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Artículos de revistas sobre el tema "Fetal growth retardation"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 25 de julio de 2025

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1

M N, Dharmavijaya, Kala K, Sujata Datti, Anupama Rani V, Kumar Kumar, and Guruprasad G A. "Antepartum Fetal Surveillance in Intra Uterine Growth Retardation." JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 03, no. 1 (2013): 27–31. http://dx.doi.org/10.58739/jcbs/v03i1.6.

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2

Lazareva, V. K., R. S. Zamaleeva, and N. A. Cherepanova. "Clinical significance of regulatory antibodies content evaluation in pregnant women with fetal growth retardation." Kazan medical journal 95, no. 6 (2014): 836–40. http://dx.doi.org/10.17816/kmj1990.

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Aim. To identify the possibility of fetal growth retardation prediction at early stages of pregnancy by revealing changes in the content of some regulatory autoantibodies. Methods. A comprehensive examination of 388 pregnant women at risk of gestational complications was performed. After standardization of groups 185 pregnant women were selected for the analysis. Out of these, 80 patients with fetal growth retardation were included into the main group, 80 matched pairs were selected from the group of pregnant women at risk of fetal growth retardation (comparison group). The control group consi

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3

Vetter, K. "Treatment options for fetal growth retardation (intrauterine growth retardation, IUGR)." Der Gynäkologe 34, no. 12 (2001): 1124–27. http://dx.doi.org/10.1007/s001290101082.

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4

&NA;. "Aspirin prevents fetal growth retardation." Inpharma Weekly &NA;, no. 793 (1991): 1. http://dx.doi.org/10.2165/00128413-199107930-00001.

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5

NUREDINI-DEMIRI, Besa, Kefser LUSJANI, Luljeta BEQIRI, Esma IBRAIMI, and Zamira BEXHETI ZYLBEARI. "PREVENTION OF FETAL GROWTH RETARDATION." International Journal of Medical Sciences - ACTA MEDICA BALKANICA 9, no. 17-18 (2024): 89–99. http://dx.doi.org/10.62792/ut.amb.v9.i17-18.p2555.

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Fetal growth restriction (FGR) has been a frequently encountered pathology in obstetrics and affects 5-10% of pregnancies. It has been one of the three main causes of perinatal deaths, after premature births and fetal malformations. In approximately one third of cases with FGR, cause or pathology was not found, which made it difficult to prevent or treat them effectively. Mostly, FGR was a consequence of insufficiency of uteroplacental circulation, placental and fetoplacental function. The term SGA (small for gestational age) has to do with constitutional growth rates and the statistical deter

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6

Kempley, S. "Doppler and fetal growth retardation." Archives of Disease in Childhood - Fetal and Neonatal Edition 70, no. 2 (1994): F160. http://dx.doi.org/10.1136/fn.70.2.f160-a.

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7

Soothill, R. W., R. A. Ajayi, and K. N. Nicolaides. "Fetal biochemistry in growth retardation." Early Human Development 29, no. 1-3 (1992): 91–97. http://dx.doi.org/10.1016/0378-3782(92)90062-l.

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8

Beattie, R. B., and M. J. Whittle. "Doppler and fetal growth retardation." Archives of Disease in Childhood 69, no. 3 Spec No (1993): 271–73. http://dx.doi.org/10.1136/adc.69.3_spec_no.271.

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9

Kopteyeva, Ekaterina V., Elizaveta V. Shelayeva, Elena N. Alekseenkova, Stanislava V. Nagorneva, Roman V. Kapustin, and Igor Yu Kogan. "Fetal growth restriction in diabetic pregnancy: a retrospective single-center study." Journal of obstetrics and women's diseases 71, no. 6 (2023): 15–27. http://dx.doi.org/10.17816/jowd115018.

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BACKGROUND: The high risk of adverse maternal and perinatal complications in patients with fetal growth restriction and diabetes mellitus requires a detailed assessment of the major risk factors and outcomes. AIM: The aim of this study was to determine the main risk factors for fetal growth retardation in pregnant women with pregestational and gestational diabetes mellitus, and to assess obstetric and perinatal outcomes in these patients. MATERIALS AND METHODS: We conducted a retrospective single-center cohort study at the premises of the Research Institute of Obstetrics, Gynecolog

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10

Warshaw, Joseph B. "Intrauterine Growth Retardation." Pediatrics In Review 8, no. 4 (1986): 107–14. http://dx.doi.org/10.1542/pir.8.4.107.

