucose levels. There was no significant difference between the middle cerebral artery PI in the diabetic and control groups. This observation indicates that there was no redistribution in the fetal circulation in the fetuses of the diabetic group. There was also non correlation between the MCA Doppler indices and the glycemic control. Histopathologic studies of the placental bed showed marked difference between the diabetic group and the control group as regards lack of physiologic changes and arteriosclerotic changes, which emphasizes the effect of diabetes on the placental bed vasculature. Conclusion: Abnormal umbilical artery waveform analysis is one of significant predictors of fetal compromise in diabetic pregnancy, but fetal compromise can occur in association with normal Doppler waveform analysis. In maternal diabetes the classic redistribution seen in fetal hypoxemia due to uteroplacental insufficiency may not occur in diabetic patient even in severely compromised fetuses. In maternal diabetes mellitus, maternal glycemic control has no effect on impedance to flow in the uterine and middle cerebral arteries. No relationship was found between the uterine or umbilical arteries Doppler indices and the placental bed decidual vascular pathology in diabetic pregnancies. There was no correlation between placental findings and the Doppler waveform analysis of the umbilical and the uterine arteries.
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Pham Minh, Son, Huy Nguyen Vu Quoc, and Vinh Tran Dinh. "INTRAUTERINE GROWTH RETARDATION - A REVIEW ARTICLE." Volume 8 Issue 6 8, no. 6 (December 2018): 184–95. http://dx.doi.org/10.34071/jmp.2018.6.25.
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Small for gestational age (SGA) and fetal growth restriction (FGR) is difficult to define exactly. In this pregnancy condition, the fetus does not reach its biological growth potential as a consequence of impaired placental function, which may be because of a variety of factors. Fetuses with FGR are at risk for perinatal morbidity and mortality, and poor long-term health outcomes, such as impaired neurological and cognitive development, and cardiovascular and endocrine diseases in adulthood. At present no gold standard for the diagnosis of SGA/FGR exists. The first aim of this review is to: summarize areas of consensus and controversy between recently published national guidelines on small for gestational age or fetal growth restriction; highlight any recent evidence that should be incorporated into existing guidelines. Another aim to summary a number of interventions which are being developed or coming through to clinical trial in an attempt to improve fetal growth in placental insufficiency. Key words: fetal growth restriction (FGR), Small for gestational age (SGA)
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Mureșan, Daniel, Ioana Cristina Rotar, and Florin Stamatian. "The usefulness of fetal Doppler evaluation in early versus late onset intrauterine growth restriction. Review of the literature." Medical Ultrasonography 18, no. 1 (March 1, 2016): 103. http://dx.doi.org/10.11152/mu.2013.2066.181.dop.
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Intrauterine growth restriction (IUGR) represents a serious condition that can lead to increased perinatal morbidity, mortality and postnatal impaired neurodevelopment. There are two distinct phenotypes of IUGR: early onset and late onset IUGR with different onset, patterns of evolution and fetal Doppler profile. In early onset preeclampsia the main Doppler modifications are at the level of umbilical artery, with progressive augmentation of the pulsatility index to absent or reverse end diastolic flow. The modifications of the cerebral, cardiac and ductus venosus circulation are generally present, but with different sequences. The late onset IUGR is determined by third trimester placental insufficiency that entails fetal hypoxia. The cerebro-placental ratio (CPR) and the pulsatility index of the middle cerebral artery (PI MCA) seems to be the main markers for both diagnosis and obstetrical management while umbilical Doppler PI is frequently normal. Also the sequence of Doppler alterations is neither specific nor complete. New protocols for the diagnosis and management of late onset IUGR need to be implemented.
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Heazell, Alexander E. P., Christopher J. Weir, Sarah J. E. Stock, Catherine J. Calderwood, Sarah Cunningham Burley, J. Frederik Froen, Michael Geary, et al. "Can promoting awareness of fetal movements and focusing interventions reduce fetal mortality? A stepped-wedge cluster randomised trial (AFFIRM)." BMJ Open 7, no. 8 (August 2017): e014813. http://dx.doi.org/10.1136/bmjopen-2016-014813.
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BackgroundIn 2013, the stillbirth rate in the UK was 4.2 per 1000 live births, ranking 24th out of 49 high-income countries, with an annual rate of reduction of only 1.4% per year. The majority of stillbirths occur in normally formed infants, with (retrospective) evidence of placental insufficiency the most common clinical finding. Maternal perception of reduced fetal movements (RFM) is associated with placental insufficiency and increased risk of subsequent stillbirth.This study will test the hypothesis that the introduction of a package of care to increase women's awareness of the need for prompt reporting of RFM and standardised management to identify fetal compromise with timely delivery in confirmed cases, will reduce the rate of stillbirth. Following the introduction of a similar intervention in Norway the odds of stillbirth fell by 30%, but the efficacy of this intervention (and possible adverse effects and implications for service delivery) has not been tested in a randomised trial.MethodsWe describe a stepped-wedge cluster trial design, in which participating hospitals in the UK and Ireland will be randomised to the timing of introduction of the care package. Outcomes (including the primary outcome of stillbirth) will be derived from detailed routinely collected maternity data, allowing us to robustly test our hypothesis. The degree of implementation of the intervention will be assessed in each site. A nested qualitative study will examine the acceptability of the intervention to women and healthcare providers and identify process issues including barriers to implementation.Ethics and disseminationEthical approval was obtained from the Scotland A Research Ethics Committee (Ref 13/SS/0001) and from Research and Development offices in participating maternity units. The study started in February 2014 and delivery of the intervention completed in December 2016. Results of the study will be submitted for publication in peer-reviewed journals and disseminated to local investigating sites to inform education and care of women presenting with RFM.Trial registration numberwww.clinicaltrials.govNCT01777022.VersionProtocol Version 4.2, 3 February 2017.
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ANG, Christine, and Mary Ann LUMSDEN. "Diabetes and the maternal resistance vasculature." Clinical Science 101, no. 6 (November 21, 2001): 719–29. http://dx.doi.org/10.1042/cs1010719.
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Diabetes is the most common endocrine disorder worldwide, with complications that include the development of both macro- and micro-vascular disease that contribute significantly to patient morbidity and mortality. The severity of diabetic complications is amplified during pregnancy, resulting in a higher incidence of adverse pregnancy outcomes such as pre-eclampsia, placental insufficiency and stillbirth than in non-diabetics. Vascular dysfunction is thought to underlie many of these complications, with the greatest impact occurring at the level of the resistance vasculature, where alterations in vascular reactivity can significantly affect blood flow and tissue perfusion. It is likely that problems associated with diabetic pregnancies are related, in part, to abnormal vascular function, particularly dysfunction of the vascular endothelium.
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Vdovichenko, Yu P., and V. O. Golyanovskyi. "Determining diagnostic markers of intrautering growth retardation in early pregnancy." Reproductive health of woman 1 (February 26, 2021): 61–65. http://dx.doi.org/10.30841/2708-8731.1.2021.229717.
