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Thematische Bibliographien / Fetal growth retardation / Zeitschriftenartikel

Zeitschriftenartikel zum Thema „Fetal growth retardation“

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Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 3. März 2023

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1

M N, Dharmavijaya, Kala K, Sujata Datti, Anupama Rani V, Kumar Kumar und Guruprasad G A. „Antepartum Fetal Surveillance in Intra Uterine Growth Retardation“. JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 03, Nr. 1 (15.03.2013): 27–31. http://dx.doi.org/10.58739/jcbs/v03i1.6.

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2

Vetter, K. „Treatment options for fetal growth retardation (intrauterine growth retardation, IUGR)“. Der Gynäkologe 34, Nr. 12 (Dezember 2001): 1124–27. http://dx.doi.org/10.1007/s001290101082.

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3

&NA;. „Aspirin prevents fetal growth retardation“. Inpharma Weekly &NA;, Nr. 793 (Juni 1991): 1. http://dx.doi.org/10.2165/00128413-199107930-00001.

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4

Kempley, S. „Doppler and fetal growth retardation.“ Archives of Disease in Childhood - Fetal and Neonatal Edition 70, Nr. 2 (01.03.1994): F160. http://dx.doi.org/10.1136/fn.70.2.f160-a.

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5

Soothill, R. W., R. A. Ajayi und K. N. Nicolaides. „Fetal biochemistry in growth retardation“. Early Human Development 29, Nr. 1-3 (Juni 1992): 91–97. http://dx.doi.org/10.1016/0378-3782(92)90062-l.

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6

Beattie, R. B., und M. J. Whittle. „Doppler and fetal growth retardation.“ Archives of Disease in Childhood 69, Nr. 3 Spec No (01.09.1993): 271–73. http://dx.doi.org/10.1136/adc.69.3_spec_no.271.

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7

Warshaw, Joseph B. „Intrauterine Growth Retardation“. Pediatrics In Review 8, Nr. 4 (01.10.1986): 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 decreased growth potential relates to the condition underlying growth retardation and may, of course, result in later severe handicap. Infants with nutritional intrauterine growth retardation may exhibit decreased fetal size and sparing of brain growth as an adaptive stage in the presence of lower oxygen and substrate availability. Under such conditions, a smaller size may decrease substrate and oxygen needs and improve outcome. All infants with intrauterine growth retardation, however, require follow-up and careful developmental evaluation.

8

Lazareva, V. K., R. S. Zamaleeva und N. A. Cherepanova. „Clinical significance of regulatory antibodies content evaluation in pregnant women with fetal growth retardation“. Kazan medical journal 95, Nr. 6 (15.12.2014): 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 consisted of 25 healthy pregnant women with physiological pregnancy and childbirth. Patients with fetal growth retardation were divided into three subgroups. The first subgroup consisted of 40 pregnant women with grade I of fetal growth retardation, 24 pregnant women with grade II of fetal growth retardation formed the second subgroup, and 16 pregnant women with grade III of fetal growth retardation were included into the third subgroup. Along with the standard methods of examination the serum levels of regulatory class G antibodies binding with double-stranded deoxyribonucleic acid, β2-glycoprotein, total phospholipids, human chorionic gonadotropin, collagen, pregnancy-associated plasma protein-A, insulin, and the level of anti-neutrophil cytoplasmic antibodies, on the dates of 11-14 and 26-28 weeks of pregnancy. Results. The peculiarities of the regulatory autoantibodies content in pregnant women with fetal growth retardation and in women at risk of this condition were revealed. Pregnant women with grade I and II of fetal growth retardation had higher values of autoantibodies, whereas severe forms of fetal growth retardation were characterized by diverse changes of the examined regulatory autoantibodies with a predominance of low values. In case of pregnant women at risk of fetal growth retardation changes in the content of regulatory autoantibodies were diverse. Conclusion. The revealed changes in the content of regulatory autoantibodies can be used for prediction of fetal growth retardation in pregnant women.