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Intrauterine growth retardation can result from a variety of environmental and genetic influences on fetal growth. The sequelae of intrauterine growth retardation resulting from impairment of nutrient flow include low birth weight with sparing of brain growth, polycythemia, and hypoglycemia resulting from decreased storage fuels and defective gluconeogenesis. Available data suggest that the vast majority of nutritionally growthretarded infants have normal postnatal development without significant difference in IQ or neurologic scores from normal infants. The outcome of infants in whom there is

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11

ZHELEZOVA, M. E., B. K. BEKTUR, L. I. MALTSEVA, et al. "Influence of the maternal microbiome on the development of late fetal growth retardation." Practical medicine 20, no. 5 (2022): 34–39. http://dx.doi.org/10.32000/2072-1757-2022-5-34-39.

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The purpose — to assess the possible influence of the microbiome of the vagina, oral cavity and placenta of women on the late fetal growth retardation syndrome. Material and methods. A prospective-retrospective analysis of pregnancy and childbirth in 80 pregnant women was carried out. The main group consisted of 40 women with late fetal growth retardation syndrome, the comparison group — 40 healthy pregnant women. The study of the microbiome of the vagina, oral cavity, and placenta was carried out by sequencing of nitrogenous bases in the 16S ribosomal RNA (r-RNK) genes in 15 patients with fet

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12

Fox, H. "Placentation in intrauterine growth retardation." Fetal and Maternal Medicine Review 9, no. 2 (1997): 61–71. http://dx.doi.org/10.1017/s0965539597000053.

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A baby may be small for a variety of reasons, but there are certain overt maternal and fetal factors which may lead to, or are associated with, a poor fetal growth rate. Pre-eminent amongst the maternal factors is severe pre-eclampsia and in women with this disease the smallness of the baby is almost certainly due to the inadequacy of the uteroplacental circulation. Other maternal factors of importance are cigarette smoking, drug abuse and certain infections such as malaria. The most obvious fetal factors associated with a low birth weight are congenital malformations and chromosomal abnormali

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13

Pham Minh, Son, Huy Nguyen Vu Quoc, and Vinh Tran Dinh. "INTRAUTERINE GROWTH RETARDATION - A REVIEW ARTICLE." Volume 8 Issue 6 8, no. 6 (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: su

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14

Kravchenko, E. N., and L. V. Kuklina. "Risk factors for fetal growth retardation." Problemy reproduktsii 28, no. 5 (2022): 72. http://dx.doi.org/10.17116/repro20222805172.

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15

Granstrom, Lars, Lena Granstrom, and Lars Backman. "Fetal Growth Retardation After Gastric Banding." Acta Obstetricia et Gynecologica Scandinavica 69, no. 6 (1990): 533–36. http://dx.doi.org/10.3109/00016349009013332.

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16

Chia, Chun-Chieh, and Soon-Cen Huang. "Overview of fetal growth retardation/restriction." Taiwanese Journal of Obstetrics and Gynecology 53, no. 3 (2014): 435–40. http://dx.doi.org/10.1016/j.tjog.2014.01.003.

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17

JANCIN, BRUCE. "Steroids Linked to Fetal Growth Retardation." Internal Medicine News 44, no. 5 (2011): 31. http://dx.doi.org/10.1016/s1097-8690(11)70247-5.

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18

Philip, A. G. S., and A. M. Tito. "ERYTHROBLASTOSIS AND FETAL GROWTH RETARDATION (IUGR)." Pediatric Research 22, no. 2 (1987): 231. http://dx.doi.org/10.1203/00006450-198708000-00107.

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19

Wouters, E. J. M., P. A. de Jong, P. J. H. Cornelissen, P. H. J. Kurver, W. C. van Oel, and C. L. M. van Woensel. "HbCOf decisive for fetal growth retardation?" European Journal of Obstetrics & Gynecology and Reproductive Biology 19, no. 5 (1985): 330. http://dx.doi.org/10.1016/0028-2243(85)90052-8.

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20

JANCIN, BRUCE. "Steroids Linked to Fetal Growth Retardation." Clinical Endocrinology News 6, no. 3 (2011): 39. http://dx.doi.org/10.1016/s1558-0164(11)70151-1.

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21

Alfirevic, Z., and J. P. Neilson. "Fetal growth retardation: methods of detection." Current Obstetrics & Gynaecology 3, no. 4 (1993): 190–95. http://dx.doi.org/10.1016/0957-5847(93)90037-p.