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Intrauterine growth restriction is the cause of significant increases in perinatal mortality, morbidity and problems in the development of newborns and infants. The leading place of this pathology is not accidental, because according to various authors, the frequency of perinatal loss associated with it is from 19 to 287‰ and more, the level of perinatal morbidity - from 58.7 to 88.0%.The objective: To determine certain serum and ultrasound markers during the first trimester of pregnancy and to improve the perinatal morbidity and mortality rate in women with intrauterine growth restriction. Materials and methods. A prospective study of pregnant women in the gestation period of 11 weeks 0 days – 13 weeks 6 days, which was to determine the level of plasma protein A associated with pregnancy (PAPP-A), mean platelet volume (MPV), and ultrasound placenta examination. Pregnant women were divided into 2 groups: the main group (n1-52) and the control group (n2-50). The study group consisted of women with a low PAPP-A level and changes in the mean platelet volume towards their increase. It is this group of women that is more sensitive, in our opinion, for the development of placental disorders and the occurrence of fetal growth retardation.Results. In this study, PAPP-А levels in 39 pregnant women were <0.5 MoM, and WTO levels in 36 cases were> 10 fl, which, according to the literature, can be used as markers of early prediction of ZRP.Ultrasound type of disorders of the first stage of trophoblast invasion is described as intra- and / or periplacental pathological areas, which can be considered the causes of placental insufficiency, which results in a risk of ZRP. According to the study, high specificity and sensitivity of Doppler parameters with the determination of indices (PI and IR) in the uterine arteries were established. Conclusions. The results of the study showed that performing a screening based on a detailed history and determining PAPP-A, MPV, and ultrasound examination at first trimester of pregnancy in women with the risk of IUGR allows for prophylactic treatment and monitoring of pregnancy and thus reduces neonatal morbidity and mortality.
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Hikmah, Exma Mu'tatal, Paulus Liben, and Widjiati Widjiati. "Apium graveolens Prevents Intrauterine Growth Restriction via Suppression of Antiangiogenic Factor Production." Majalah Obat Tradisional 23, no. 2 (August 31, 2018): 135. http://dx.doi.org/10.22146/mot.36112.
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Preeclampsia is the worldwide leading cause of fetomaternal morbidity and mortality which involves the placental dysfunction. A poor placentation and formed of non-dilated spiral artery caused utero-placental circulation insufficiency, resulted in inadequate supply of nutrients and oxygen to support normal aerobic growth of the fetus. Apium graveolens or celery has been widely known as antioxidant, antiinflammation and antihypertensive with flavonoid-apigenin as main active compound. Apigenin can inhibit TNF-α, HIF-1α and nitric oxide blocking as major pathophysiological pathway of preeclampsia. This study was aimed to find how the Apium graveolens can improve intrauterine growth and its correlation with suppression of anti-angiogenic factor sFlt-1 in anti-Qa2 preeclampsia animal model. Twenty female BALB/c Mus musculus were divided into 4 groups: control, anti-Qa2 and anti-Qa2 with 500 and 1000 mg/kgBW celery herbs extract. The fetal weights and lengths, placental weights and serum sFlt-1 levels were measured and analyzed with One Way ANOVA and further tested with Least Significance Difference in 95% confidence interval. The result showed a difference between control and treatments group (p≤0.05) with 1000 mg/kgBW significantly increase intrauterine growth and decrease sFlt-1, then there is a negative correlation between intrauterine weight and serum sFlt-1. This study suggests that celery herbs extract (CHE) has an apigenin-flavonoid compound which can prevent intrauterine growth restriction (IUGR) via suppression of antiangiogenic factor production in preeclampsia mice model.
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Chereshnev, V. A., S. V. Pichugova, L. G. Tulakina, A. V. Klein, T. L. Savinova, L. M. Lebedeva, and Ya B. Beikin. "Ultrastructure of placenta in antenatal fetal death." Obstetrics, Gynecology and Reproduction 12, no. 3 (November 20, 2018): 36–46. http://dx.doi.org/10.17749/2313-7347.2018.12.3.036-046.
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The current obstetrical protocols and the improved perinatal services have led to a significant decrease in the intrapartum and neonatal mortality; however, the rate of antenatal fetal death remains high. In a search for a mechanism of this abnormality, we conducted a comprehensive morphological study of the placental ultrastructure in women with antenatal fetal death. Aim: to determine the ultrastructural characteristics of the placenta in these women. Materials and methods. We analyzed 60 cases of antenatal fetal death and conducted an electron microscopic study of placental terminal chorionic villi. The placenta samples were fixed in 2.5% glutaraldehyde, then processed in alcohol at increasing concentration and acetone for dehydration, and finally polymerized in araldite resin. Ultrathin sections were obtained using an ultra-microtome and then examined with an electron microscope. Results. In 53 (88.3%) women, antenatal fetal death occurred in the early gestation period and in 7 (11.7%) women – at a period of 38-41 weeks. In the main group, the age of women ranged from 18 years to 42 years, and in the comparison group – from 22 to 37 years. In the main group, 16 (26.6%) women were in the late reproductive period (36 years and older). Among the women with antenatal fetal death, the most common diagnoses were: chronic fetoplacental insufficiency (CFPI) – 23 (39%), fetal development retardation syndrome (FDRS) – 16 (27%), and premature detachment of a normally situated placenta (PDNSP) – 10 (17%). Changes in the syncytiotrophoblast structure were detected in patients of both groups; in these changes, signs of vacuolization and destruction were most common. In women of the main group, sclerotic stroma and infiltration by mononuclears were found, whereas loosening and swelling of the stroma were detected in both groups. Changes in the vascular bed were revealed in 100% of cases with antenatal fetal death and in 40% in comparison group. Conclusion. In antenatal fetal death, the most common causes were: CFPI, FDRS, and PDNSP. In the morphological terms, there were destructive changes in the syncytiotrophoblast, edematous-destructive, sclerotic and necrotic changes in the stromal terminal chorionic villi, vascular changes (hypovascularization, stroma obliteration, stasis and erythrocyte sludging, formation of erythrocyte thrombi in the lumens of blood vessels), dysfunctional changes in endotheliocytes, and inflammatory changes.
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Bezhenar, Vitaly F., Lidia A. Ivanova, and Mikhail Yu Korshunov. "Analysis of perinatal losses in Saint Petersburg and the Leningrad region in 2006–2018." Journal of obstetrics and women's diseases 69, no. 2 (June 21, 2020): 93–102. http://dx.doi.org/10.17816/jowd69293-102.
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Hypothesis/aims of study. Prevention of the most common causes of perinatal mortality provides an opportunity to reduce perinatal losses. It is customary to distinguish between maternal, fetal and placental factors, dividing them into preventable and unavoidable subfactors. Of all nosologies, intrauterine hypoxia and asphyxia of the newborn, infectious (viral and / or microbial) damage to the placenta and fetus / newborn, and placental insufficiency (acute and chronic) are most important. The aim of this study was to analyze perinatal losses most often diagnosed in Saint Petersburg and the Leningrad Region in order to assess the possibility of developing a set of measures to reduce perinatal mortality.