9

Kopteyeva, Ekaterina V., Elizaveta V. Shelayeva, Elena N. Alekseenkova, Stanislava V. Nagorneva, Roman V. Kapustin und Igor Yu Kogan. „Fetal growth restriction in diabetic pregnancy: a retrospective single-center study“. Journal of obstetrics and women's diseases 71, Nr. 6 (07.02.2023): 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, Gynecology and Reproductology named after D.O. Ott, Saint Petersburg, Russia. The study included 103 patients with type 1 diabetes mellitus, type 2 diabetes mellitus, or gestational diabetes mellitus with fetal growth retardation who delivered a singleton neonate from January 2017 to December 2021. Based on the antenatal diagnosis, the patients were divided into the following comparison groups: group I early fetal growth retardation (n = 29), group II late fetal growth retardation (n = 27), group III small for gestational age (n = 47). Relative risk calculations were used to assess the contribution of risk factors and the risk of developing secondary outcomes. RESULTS: Pregestational diabetes mellitus was the major risk factor for early fetal growth retardation development (relative risk 1.91; 95% confidence interval 1.043.50); especially type 1 diabetes mellitus (relative risk 1.64; 95% confidence interval 1.022.74) and more than 10 years of pregestational diabetes mellitus duration (relative risk 2.62; 95% confidence interval 1.126.17). Chronic hypertension increases the risk of early fetal growth retardation (relative risk 2.11; 95% confidence interval 2.213.68), while gestational hypertension was a significant risk factor for late fetal growth retardation development (relative risk 1.81; 95% confidence interval 1.013.70). Preeclampsia is associated with both early and late forms of fetal growth retardation. Maternal characteristics, such as age over 35 years, obesity, and in vitro fertilization pregnancy, increased the risk of early fetal growth retardation development. In turn, the presence of fetal growth retardation in patients with diabetes mellitus is associated with increased risk of cesarean section, prolonged stay of the newborn in the neonatal intensive care unit (5 days), low Apgar scores (7 at the 5th minute), and neonatal hypoglycemia. Early fetal growth retardation is a significant risk factor for preterm birth (relative risk 6.23; 95% confidence interval 2.8713.42) and fetal distress (relative risk 5.51; 95% confidence interval 2.2813.33). CONCLUSIONS: Being associated with a highly increased risk of adverse obstetric and perinatal outcomes, early fetal growth retardation in diabetic pregnancy is related to pregestational diabetes mellitus, especially type 1 diabetes mellitus, with a long history, as well as with hypertension in pregnancy.

10

Kravchenko, E. N., und L. V. Kuklina. „Risk factors for fetal growth retardation“. Problemy reproduktsii 28, Nr. 5 (2022): 72. http://dx.doi.org/10.17116/repro20222805172.

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11

Granstrom, Lars, Lena Granstrom und Lars Backman. „Fetal Growth Retardation After Gastric Banding“. Acta Obstetricia et Gynecologica Scandinavica 69, Nr. 6 (Januar 1990): 533–36. http://dx.doi.org/10.3109/00016349009013332.

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12

Chia, Chun-Chieh, und Soon-Cen Huang. „Overview of fetal growth retardation/restriction“. Taiwanese Journal of Obstetrics and Gynecology 53, Nr. 3 (September 2014): 435–40. http://dx.doi.org/10.1016/j.tjog.2014.01.003.

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13

JANCIN, BRUCE. „Steroids Linked to Fetal Growth Retardation“. Internal Medicine News 44, Nr. 5 (März 2011): 31. http://dx.doi.org/10.1016/s1097-8690(11)70247-5.

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14

Philip, A. G. S., und A. M. Tito. „ERYTHROBLASTOSIS AND FETAL GROWTH RETARDATION (IUGR)“. Pediatric Research 22, Nr. 2 (August 1987): 231. http://dx.doi.org/10.1203/00006450-198708000-00107.

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15

Wouters, E. J. M., P. A. de Jong, P. J. H. Cornelissen, P. H. J. Kurver, W. C. van Oel und C. L. M. van Woensel. „HbCOf decisive for fetal growth retardation?“ European Journal of Obstetrics & Gynecology and Reproductive Biology 19, Nr. 5 (Mai 1985): 330. http://dx.doi.org/10.1016/0028-2243(85)90052-8.

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16

JANCIN, BRUCE. „Steroids Linked to Fetal Growth Retardation“. Clinical Endocrinology News 6, Nr. 3 (März 2011): 39. http://dx.doi.org/10.1016/s1558-0164(11)70151-1.

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17

Alfirevic, Z., und J. P. Neilson. „Fetal growth retardation: methods of detection“. Current Obstetrics & Gynaecology 3, Nr. 4 (Dezember 1993): 190–95. http://dx.doi.org/10.1016/0957-5847(93)90037-p.

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18

Geipel, A., und U. Gembruch. „Fetal growth retardation in twin gestations“. Der Gynäkologe 34, Nr. 12 (Dezember 2001): 1138–44. http://dx.doi.org/10.1007/s001290101056.