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22

Geipel, A., and U. Gembruch. "Fetal growth retardation in twin gestations." Der Gynäkologe 34, no. 12 (2001): 1138–44. http://dx.doi.org/10.1007/s001290101056.

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23

Kudryavtseva, E. V., V. V. Kovalev, A. A. Dektyarev, and I. I. Baranov. "Predicting fetal growth retardation: mathematical modeling." Obstetrics, Gynecology and Reproduction 16, no. 6 (2023): 664–75. http://dx.doi.org/10.17749/2313-7347/ob.gyn.rep.2022.328.

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Introduction. Annually, more than 13 million neonates are born with fetal growth retardation (FGR) worldwide. FGR increases prenatal mortality and morbidity. Due to no effective treatments for FGR are available, its prevention and prognosis are of extreme relevance.Aim: development of prognostic clinical and anamnestic mathematical model for assessing a risk of developing FGR during pregnancy.Materials and Methods. A prospective, controlled, open, continuous study was performed. The main group (1) included 75 patients who had FGR during pregnancy; the control group (2) consisted of 414 women w

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24

Kramer, Michael S., Marielle Olivier, Frances H. McLean, Geoffrey E. Dougherty, Diana M. Willis, and Robert H. Usher. "Determinants of Fetal Growth and Body Proportionality." Pediatrics 86, no. 1 (1990): 18–26. http://dx.doi.org/10.1542/peds.86.1.18.

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Previous studies of fetal growth and body proportionality have been based on error-prone gestational age estimates and on inappropriate comparisons of infants with dissimilar birth weights. Based on a cohort of 8719 infants with validated (by early ultrasonography) gestational ages and indexes of body proportionality standardized for birth weight, potential maternal and fetal determinants of fetal growth and proportionality were assessed. Maternal history of previous low birth weight infants, pregnancy-related hypertension (particularly if severe), diabetes, prepregnancy weight, net gestationa

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25

Maršál, Karel. "Antenatal Diagnosis of Intrauterine Growth Retardation by Ultrasound." International Journal of Technology Assessment in Health Care 8, S1 (1992): 160–69. http://dx.doi.org/10.1017/s0266462300013064.

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AbstractUltrasound estimation of fetal weight or ultrasound measurement of fetal abdomen alone enables identification of small-for-gestational-age fetuses. A prerequisite for this is a reliable dating of pregnancy, which is provided by a routine ultrasound screening in the first half of gestation. The fetal growth can be followed by serial fetometric measurements. As a standard, charts of intrauterine growth based on the ultrasonic measurement can be used. As a secondary diagnostic test for monitoring fetal health in pregnancies suspected of intrauterine growth retardation, Doppler ultrasound

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26

Soldatova, Soldatova E. E., Kan N. E. Kan, Tyutyunnik V. L. Tyutyunnik, and Volochaeva M V. Volochaeva M. "Fetal growth retardation in the context of fetal programming." Akusherstvo i ginekologiia 8_2022 (August 30, 2022): 5–10. http://dx.doi.org/10.18565/aig.2022.8.5-10.

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27

Yusenko, S. R., S. V. Nagorneva, and I. Yu Kogan. "Changes in fetal cerebral hemodynamics in fetal growth retardation." Russian Bulletin of Obstetrician-Gynecologist 24, no. 3 (2024): 36. http://dx.doi.org/10.17116/rosakush20242403136.

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28

Zhang, Jun. "Fetal gender and fetal growth retardation: Fact or artifact?" American Journal of Obstetrics and Gynecology 172, no. 6 (1995): 1947–48. http://dx.doi.org/10.1016/0002-9378(95)91447-1.

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29

Carrión Ordoñez, José Gonzalo, María Elisa Carrión Barreto, Gleici Da Silva Castro Perdoná, and Natielle Gonçalves de Sá. "Evaluación de los índices biométricos fetales para el diagnóstico del Retardo del Crecimiento Fetal." Revista Médica del Hospital José Carrasco Arteaga 14, no. 3 (2023): 166–72. http://dx.doi.org/10.14410/2022.14.3.ao.25.