Study design, materials and methods. The analysis of perinatal losses in Saint Petersburg and the Leningrad Region in 20062018 is based on the official reports of the Saint Petersburg State Budgetary Healthcare Institution Medical Information and Analytical Center and the Leningrad Regional State Budgetary Healthcare Institution Medical Information and Analytical Center, as well as the reports of the Leningrad Regional Pathological and Anatomical Bureau (LRPAB).
Results. The main causes of perinatal losses in Saint Petersburg and the Leningrad Region for 20062018 were: fetal hypoxia (acute and chronic), intrauterine infections, respiratory distress syndrome (for premature babies), congenital malformations, and chromosomal abnormalities. Throughout the period, intrauterine hypoxia and asphyxia of the newborn (which are the pathology manifestation, not etiology) were indicated as leading diagnoses in the conclusions of perinatal death. Moreover, according to the LRPAB pathomorphological findings, intrauterine infections were the leading (over 60% of cases) cause of perinatal losses over the years. During the analyzed period in Saint Petersburg and the Leningrad Region, a high frequency of individual states arising in the perinatal period remained unchanged without determination of a specific diagnosis, which significantly complicates our analysis.
Conclusion. For an adequate diagnosis of the etiological mechanisms of perinatal losses, it is necessary to improve histological examination of the afterbirth and pathomorphological examination of the fetus / newborn using virological and immunological tests. It is also necessary to change the structure of statistical reports, obliging medical institutions to indicate the exact cause of perinatal death, excluding whenever possible the diagnoses of intrauterine hypoxia and asphyxia in labor that indicate no etiological diagnosis explaining the occurrence of hypoxia / asphyxia.
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Kohan-ghadr, H. R., R. Lefebvre, G. Fecteau, L. C. Smith, and J. Durocher. "48 MORPHOLOGICAL ANOMALIES OF FETAL MEMBRANES DURING GESTATION IN BOVINE CLONES DERIVED BY SOMATIC NUCLEAR TRANSFER." Reproduction, Fertility and Development 18, no. 2 (2006): 133. http://dx.doi.org/10.1071/rdv18n2ab48.
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High pregnancy loss and prenatal morbidity and mortality encountered in cloned animals might be explained by placental nutritional or steroidogenic insufficiency that would indirectly compromise fetal survival (Hashizume et al. 2002 Cloning and Stem Cells 4(3), 197-209). Our hypothesis is that ultrasonographic characterization of placenta in bovine clones could be used to predict anomalies in fetal development and well-being during pregnancy. We examined surrogate heifers bearing cloned fetuses (n = 37) and fetuses obtained by traditional embryo transfer (n = 5) in three stages of gestation (Day 70, 100 and 200). Morphological parameters based on direct ultrasonographic observations were collected: thickness and shape of amniotic membrane, utero-placental thickness, placentomes shape and length in fetal area, and umbilical cord shape and appearance. Analysis was done using repeated measures linear model, with day as a repeated factor. Of all clone pregnancies, 30 females were still pregnant at Day 70 and only 16 reached Day 100, from which 63% had different degrees of amniotic and/or umbilical cord anomalies. No placental anomalies or abortions were observed in the control group. The amniotic membrane abnormalities observed at Day 100 were irregularities and presence of nodules (rosary-like) in the cross-sectional view of the membrane. Hyperechogenic spikes or irregularities around the umbilical cord were observed at Day 100 in 38% of the clones (n = 6) and all of them also had amniotic anomalies. From the clone pregnancies with amniotic and/or umbilical cord problems, 30% aborted between Days 100 and 200, and for those that went to term (Days 264-278; n = 7), all calves but one died at birth or during the first month of life. Statistical analysis results showed that placentomes in cloned embryos were larger than those in control embryos (P = 0.003; least-squares mean (LSM) for clone = 4.34 cm, control = 2.97 cm) in all three stages of gestation. During the same period, amniotic membranes of clones became thicker compared to those of the control group (P = 0.0001; LSM for clone = 0.25 cm, control = 0.11 cm). Variation in utero-placental thickness was also observed. At Day 70, the utero-placental layer was thicker in clones in comparison to controls (LSM for clone = 0.32 cm, control = 0.30 cm) before it became thinner at Day 200 (LSM for clone = 0.38 cm, control = 0.40 cm). The present results showed that morphological anomalies of placentomes, amniotic membrane and umbilical cord appear during gestation of bovine cloned fetuses that could potentially compromise normal fetal development. Also, ultrasonographic monitoring of pregnancies of cloned animals is a useful tool to characterize the fetal membrane changes. This work was funded by a Strategic Project Grant from the Natural Sciences and Engineering Research Council (NSERC) Canada.
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Bertucci, Micka C., Jan M. Loose, Euan M. Wallace, Graham Jenkin, and Suzanne L. Miller. "Anti-inflammatory therapy in an ovine model of fetal hypoxia induced by single umbilical artery ligation." Reproduction, Fertility and Development 23, no. 2 (2011): 346. http://dx.doi.org/10.1071/rd10110.
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Perinatal morbidity and mortality are significantly higher in pregnancies complicated by chronic hypoxia and intrauterine growth restriction (IUGR). Clinically, placental insufficiency and IUGR are strongly associated with a fetoplacental inflammatory response. To explore this further, hypoxia was induced in one fetus in twin-bearing pregnant sheep (n = 9) by performing single umbilical artery ligation (SUAL) at 110 days gestation. Five ewes were administered the anti-inflammatory drug sulfasalazine (SSZ) daily, beginning 24 h before surgery. Fetal blood gases and inflammatory markers were examined. In both SSZ- and placebo-treated ewes, SUAL fetuses were hypoxic and growth-restricted at 1 week (P < 0.05). A fetoplacental inflammatory response was observed in SUAL pregnancies, with elevated pro-inflammatory cytokines, activin A and prostaglandin E2. SSZ did not mitigate this inflammatory response. It is concluded that SUAL induces fetal hypoxia and a fetoplacental inflammatory response and that SSZ does not improve oxygenation or reduce inflammation. Further studies to explore whether alternative anti-inflammatory treatments may improve IUGR outcomes are warranted.
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Venzkovskaya, Irina, and Anastasiіa Padchenko. "THE ROLE OF THE PIGF/SFLT-1 RELATIONSHIP IN PREDICTING PREECLAMPSIA (LITERATURE REVIEW)." Ukrainian Scientific Medical Youth Journal, no. 1(109) (April 5, 2019): 25–34. http://dx.doi.org/10.32345/usmyj.1(109).2019.25-34.