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19

Kudryavtseva, E. V., V. V. Kovalev, A. A. Dektyarev und I. I. Baranov. „Predicting fetal growth retardation: mathematical modeling“. Obstetrics, Gynecology and Reproduction 16, Nr. 6 (14.01.2023): 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 with favorable pregnancy outcome. All subjects underwent examination, including collecting medical history, a complex of prenatal diagnostics in the first trimester of pregnancy – ultrasound, Doppler uterine arteries, serum level of pregnancy-associated plasma protein-A (PAPP-A), free beta-subunit of human chorionic gonadotropin (β-hCG), placental growth factor (PlGF), and non-invasive prenatal test (NIPT).Results. To determine the relative contribution of each individual trait to the formation of FGR risk and develop a prognostic index, a discriminant analysis was carried out, on the basis of which a prognostic F-index was developed. The formula for calculating the F-index includes the age of pregnant woman, obstetric history data, method of conception, recorded nicotine addiction in pregnancy, detected uterine fibroids, body mass index, biochemical parameters (PAPP-A, β-hCG, PlGF), nuchal translucency of the fetus, the pulsation index of the uterine artery, the level of the fetal fraction and fetal gender (determined during NIPT). The parameters of sensitivity and specificity of the FGR prognosis were 90.1 and 82.18 % respectively, the method effectiveness was 83.97 %.Conclusion. The method developed for predicting FGR can be used in clinical practice to form risk groups for FGR development and choose tactics for pregnancy management.

20

Fox, H. „Placentation in intrauterine growth retardation“. Fetal and Maternal Medicine Review 9, Nr. 2 (Mai 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 abnormalities, and there the failure of the fetus to achieve a normal weight is clearly an expression of a generalised disorder of growth and is unrelated to the adequacy or otherwise of the placenta. If cases such as these are removed from consideration, there remains an important residue of unduly small infants who are delivered after an apparently uncomplicated pregnancy, are free from congenital malformations and have a normal karotype; it is this group which is considered here.

21

Pham Minh, Son, Huy Nguyen Vu Quoc und Vinh Tran Dinh. „INTRAUTERINE GROWTH RETARDATION - A REVIEW ARTICLE“. Volume 8 Issue 6 8, Nr. 6 (Dezember 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)

22

Soldatova, Soldatova E. E., Kan N. E. Kan, Tyutyunnik V. L. Tyutyunnik und Volochaeva M V. Volochaeva M. „Fetal growth retardation in the context of fetal programming“. Akusherstvo i ginekologiia 8_2022 (30.08.2022): 5–10. http://dx.doi.org/10.18565/aig.2022.8.5-10.

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23

Zhang, Jun. „Fetal gender and fetal growth retardation: Fact or artifact?“ American Journal of Obstetrics and Gynecology 172, Nr. 6 (Juni 1995): 1947–48. http://dx.doi.org/10.1016/0002-9378(95)91447-1.

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24

ZHELEZOVA, M. E., B. K. BEKTUR, L. I. MALTSEVA, T. V. GRIGORYEVA, E. A. BOULYGINA, D. R. KHUSNUTDINOVA und E. A. ZIATDINOVA. „Influence of the maternal microbiome on the development of late fetal growth retardation“. Practical medicine 20, Nr. 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 fetal growth retardation and 8 healthy pregnant women. The Fast-DNA SPIN Kit was used to isolate the DNA material. The isolated DNA was subjected to subsequent PCR amplification followed by sequencing with forward primers and reagent kits. Results. The vaginal microbiome in women of both observation groups was characterized by the predominance of Lactobacillus, the content of which was more than 90%. The oral microbiome in both observation groups was marked by the predominance of two main bacterial types — Firmicutes and Prevotella, while Streptococcus was dominant in women with fetal growth retardation. In the placenta of women with fetal growth retardation, the bacterial diversity was significantly lower than in healthy pregnant women. The oral and placental microbiome influences the development of the late fetal growth retardation syndrome. Conclusion. The influence of the altered maternal microbiome on the formation of late fetal growth retardation is not excluded.

25

Maršál, Karel. „Antenatal Diagnosis of Intrauterine Growth Retardation by Ultrasound“. International Journal of Technology Assessment in Health Care 8, S1 (Januar 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 evaluation of fetal and uteroplacental hemodynamics provided useful for early detection of imminent fetal distress.