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BACKGROUND: Fetal Growth Restriction occurs when a fetus does not reach its intrauterine growth potential due to genetic and/or environmental factors; it is associated with increased perinatal mortality and morbidity and also predisposes to the development of chronic disorders in adulthood. The aim of this study was to evaluate the accuracy of the Biometric Indices: Femur Length/Abdominal Circumference (FL/AC); Transverse Cerebellar Diameter/Abdominal Circumference (TCD/AC) and Humerus, Cerebellum, Femur/Abdominal Circumference Equation (HCF/AC); in predicting fetal growth retardation. METHODS

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30

Goryunova, Aleksandra G., M. S. Simonova, and A. V. Murashko. "Fetal growth retardation syndrome and adaptation of the placenta." V.F.Snegirev Archives of Obstetrics and Gynecology 3, no. 2 (2016): 76–80. http://dx.doi.org/10.18821/2313-8726-2016-3-2-76-80.

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There are considered modern data on etiology, pathogenesis, course of the pregnancy, methods of diagnosing of the fetal growth retardation syndrome. There is presented information about the role of growth factors and their receptors, as well as modern views on the problem of placental insufficiency as a major cause of fetal growth retardation syndrome.

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31

Gulyaeva, Olga N., Anastasiya S. Kazitskaya, Olga A. Zagorodnikova, Lyudmila V. Renge, and Anna G. Zhukova. "Gene polymorphism of the xenobiotic biotransformation system and the intrauterine fetal growth retardation in female workers of industrial enterprises." Russian Journal of Occupational Health and Industrial Ecology 61, no. 6 (2021): 415–20. http://dx.doi.org/10.31089/1026-9428-2021-61-6-415-420.

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Intrauterine growth retardation is recognized as one of the leading causes of incidence and mortality in infancy and early childhood in all the countries of the world. The causes and mechanisms of development of this process are decisive when choosing the tactics of nursing such children. Of particular importance is the understanding of the functioning of the mother-placenta-fetus system, in particular the mechanisms of suppression of the detoxification function of the placenta in connection with the polymorphisms of the genes of the I and II phases of the xenobiotic biotransformation system.

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32

Degtyareva, E. A., O. A. Zakharova, M. A. Kufa, M. G. Kantemirova, and V. E. Radzinskiy. "The efficacy of prognosis and early diagnostics of fetal growth retardation." Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 63, no. 6 (2018): 37–45. http://dx.doi.org/10.21508/1027-4065-2018-63-5-37-45.

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The fetal growth retardation takes one of the leading places in the structure of perinatal morbidity and mortality. The frequency of this pregnancy complication in Russia is high – from 3% to 24% among full-term infants and from 18% to 46% among premature newborns. The article analyzes the capabilities of various diagnostic methods for predicting fetal growth retardation. The more indicators are included in the review the more effective isitsreliability in the formation of risk groupsforthis pathology and more effective measures to prevent fetal growth retardation can be taken.Conflict of inte

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33

Fay, Roger A., and David A. Ellwood. "Categories of intrauterine growth retardation." Fetal and Maternal Medicine Review 5, no. 4 (1993): 203–12. http://dx.doi.org/10.1017/s0965539500000899.

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Originally all low birthweight infants were considered to be premature. When prematurity was redefined in terms of gestational age (SGA) and not preterm. With the large scale collection of obstetric data the distributions of birthweight at different gestational ages were described and from these, infants who were SGA could be defined. SGA became synonymous with terms such as growth retardation, but it soon became appearent that the two were not necessarily interchangeable. Scott and Usher found that it was the degree of soft tissue wasting rather than birthweight that related to poor perinatal

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34

Naeem, Muhammad Ahmad, Humaira Rauf, Sayeda Kiran Aftab, Fatima Mahrukh, Akash John, and Warda Kiran. "Prevalence of Intrauterine Growth Retardation on Antenatal Ultrasound Scan in Lahore, Pakistan." Lahore Garrison University Journal of Life Sciences 6, no. 04 (2022): 350–59. http://dx.doi.org/10.54692/lgujls.2022.0604234.

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Fetal growth retardation is described as infants whose weights are much less than expected. Population based norms are used to categorize abnormal growths. The objective of the study was to determine the frequency of intrauterine growth retardation on antenatal ultrasound scan. It was an observational descriptive study conducted at the Radiology Department of Fatima Memorial Hospital, Shadman Lahore. Patients visited the Ultrasound Department for Obstetric scan. The study was conducted in 6 months from January to June in 2022. The sample size of 87 was calculated for study with expected rate o

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35

Alsat, E., C. Marcotty, R. Gabriel, et al. "Molecular approach to intrauterine growth retardation: an overview of recent data." Reproduction, Fertility and Development 7, no. 6 (1995): 1457. http://dx.doi.org/10.1071/rd9951457.