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Endothelial vascular dysfunction is an important link in the pathogenesis of preeclampsia – a pathological condition that occupies a leading position in the structure of maternal morbidity and mortality, perinatal mortality and intrauterine growth retardation. Assessment of the state of vascular endothelium during pregnancy is currently an informative method for predicting the development of this disease. The article summarizes the significance of the most studied specific biochemical markers of endothelial dysfunction, such as soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF), in relation to the prognosis and diagnosis of preeclampsia. Since the etiopathogenesis of preeclampsia is caused by the development of endothelial insufficiency and impaired vascular formation in the mother-placenta-fetus system, the choice of angiogenesis biomarkers as screening tests is justified from a logical point of view. As a screening indicator of the risk of preeclampsia, the most reliable determination of the ratio sFlt-l/PIGF, which reflects the change in both biomarkers during preeclampsia, is more pronounced than a separate definition of any of these factors. In women with the pathological course of the gestational process, in several weeks before the onset of the first clinical symptoms, a decrease in PlGF concentration and a significant increase in sFlt-1 concentration are observed in 92.5% of cases, which makes it possible to determine the risk of gestosis long before the onset of its severe clinical manifestations and to develop an optimal management for patients with this pathology. This topic is relevant, since the prevalence of preeclampsia according to different authors varies from 3 to 8% among pregnant women in developed countries. In general, up to 10-15% of maternal deaths are associated with preeclampsia and eclampsia.
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Mazarico, Edurne, Anna Peguero, Marta Camprubí, Carlota Rovira, Maria Dolores Gomez Roig, Daniel Oros, Patricia Ibáñez-Burillo, et al. "Study protocol for a randomised controlled trial: treatment of early intrauterine growth restriction with low molecular weight heparin (TRACIP)." BMJ Open 8, no. 10 (October 2018): e020501. http://dx.doi.org/10.1136/bmjopen-2017-020501.
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IntroductionThe incidence of intrauterine growth restriction (IUGR) is estimated at about 3% of pregnancies, and it is associated with 30% of all perinatal mortality and severe morbidity with adverse neurodevelopmental and cardiovascular health consequences in adult life. Early onset IUGR represents 20%–30% of all cases and is highly associated with severe placental insufficiency. The existing evidence suggests that low molecular weight heparin (LMWH) has effects beyond its antithrombotic action, improving placental microvessel structure and function of pregnant women with vascular obstetric complications by normalising proangiogenic and antiapoptotic protein levels, cytokines and inflammatory factors. The objective of our study is to demonstrate the effectiveness of LMWH in prolonging gestation in pregnancies with early-onset IUGR.Methods and analysisThis is a multicentre, triple-blind, parallel-arm randomised clinical trial. Singleton pregnancies qualifying for early (20–32 weeks at diagnosis) placental IUGR (according to Delphi criteria) will be randomised to subcutaneous treatment with bemiparin 3500 IU/0.2 mL/day or placebo from inclusion at diagnosis to the time of delivery. Analyses will be based on originally assigned groups (intention-to-treat). The primary objective will be analysed by comparing gestational age and prolongation of pregnancy (days) in each group with Student’s t-tests for independent samples and by comparing Kaplan-Maier survival curves (from inclusion to delivery, log-rank test). A linear regression model for gestational age at birth will consider the following covariates: gestational age at inclusion (continuous) and pre-eclampsia (binary).Ethics and disseminationThe study will be conducted in accordance with the principles of Good Clinical Practice. This study was approved by the Clinical Research Ethics Committee (CEIC) of Sant Joan de Déu Hospital, on 13 July 2017. The trial is registered in the public registrywww.clinicaltrial.gov. according to Science Law 14/2011, and the results will be published in an open access journal.Trial registration numberNCT03324139; Pre-results.
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Haughey, K. G. "Perinatal lamb mortality - its investigation, causes and control." Journal of the South African Veterinary Association 62, no. 2 (June 30, 1991): 78–91. http://dx.doi.org/10.4102/jsava.v62i2.1599.
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Methods of investigating perinatal loss in grazing sheep flocks are reviewed and evaluated. The "wet-dry" method is the simplest method for assessing minimal prevalence, whereas the differences between the numbers of single and twin foetuses present at ultrasonic determination of litter size during pregnancy, and the numbers of single and twin lambs present at lamb-marking, is the most precise. The veterinary investigation of field mortality involves full autopsy of a representative sample of dead lambs, a history of prenatal nutrition, disease and husbandry, as well as a qualitative estimate of weather conditions over the period of lamb collection. Pathological processes may be identified in over 95% of deaths and the specific cause determined in about 75% of deaths. The identification of the specific causes in the remainder of deaths, all classified as the starvation-mismothering-exposure (SME) complex, requires intensive, costly, on-site observation, and physiological and biochemical assessment. The probable causes of these deaths include prenatal physiological handicaps resulting from placental insufficiency, aberrant parent-offspring behaviour, management-induced mismothering, misadventure, inadequate milk supply or teat and udder abnormalities, and cold-induced starvation. The gross pathology and pathophysiology of birth stress and the SME complex, which are associated with at least 80% of mortality, are summarised. Birth injury to the foetal central nervous system, characterised by cranial and spinal meningeal haemorrhage is exclusive to parturient deaths and the SME complex. Observed flock prevalences range from 81% to 100% in parturient deaths, and 20% to 57% in the SME complex. The high total prevalence and experimental evidence, indicate the major causal role of birth stress in the pathogenesis of these entities. Lethal congenital malformations, infections (both congenital and acquired after birth), trace element deficiencies and predation are reviewed as minor causes. The new understanding of the pathogenesis of perinatal lamb mortality, recognises the heritable nature of birth mass, maternal pelvic dimensions, parent-offspring behaviour, and the resistance of neonates to cold. Control measures need to incorporate selection for maternal rearing ability, further refinement of prenatal nutritional management of twin-bearing ewes, disease control, provision of shelter for lambing flocks, and avoidance of husbandry: practices which frustrate innate parent-offspring behaviour. A selection programme is summarised.
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Semenova, Tatyana Valeryevna, Olga Nikolayevna Arzhanova, Olesya Nikolayevna Bespalova, Yuliya Pavlovna Milyutina, Valentina Mikhaylovna Prokopenko, Lyudmila Borisovna Zubzhitskaya, and Aleksandr Vartanovich Arutyunyan. "Peculiarities of pregnancy course and pregnancy outcomes in tobacco smoking." Journal of obstetrics and women's diseases 63, no. 2 (June 15, 2014): 50–58. http://dx.doi.org/10.17816/jowd63250-58.
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Tobacco is an urgent problem in Russia and in the world. Recent years have seen increased prevalence of smoking among the population. Tobacco dependence is included in the international classification of diseases, the American Psychiatric Association. From habit associated increase in the frequency of chronic diseases, mortality. In Russia smokes about 30 % of women and half of them continue to smoke during pregnancy. Proved that chronic nicotine intoxication has a negative effect on the pregnancy and fetus, worsens perinatal outcomes. It is also known that when tobacco smoking increases the level of homocysteine in the body, which in turn have toxic effects on vasculature. With many gestational hyperhomocysteinemia associated complications (gestoses, placental insufficiency, miscarriage and other). Already, there are methods of prevention and treatment of hyperhomocysteinemia. However, studies on folate metabolism in pregnant smoking a little. No clear approaches to the maintenance and inspection of this group of patients. I would like to draw attention to the state of folate metabolism in pregnant women with nicotine intoxication, reveal features of pregnancy, methods of prevention and treatment of gestational complications.
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Mielikova, Tatiana Anatolevna, and Dmitrii Nikolaevich Shapoval. "CURRENT APPROACHES TO TREAT GESTATIONAL PERIOD COMPLICATIONS IN WOMEN WITH GRAVES’ DISEASE." International Medical Journal, no. 4 (February 26, 2020): 31–34. http://dx.doi.org/10.37436/2308-5274-2019-4-7.
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The most common cause of hyperthyroidism in pregnant women is recognized by Graves' disease. Because it leads to serious complications in the mother and fetus, timely correction of disorders of homeostasis provides a successful outcome of pregnancy. In order to study the effectiveness of the drug with the active substance sulodexide in pregnant women with Graves' disease, 28 women were examined for the possibility of reducing obstetric and perinatal complications. They performed general clinical examinations, performed an extensive hemostasis, determined the fetal fetal condition. It has been found that the development of chronic syndrome of disseminated intravascular coagulation is characteristic for pregnant women and as a result this aggravates the gestational period for the mother and fetus. Supplementation of the standard protocol of treatment with anticoagulant sulodexide has led to an improvement in the parameters of the coagulation unit of hemostasis, and was also characterized by anti−adhesive and antithrombotic action. Clinically, the effectiveness of this therapy was manifested by the elimination of symptoms of placental insufficiency, the threat of pregnancy termination, preeclampsia, delayed fetal fetal development, thrombotic complications. The results obtained in this study indicate that the use of sulodexide anticoagulant has contributed to a reliable normalization of the hemostatic index, improved blood supply to the placental and fetal complex, which reduced an obstetric pathology occurrence and perinatal mortality. Thus, we can recommend to include natural anticoagulant sulodexide into standard protocol of treatment for patients with Graves' disease, because it has no side effects, unlike other anticoagulant drugs and can be safe for pregnant women. Key words: hemostasis, pregnancy, Graves' disease, sulodexide.
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Chen, Hong, Xiaobo Zhou, Ting-Li Han, Philip N. Baker, Hongbo Qi, and Hua Zhang. "Decreased IL-33 Production Contributes to Trophoblast Cell Dysfunction in Pregnancies with Preeclampsia." Mediators of Inflammation 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/9787239.
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Preeclampsia (PE) is a life-threatening pregnancy complication which is related to aggradation of risk regarding fetal and maternal morbidity and mortality. Dysregulation of systemic inflammatory response and dysfunction of trophoblast cells have been proposed to be involved in the development and progression of PE. Some studies have demonstrated that interleukin-33 (IL-33) is an immunomodulatory cytokine that is associated with the immune regulation of tumor cells. However, little is known whether IL-33 and its receptor ST2/IL-1 R4 could regulate trophoblast cells, which are associated with the pathogenesis of PE. In this study, our target is to explore the impact of IL-33 on trophoblast cells and elucidate its underlying pathophysiological mechanisms. Placental tissues from the severe PE group (n=11) and the normotensive pregnant women’s group (n=11) were collected for the protein expression and distribution of IL-33 along with its receptor ST2/IL-1 R4 via Western blot analysis and immunohistochemistry, respectively. We discovered that the level of IL-33 was decreased in placental tissues of pregnant women with PE, while no distinction was observed in the expression of ST2/IL-1 R4. These results were further verified in villous explants which were treated with sodium nitroprusside with different concentrations, to simulate the pathological environment of PE. To investigate IL-33 effects on trophoblast cells separately, IL-33 shRNA was introduced into HTR8/SVneo cells and villi. IL-33 shRNA weakened the proliferation, migration, and invasion capacity of HTR8/SVneo cells. The migration distance of villous explants was also markedly decreased. The reduced invasion of trophoblast cells is a result of IL-33 knockdown which could be related to the decline of MMP2/9 activity and the increased utterance of TIMP1/2. Overall, our findings demonstrated that the reduction of IL-33 production was connected with the reduced functional capability of trophoblast cells, thus inducing placental insufficiency that has been linked to the development of PE.
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Kapustin, Roman V., Natalia V. Borovik, Ekaterina V. Musina, Olga N. Arzhanova, Maria I. Yarmolinskaya, Elena N. Alekseyenkova, Olga V. Kovalchuk-Kovalevskaya, and Yury A. Petrov. "Pregnancy and delivery in a patient with a 40-year history of type 1 diabetes mellitus and antiphospholipid syndrome." Journal of obstetrics and women's diseases 67, no. 6 (December 15, 2018): 93–99. http://dx.doi.org/10.17816/jowd67693-99.
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Type 1 diabetes mellitus is a condition associated with an increased risk of adverse perinatal outcomes such as spontaneous abortions, preterm birth, placental insufficiency, congenital malformations, and perinatal mortality. Diabetes mellitus combined with cardiovascular diseases in women during pregnancy often leads to hypertensive disorders and pre-eclampsia. The severity of the microvascular diabetic complications and frequency of hypoglycemic episodes, particularly in early pregnancy, are related to the risk of pre-eclampsia. We report the case of pregnancy and delivery of a live newborn in a 42-year-old woman with type 1 diabetes mellitus, pre-existing hypertension, heritable thrombophilia, and antiphospholipid syndrome. She had a 40-year history of type 1 diabetes mellitus with well-controlled diabetic nephropathy and retinopathy. The woman had been receiving continuous subcutaneous insulin therapy for the last five years, which allowed maintaining an appropriate glycemic control during pregnancy. Multidisciplinary supervision of course of pregnancy was carried out from the pre-gravidity stage until delivery and postpartum. In spite of the severe pre-eclampsia and preterm delivery by cesarean section at 36 weeks, she and newborn could avoid the intensive unit care and discharge from perinatal center without any complications.
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Rains, Marcelo E., Colin B. Muncie, Yi Pang, Lir-Wan Fan, Lu-Tai Tien, and Norma B. Ojeda. "Oxidative Stress and Neurodevelopmental Outcomes in Rat Offspring with Intrauterine Growth Restriction Induced by Reduced Uterine Perfusion." Brain Sciences 11, no. 1 (January 8, 2021): 78. http://dx.doi.org/10.3390/brainsci11010078.
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Intrauterine growth restriction (IUGR) is a major cause of morbidity and mortality and is worldwide associated with delayed neurodevelopment. The exact mechanism involved in delayed neurodevelopment associated with IUGR is still unclear. Reduced uterine perfusion (RUP) is among the main causes of placental insufficiency leading to IUGR, which is associated with increases in oxidative stress. This study investigated whether oxidative stress is associated with delayed neurodevelopment in IUGR rat pups. Pregnant rats were exposed to RUP surgery on gestational day 14 to generate IUGR rat offspring. We evaluated offspring’s morphometric at birth, and neurodevelopment on postnatal day 21 (PD21) as well as markers of oxidative stress in plasma and brain. Offspring from dams exposed to RUP showed significant (p < 0.05) lower birth weight compared to controls, indicating IUGR. Motor and cognitive deficits, and levels of oxidative stress markers, were significantly (p < 0.05) elevated in IUGR offspring compared to controls. IUGR offspring showed significant (p < 0.05) negative correlations between brain lipid peroxidation and neurocognitive tests (open field and novel object recognition) in comparison with controls. Our findings suggest that neurodevelopmental delay observed in IUGR rat offspring is associated with increased levels of oxidative stress markers.