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Consideration of the abnormal regulation of fetal growth leading to intrauterine growth retardation must take account of the fundamental differences between the regulation of growth before and after birth. The significance of endocrine regulators of growth differs greatly in utero. During the first trimester of pregnancy, embryonic growth might be controlled at the level of the individual organs by nutrient supply and by locally active growth factors. Later, fetal growth depends essentially upon materno-placental cooperation in delivering nutrients to the fetus. Therefore the major role of hor

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36

Severi, F. M., G. Rizzo, C. Bocchi, D. D’Antona, M. S. Verzuri, and D. Arduini. "Intrauterine Growth Retardation and Fetal Cardiac Function." Fetal Diagnosis and Therapy 15, no. 1 (2000): 8–19. http://dx.doi.org/10.1159/000020969.

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37

Snijders, Rosalinde, and Jon Hyett. "Fetal testing in intra-uterine growth retardation." Current Opinion in Obstetrics and Gynecology 9, no. 2 (1997): 91–95. http://dx.doi.org/10.1097/00001703-199704000-00003.

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38

Weir, P. E., J. N. Oats, Rhonda Holdsworth, and R. Cross. "Histocompatibility Antigens and Intrauterine Fetal Growth Retardation." Australian and New Zealand Journal of Obstetrics and Gynaecology 25, no. 2 (1985): 108–10. http://dx.doi.org/10.1111/j.1479-828x.1985.tb00619.x.

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39

James, D. "Diagnosis and management of fetal growth retardation." Archives of Disease in Childhood 65, no. 4 Spec No (1990): 390–94. http://dx.doi.org/10.1136/adc.65.4_spec_no.390.

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40

Sheppard, Brian, and John Bonnar. "Uteroplacental Hemostasis in Intrauterine Fetal Growth Retardation." Seminars in Thrombosis and Hemostasis 25, no. 05 (1999): 443–46. http://dx.doi.org/10.1055/s-2007-994947.

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41

Hubinont, C., N. M. Fisk, U. Nicolini, C. H. Rodeck, and R. D. Johnson. "Fetal alpha-fetoprotein concentration in growth retardation." BJOG: An International Journal of Obstetrics and Gynaecology 96, no. 10 (1989): 1233–34. http://dx.doi.org/10.1111/j.1471-0528.1989.tb03204.x.

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42

Avni, F. "Fetal renal hyperechogenicity in intrauterine growth retardation." Pediatric Nephrology 17, no. 3 (2002): 222. http://dx.doi.org/10.1007/s00467-001-0772-3.

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43

Rizzo, Giuseppe, and Domenico Arduini. "Fetal cardiac function in intrauterine growth retardation." American Journal of Obstetrics and Gynecology 165, no. 4 (1991): 876–82. http://dx.doi.org/10.1016/0002-9378(91)90431-p.

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44

Parkes, M. J., and D. J. Hill. "Lack of growth hormone-dependent somatomedins or growth retardation in hypophysectomized fetal lambs." Journal of Endocrinology 104, no. 2 (1985): 193–99. http://dx.doi.org/10.1677/joe.0.1040193.

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ABSTRACT Fetal lambs were hypophysectomized and, after 8 days of recovery, given infusions of GH, prolactin, thyroxine and insulin with glucose. Hypophysectomy caused no consistent reduction in fetal plasma somatomedin-like activity. Fetal infusions of GH or prolactin caused no consistent change in plasma somatomedin-like activity. It was concluded that fetal somatomedin-like activity is not GH dependent. After hypophysectomy fetal lambs showed no reduction in body weight or length at term. J. Endocr. (1985) 104, 193–199

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45

Pickard, MR, AJ Leonard, LM Ogilvie, et al. "Maternal hypothyroidism in the rat influences placental and liver glycogen stores: fetal growth retardation near term is unrelated to maternal and placental glucose metabolic compromise." Journal of Endocrinology 176, no. 2 (2003): 247–55. http://dx.doi.org/10.1677/joe.0.1760247.