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Rains, Marcelo E., Colin B. Muncie, Yi Pang, Lir-Wan Fan, Lu-Tai Tien, and Norma B. Ojeda. "Oxidative Stress and Neurodevelopmental Outcomes in Rat Offspring with Intrauterine Growth Restriction Induced by Reduced Uterine Perfusion." Brain Sciences 11, no. 1 (January 8, 2021): 78. http://dx.doi.org/10.3390/brainsci11010078.
Full textAbstract:
Intrauterine growth restriction (IUGR) is a major cause of morbidity and mortality and is worldwide associated with delayed neurodevelopment. The exact mechanism involved in delayed neurodevelopment associated with IUGR is still unclear. Reduced uterine perfusion (RUP) is among the main causes of placental insufficiency leading to IUGR, which is associated with increases in oxidative stress. This study investigated whether oxidative stress is associated with delayed neurodevelopment in IUGR rat pups. Pregnant rats were exposed to RUP surgery on gestational day 14 to generate IUGR rat offspring. We evaluated offspring’s morphometric at birth, and neurodevelopment on postnatal day 21 (PD21) as well as markers of oxidative stress in plasma and brain. Offspring from dams exposed to RUP showed significant (p < 0.05) lower birth weight compared to controls, indicating IUGR. Motor and cognitive deficits, and levels of oxidative stress markers, were significantly (p < 0.05) elevated in IUGR offspring compared to controls. IUGR offspring showed significant (p < 0.05) negative correlations between brain lipid peroxidation and neurocognitive tests (open field and novel object recognition) in comparison with controls. Our findings suggest that neurodevelopmental delay observed in IUGR rat offspring is associated with increased levels of oxidative stress markers.
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Kovtun, O. P., P. B. Tsyvian, T. V. Markova, and T. V. Chumarnaya. "Remodeling of the Heart of the Premature Child." Annals of the Russian academy of medical sciences 75, no. 6 (November 15, 2020): 631–37. http://dx.doi.org/10.15690/vramn1268.
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Epidemiological studies consistently have suggested an association between low birth weight and increased rate of cardiovascular morbidity and mortality in adult life. Preterm birth, as one of the leading causes of the low birth weight, is associated with cardiovascular remodeling which consists of changes in heart chambers geometry and contraction-relaxation mode, ventricular hypertrophy, arterial wall structure and density changes. Several types of preterm birth are discussed: prematurity, associated with placental insufficiency and fetal growth restriction, preterm leaking of amniotic fluid, and twin pregnancy. DNA methylation process under the influence of epigenetic factors of the intrauterine and early postnatal development is suggested as a one of the main mechanism of cardiovascular remodeling in preterm infants. The other mechanisms of cardiovascular remodeling are discussed in terms of the modern intrauterine programming concept. The early diagnostics and prevention of cardiovascular diseases in preterm born children are discussed. The treatment during prenatal and early postnatal periods as well as prevention of the remodeling causes could diminish and even reverse the development of the negative cardiovascular events and diseases in later life according to the so called concept of one thousand days opportunities window.
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Kamilova, M. Ya, P. A. Dzhonmakhmadova, and F. R. Ishan-Khodzhaeva. "The Relationship of Rates and Causes of Stillbirth to Obstetric Facility Level." Doctor.Ru 19, no. 8 (2020): 61–65. http://dx.doi.org/10.31550/1727-2378-2020-19-8-55-61-65.
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Study Objective: To compare the rates and causes of stillbirth in level 2 and 3 obstetric institutions. Study Design: This was a retrospective group study. Materials and Methods: Statistical data and labor and delivery histories of women who experienced stillbirth and were admitted to obstetric facilities (two level 2 facilities and one level 3 facility) between January and June 2019 were reviewed. Retrospective analysis was done of their labor and delivery histories, and the cases of stillbirth were clinically analyzed, using the ReCoDe classification. Study Results: The frequency of stillbirth was higher in the level 3 hospital. Irrespective of the level of hospital, mortality in the antenatal period dominated (four out of six cases in the level 2 facilities and 104 out of 129 in the level 3 facility); it was more often due to congenital malformations in the level 2 facilities and to intrauterine growth restriction (IUGR) or placental insufficiency in the level 3 facility. In the level 3 hospital, the most common causes of intranatal fetal death included maternal (pre-eclampsia and extragenital diseases) and fetal (IUGR) disorders that developed before labor. The risk factors for stillbirth were inadequate quality of medical services and factors related to the woman or family, such as late registration for prenatal care, non-compliance with doctors’ recommendations, etc. Conclusion: The actual causes, as established in this study, of negligence leading to stillbirth demonstrate that there is potential for reducing perinatal mortality. Keywords: stillbirth, antenatal and intranatal fetal death, ReCoDe classification, causes of stillbirth, perinatal audit.
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Bhat, Swathi, Ambika H. E., Lepakshi B. G., and Savitha C. S. "Pregnancy outcome in low risk pregnancy with decreased amniotic fluid index." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 3 (February 19, 2017): 887. http://dx.doi.org/10.18203/2320-1770.ijrcog20170550.
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Background: To evaluate whether oligohydramnios (AFI≤5) has any significance in the outcome of low risk pregnancies. Normal amniotic fluid index in pregnancy is one of the indicators of fetal well-being. In a term pregnancy, oligohydramnios, a condition associated with AFI≤5, could be a sign of placental insufficiency. An association of low AFI with complications like pregnancy induced hypertension, consistently leads to poor fetal outcome. A need to deliver the fetus by cesarean section often arises. Occasionally one comes across a full-term pregnancy with AFI ≤5 with no known high risk factors; this could lead to increased cesarean section rates. Thus, it becomes necessary to evaluate if AFI ≤5 in the absence of other risk factors has any significance on obstetric outcome.Methods: Prospective case controlled study was done. Fifty women with term pregnancies and (AFI≤5) cm not associated with any other high risk factors were enrolled for the study. They were matched with fifty controls with normal AFI.Results: Except for a slight increase in variable deceleration in the study group, no differences were noted with fetal heart rate recordings in NST. Decreased AFI was not associated with increased cesarean section rates, instrumental deliveries or meconium stained amniotic fluid. Severe asphyxia, NICU admission or perinatal mortality was not noted in either group.Conclusions: When a low risk pregnancy is associated with Oligohydramnios (AFI≤5), it does not have any deleterious effect on labor outcome or perinatal outcome.
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Borisova, Daria S., and Valerii P. Chashchin. "Reproductive health and demographic characteristics of the population residing in a coal-mining region in the Arctic zone." Hygiene and sanitation 100, no. 8 (August 31, 2021): 826–32. http://dx.doi.org/10.47470/0016-9900-2021-100-8-826-832.