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Maternal hypothyroidism impairs fetal growth in the rat, but the mechanisms by which this occurs are unknown. Since the fetus derives its glucose supply from the mother, and maternal thyroidectomy may disturb maternal and placental glucose metabolism, we postulated that maternal and/or placental glucose metabolic compromise may contribute to fetal growth retardation in hypothyroid dams. Feto-placental growth, tissue glycogen stores and glucose levels in sera and amniotic fluid were determined in rat dams partially thyroidectomized (TX) before pregnancy and in euthyroid controls. Fetal body wei

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46

Orudzhova, E. A., N. A. Samburova, E. V. Anichkova, K. E. Gotsiridze, and V. O. Bitsadze. "Thrombophilia in the pathogenesis of fetal growth retardation." Obstetrics, Gynecology and Reproduction 15, no. 2 (2021): 189–200. http://dx.doi.org/10.17749/2313-7347/ob.gyn.rep.2021.223.

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Fetal growth retardation (FGR) is a complication of pregnancy that determines perinatal morbidity and mortality. It is a complex and multifaceted medical problem that does not lose its relevance. Impaired fetal development and delayed growth result from various etiopathogenesis of pathological processes occurring in the "mother–placenta–fetus" interface. Thrombophilia is one of the factors that can initiate disturbed placental function and the utero-placental blood flow. Here we describe the clinical FGR variants and etiopathogenetic factors of developing this complication of pregnancy (placen

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47

Thureen, P. J., K. A. Trembler, G. Meschia, E. L. Makowski, and R. B. Wilkening. "Placental glucose transport in heat-induced fetal growth retardation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 3 (1992): R578—R585. http://dx.doi.org/10.1152/ajpregu.1992.263.3.r578.

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In six ewes heat stressed from 39 to 125 days gestation and studied in a normothermic environment at 135 days, fetal and placental masses were less than in control sheep (1,645 vs. 3,112 and 149 vs. 356 g, respectively, P less than 0.01). Umbilical glucose uptakes (Rf,UP) were measured keeping maternal arterial plasma glucose at 70 mg/dl at spontaneously occurring fetal plasma glucose values (state A) and at two additional fetal glucose levels, to determine the transplacental glucose difference (delta) vs. Rf,UP relation. At normal delta of 49.2 mg/dl, Rf,UP was less in the experimental group

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48

POSOKHOVA, S. P., A. D. SHYROKA, and O. U. KUCHERENKO. "EARLY FETAL GROWTH RETARDATION IN PREGNANT WOMEN WITH HYPERTENSIVE DISORDERS." Scientific digest of association of obstetricians and gynecologists of Ukraine, no. 1(51) (October 11, 2023): 40–55. http://dx.doi.org/10.35278/2664-0767.1(51).2023.294845.

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Fetal growth retardation (FGR) is a complication of pregnancy that develops due to placental insufficiency and leads to the birth of a child with mass and growth parameters below the 10th percentile for a given gestational age. Newborns with FGR are at high risk of developing motor, neurological, cognitive and learning disorders, as well as cerebral palsy. Purpose. To determine the frequency, risk factors and perinatal outcomes in case of early fetal growth retardation (up to 32 weeks of gestation) in pregnant women with hypertensive disorders. Materials and methods. A retrospective analysis o

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Chareonsirisuthigul, Takol, Suchin Worawichawong, Rachanee Parinayok, Patama Promsonthi, and Budsaba Rerkamnuaychoke. "Intrauterine Growth Retardation Fetus with Trisomy 16 Mosaicism." Case Reports in Genetics 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/739513.

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Fetal trisomy 16 is considered uniformly lethal early in gestation. It has been reported to be associated with the variability of clinical features and outcomes. Mosaic trisomy 16 leads to a high risk of abnormality in prenatal cases. Intrauterine growth retardation (IUGR) is a common outcome of mosaic trisomy 16. Herein, we report on the case of Thai male IUGR fetus with trisomy 16 mosaicism. The fetal body was too small. Postmortem investigation of placenta revealed the abnormality including small placenta with furcated cord insertion and single umbilical cord artery. Cytogenetic study demon

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Basystyi, O. V. "Morphofunctional сhanges in the рlacenta of рregnant with Intrauterine growth retardation". HEALTH OF WOMAN, № 8(114) (30 жовтня 2016): 55–58. http://dx.doi.org/10.15574/hw.2016.114.55.

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The objective: to reveal morphofunctional changes in the placenta of pregnant with intrauterine growth retardation of different severity. Patients and Methods. The study included 100 pregnant (from 23 to 40 weeks of gestation). The main group consisted of 80 pregnant women with intrauterine growth retardation of different severity. The control group consisted of 20 women with physiological course of pregnancy. The patients of the main group were divided into three clinical groups regarding intrauterine growth retardation staging. Group I included 38 pregnant with stage 1 IUGR, 22 pregnant wome

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