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Introduction. The study was conducted to identify the main trends in reproductive, maternal, and newborn’s health to justify additional measures to achieve sustainable demographic development of industrial regions in the Arctic zone of the Russian Federation (AZRF). Material and methods. The study was carried out using reporting and statistical materials characterizing the main demographic and health statistics of the reproductive health in the female population of Vorkutinsky municipal district (16 settlements), summarized in the “Demographic Yearbook of the Komi Republic” (2015-2019), and the annual reports of medical organizations providing obstetric and gynaecological medical care to the population of Vorkuta. Results. As in many other areas of the Russian Arctic, in the city of Vorkuta, there were observed: a population decline from 60.4 in 2015 to 54.2 thousand people in 2019, a decrease in the number of women at reproductive age from 19.9 to 19.2 thousand people, as well as a significant increase in the frequency of preterm birth (PB) (from 2,2% to 8,4%) mainly due urogenital infection (42,3%), chronic placental insufficiency (CPF) (27%), multiple pregnancies (11,5%), preeclampsia (7,7%), cervical incompetence (7,7%), uterine scar inconsistency (3,8%). The incidence of PB among primiparous women was significantly lower than that among multiparous women - 34.6% and 65.3%, respectively. The frequency of abortions increased from 15.4 to 20.9 per 1000 women of reproductive age, and there was an increase by 16.3% in the rate of spontaneous abortions among women 18-44 years of age at the pregnancy terms from 12 to 22 weeks. Perinatal mortality during the study period increased from 7.5 ‰ to 12.7 ‰ in 2019. (on average in Russia 7.23 ‰). The stillbirth rate was 9.5 ‰ (on average in Russia 5.51 ‰). The main cause of stillbirth in the study period was intrauterine asphyxia due to the decompensated chronic placental insufficiency. Among the possible reasons for increased fetal infantile losses is a significant proportion in the general population of the Vorkuta of workers exposed to adverse occupational risk factors (25.7% compared to 14.1% in the Russian Arctic as a whole). Conclusion. Among the population living in the area of the Pechora coal basin, the risk remains for an increase in the demographic crisis phenomena mainly due to the rise in the frequency of pregnancy disorders and, above all, a high level of fetal-infantile losses. To solve one of the main tasks of national security to prevent further depopulation of the Arctic regions, set in the Decree of the President of the Russian Federation*, it is necessary besides socioeconomic measures to preserve the population number, to develop and implement programs to effectively reduce fetal-infantile losses, including those potentially associated with adverse occupational exposure to reproductive risk factors.
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Andersen, Judith C. "Tinzaparin in Problem Pregnancy (TIPP): Retrospective Analysis of Therapeutic Outcomes in High-Risk Pregnant Patients Treated with Tinzaparin." Blood 104, no. 11 (November 16, 2004): 4087. http://dx.doi.org/10.1182/blood.v104.11.4087.4087.
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Abstract BACKGROUND: Pregnancy represents a “physiologic” maternal thrombophilic state, with presumed evolutionary goals of ensuring secure fetal implantation, placental stability, and control of peripartum maternal bleeding. Specific pregnancy-induced maternal changes include increased activated Protein C resistance; decreased active Protein S; increased levels of vitamin K-dependent procoagulants, factor VIII, von Willebrand factor, and fibrinogen; and increased levels of plasminogen activator inhibitor (PAI-1). Superposition of pregnancy upon inherited or acquired thrombophilias may have untoward consequences for both mother and fetus. Venous thromboembolism (the leading cause of maternal morbidity and mortality in pregnancy) is five times more likely to occur in pregnant women than in nonpregnant women of similar age. Placental insufficiency and recurrent fetal loss are strongly associated with inherited and acquired thrombophilia, and antithrombotic interventions with aspirin, unfractionated heparin and low molecular weight heparins (LMWHs) have decreased maternal morbidity and improved fetal outcome. LMWHs offer decreased incidence of bleeding, heparin-induced thrombocytopenia with thrombosis (HITT), and osteoporosis, as well as predictable dosing efficacy. An industry sponsored series of roundtable discussions with US hematology and high-risk obstetrics practitioners revealed that a collective deterrent to use of tinzaparin (the most recently introduced LMWH with favorable pharmacokinetics and once-daily dosing) was the limited amount of published safety and efficacy data in this patient population. STUDY DESIGN: Fifty pregnancies in women treated with tinzaparin between January 2003, and June 2004, in American maternal/fetal medicine programs for high risk from prior pregnancy-associated VTE, presence of high risk pre-existing thrombophilias, or recurrent fetal loss are undergoing retrospective analysis for maternal and fetal outcomes; safety; and compliance with therapy. A specific identifier-blind data collection tool will capture historical and examination data and diagnostic studies that establish and follow risk as well as tabulate antithrombotic and adjunctive medication/supplement regimens. “Live birth” and “fetal loss” questionnaires will capture maternal and fetal course, complications, anesthesia and delivery decisions, and tissue pathology, as appropriate. RESULTS: Data analysis will be complete by late November 2004. In the absence of large randomized trials of efficacy and safety, such a study may provide guidelines for safe and effective use of tinzaparin in American high-risk pregnancy.
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Sultana, Sharmin, Parul Akhter, Seema Rani Dabee, Saida Akter, and Mst Rahima Khatun. "Serum C-reactive protein concentration in preeclamptic women: Effect on pregnancy outcome." Bangabandhu Sheikh Mujib Medical University Journal 8, no. 1 (July 26, 2016): 30. http://dx.doi.org/10.3329/bsmmuj.v8i1.28917.
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<p><strong>Background:</strong> Preeclampsia is a multisystem disorder of unknown etiology characterized by development of hypertension to the extent of 140/90 mm of Hg or more with proteinuria after the 20th gestational week in a previously normotensive and non protein uric women. According to the National High blood presure Working group (NHBPEP) and American college of obstetricans and Gynecologiests (ACOG) hypertension in pregnancy is defined as a diastolic blood pressure of 90 mm Hg or higher after 20 weeks of gestation in a woman with previously normal blood pressure (NHBPEP, 2000; ACOG, 2002). If the disease is allowed to progress to the HELLP syndrome or eclampsia, maternal morbidity and mortality increases. The majority of perinatal losses are related to placental insufficiency, which causes intrauterine growth retardation, prematurity associated with preterm delivery, or abruptio placentae.</p><p><strong> Objectives:</strong> This study tried to explore the effect of serum C reactive protein concentration in preeclamptic women and its effect on pregnancy outcome.</p><p><strong>Methods:</strong> This case control study included 60 third trimester pregnant women (30 normotensive and 30 preeclamptic) who attended Department of Obstetrics and Gynaecology, BIRDEM and DMCH, during July 2009 and June 2010. Estimation of serum C reactive protein (CRP) concentrations was done by liquid phase immunoprecipitation assay and turbulometry at DMC.</p><p><strong>Results:</strong> Mean (±SD) age showed no significant difference between groups; however, BMI, SBP, DBP and CRP were significantly (P<0.001) high in case group. Gravidity and ANC showed no significant variation between groups. CRP concentration was significantly high case group. Gestational age was significantly low in case group resulting in higher preterm delivery. No significant variation was observed regarding fetal outcome; however, birth weight was significantly low and neonatal complication was also significantly high in case group.</p><p><strong>Conclusion:</strong> CRP concentration was high in preeclamptics resulting in adverse pregnancy outcome.</p>
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Raznatovska, О. М., S. I. Tertishniy, V. G. Syusyuka, A. V. Fedorec, T. K. Sahaidak, T. A. Grekova, M. O. Shalmina, and S. M. Makhonchuk. "Clinical course of pregnancy and postpartum in a multidrug-resistant tuberculosis/HIV co-infected patient receiving bedaquiline-containing regimen as antimycobacterial therapy." Infusion & Chemotherapy, no. 4 (December 20, 2019): 23–30. http://dx.doi.org/10.32902/2663-0338-2019-4-23-30.
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Background. According to World Health Organization (WHO), experimental studies performed in rats and rabbits have revealed no evidence of harmful side effects of bedaquiline to the fetus. WHO points out that, given the lack of adequate and controlled studies on the effects of bedaquiline on the fetus in pregnant women, and the fact that drug data regarding teratogenicity are limited to nonclinical animal data, this drug may be used when an effective treatment regimen cannot otherwise be provided. However, WHO recommends thorough registering treatment, pregnancy, and postpartum bedaquiline-related outcomes to provide data on appropriate dosing for multidrug-resistant tuberculosis (MDR-TB) treatment during pregnancy and postpartum. However, in the modern literature, there are no data about attributable to bedaquiline adverse events in MDR-TB/HIV co-infected pregnant women and their fetus as well as during the postpartum period.
Objective. To update the literature data with the clinical features of pregnancy and postpartum period in a MDR-TB/HIV co-infected patient receiving a bedaquiline-containing regimen as antimycobacterial therapy in the third trimester based on an example from own clinical experience.
Methods. We report the clinical case of pregnancy course in the MDR-TB/HIV co-infected woman treated with the bedaquiline-containing regimen as antimycobacterial therapy in the third trimester.
Results. In the clinical case presented, the patient demonstrated an initial poor adherence to treatment for both MDR-TB and HIV infection resulting in tuberculous process and HIV rapid progression. Since the patient refused the option of undergoing the therapeutic abortion prior to 22 gestational weeks as the pregnancy was intended, the antimycobacterial therapy regimen was modified by bedaquiline inclusion at 30 weeks’ gestation (the third trimester) for the maternal and neonatal mortality prevention. However, there was no sputum smear conversion on the antimycobacterial therapy regimen including bedaquiline, the patient presented with the signs of endogenous intoxication and nephropathy. Relatedly, neonatal transabdominal ultrasound revealed intrauterine growth retardation, worsening fetoplacental insufficiency (reverse flow) and intrauterine dystrophy. There was abundant placental calcification. Taking into account breech presentation, II degree intrauterine growth retardation, III degree fetoplacental insufficiency (reverse flow), oligohydramnios, fetal distress syndrome and bilateral pyelectasis, the patient was transferred to the Perinatal Centre for planned caesarean section at the 32nd week of gestation. The premature female infant was declared dead some hours later. In the postpartum period, the patient continued the initiated bedaquilinebased antimycobacterial therapy and antiretroviral therapy. However, positive clinical-radiological dynamics and sputum smear conversion have not been achieved.
Conclusions. The clinical case presented confirms the literature data that the features of pregnancy and postpartum period in patients with MDR-TB/HIV co-infection are characterized by such complications development as preterm delivery, early neonatal mortality, intrauterine growth retardation, distress syndrome, etc.
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Zelinka-Khobzey, M. M. "PECULIARITIES OF PREGNANCY COURSE IN WOMEN WITH CONCOMITANT OBESITY WHO TAKE THERAPEUTIC AND PROPHYLACTIC COMPLEX AIMED TO PREVENT PREECLAMPSIA." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 21, no. 2 (June 17, 2021): 51–56. http://dx.doi.org/10.31718/2077-1096.21.2.51.
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The rapid growth in the incidence of overweight and obesity among women of childbearing age is posing specific issues related to their pregnancy, thereupon choosing adequate and effective tactics for the prevention of preeclampsia in women with concomitant obesity who are at high risk group for this complication is of undoubted relevance. The aim of this study is to assess the occurrence and characteristic of obstetric and prenatal complications in women with concomitant obesity, who receive therapeutic and prophylactic complex designed to prevent the development of preeclampsia. We studied the course of pregnancy of 255 women, who were divided into 3 groups according to the class of obesity, and then, in turn, were subdivided into subgroups taking into account the presence of preeclampsia and the therapeutic and prophylactic complex course. The high efficiency of the therapeutic and prophylactic complex including L-arginine and diosmin for obese women enables to reduce the manifestations of endothelial dysfunction, the occurrence of preeclampsia and its severe forms; to lower down the occurrence of other complications during the pregnancy (risks of premature birth, placental insufficiency, distress and foetal growth retardation); to avoid perinatal mortality and improve the condition of the foetus. Applying this pathogenetically grounded therapeutic and prophylactic complex we elaborated (acetylsalicylic acid, L-arginine, calcium supplements and semisynthetic diosmin) to prevent the occurrence of preeclampsia in pregnant women with concomitant obesity, who are at high-risk group, promotes the reduction of occurrence and intensity of obstetric and prenatal complications resulted from endothelial dysfunction. We can suggest the therapeutic and prophylactic complex for pregnant women with concomitant obesity as effective therapy because no cases of severe and early preeclampsia have been registered.
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Iwahashi, Naoyuki, Midori Ikezaki, Kazuchika Nishitsuji, Madoka Yamamoto, Ibu Matsuzaki, Naoki Kato, Naoyuki Takaoka, et al. "Extracellularly Released Calreticulin Induced by Endoplasmic Reticulum Stress Impairs Syncytialization of Cytotrophoblast Model BeWo Cells." Cells 10, no. 6 (May 24, 2021): 1305. http://dx.doi.org/10.3390/cells10061305.
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The pregnancy-specific syndrome preeclampsia is a major cause of maternal mortality throughout the world. The initial insult resulting in the development of preeclampsia is inadequate trophoblast invasion, which may lead to reduced maternal perfusion of the placenta and placental dysfunction, such as insufficient trophoblast syncytialization. Endoplasmic reticulum (ER) stress has been implicated in the pathology of preeclampsia and serves as the major risk factor. Our previous studies suggested critical roles of calreticulin (CRT), which is an ER-resident stress response protein, in extravillous trophoblast invasion and cytotrophoblast syncytialization. Here, we studied the mechanism by which ER stress exposes the placenta to the risk of preeclampsia. We found that CRT was upregulated in the serum samples, but not in the placental specimens, from preeclamptic women. By using BeWo cells, an established model of cytotrophoblasts that syncytialize in the presence of forskolin, we demonstrated that thapsigargin-induced ER stress caused extracellular release of CRT from BeWo cells and that the extracellular CRT suppressed forskolin-induced release of β-human chorionic gonadotropin and altered subcellular localization of E-cadherin, which is a key adhesion molecule associated with syncytialization. Our results together provide evidence that induction of ER stress leads to extracellular CRT release, which may contribute to placental dysfunction by suppressing cytotrophoblast syncytialization.