26

Kramer, Michael S., Marielle Olivier, Frances H. McLean, Geoffrey E. Dougherty, Diana M. Willis und Robert H. Usher. „Determinants of Fetal Growth and Body Proportionality“. Pediatrics 86, Nr. 1 (01.07.1990): 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 gestational weight gain, cigarette smoking, height, parity, and fetal sex were all significantly associated with fetal growth in the expected directions. Consistent with previous reports, maternal age, marital status, and onset or total amount of prenatal care had no significant independent effects. Fetal growth ratio (relative weight for gestational age), pregnancy-related hypertension, fetal sex, and maternal height were the only significant determinants of proportionality. Infants who were growth-retarded, those with taller mothers, those whose mothers had severe pregnancy-related hypertension, and males tended to be longer and thinner and had larger heads for their weight, although these variables explained only a small fraction of the variance in the proportionality measures. Among infants with intrauterine growth retardation, gestational age was not independently associated with proportionality (in particular, late term and postterm infants did not tend to be more disproportional), a finding that does not support the hypothesis that earlier onset of growth retardation leads to more proportional growth retardation. The results raise serious questions about previous studies of proportionality, particularly those suggesting a nutritional etiology for proportional intrauterine growth retardation. They also emphasize the importance of controlling for degree of growth retardation, maternal stature, and pregnancy-related hypertension in evaluating the prognostic consequences of proportionality for mortality, morbidity, and functional performance.

27

Fay, Roger A., und David A. Ellwood. „Categories of intrauterine growth retardation“. Fetal and Maternal Medicine Review 5, Nr. 4 (November 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 outcome. Miller and Hassanein stated that: “birthweight by itself is not a valid measure of fetal growth impairment”. They used Rorher’s Ponderal Index (weight (g) × 100/length (cm)) to diagnose the malnourished or excessively wasted infants with reduced soft tissue mass. Most studies of intrauterine growth retardation (IUGR) still use low birthweight for gestational age centile as their only definition of IUGR or only study infants who have a low birthweight. Altman and Hytten expressed disquiet about this definition and stated: “There is now an urgent need to establish true measures of fetal growth from which deviations indicating genuine growth retardation can be derived” and that “it is particularly important that some reliable measures of outcome should be established”. In large series of term deliveries published recently, two groups of IUGR infants with different growth patterens have been identified. These studies confirm that birthweight alone is inadequate to define the different types of IUGR. They established that low Ponderal Index (PI) is a measure of IUGR associated with an increased incidence of perinatal problems and that it is time to re-evaluate IUGR in terms of the different types of aberrant fetal growth.

28

Severi, F. M., G. Rizzo, C. Bocchi, D. D’Antona, M. S. Verzuri und D. Arduini. „Intrauterine Growth Retardation and Fetal Cardiac Function“. Fetal Diagnosis and Therapy 15, Nr. 1 (2000): 8–19. http://dx.doi.org/10.1159/000020969.

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29

Snijders, Rosalinde, und Jon Hyett. „Fetal testing in intra-uterine growth retardation“. Current Opinion in Obstetrics and Gynecology 9, Nr. 2 (April 1997): 91–95. http://dx.doi.org/10.1097/00001703-199704000-00003.

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30

Weir, P. E., J. N. Oats, Rhonda Holdsworth und R. Cross. „Histocompatibility Antigens and Intrauterine Fetal Growth Retardation“. Australian and New Zealand Journal of Obstetrics and Gynaecology 25, Nr. 2 (Mai 1985): 108–10. http://dx.doi.org/10.1111/j.1479-828x.1985.tb00619.x.

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31

James, D. „Diagnosis and management of fetal growth retardation.“ Archives of Disease in Childhood 65, Nr. 4 Spec No (01.04.1990): 390–94. http://dx.doi.org/10.1136/adc.65.4_spec_no.390.

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32

Sheppard, Brian, und John Bonnar. „Uteroplacental Hemostasis in Intrauterine Fetal Growth Retardation“. Seminars in Thrombosis and Hemostasis 25, Nr. 05 (Oktober 1999): 443–46. http://dx.doi.org/10.1055/s-2007-994947.

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33

Hubinont, C., N. M. Fisk, U. Nicolini, C. H. Rodeck und R. D. Johnson. „Fetal alpha-fetoprotein concentration in growth retardation“. BJOG: An International Journal of Obstetrics and Gynaecology 96, Nr. 10 (Oktober 1989): 1233–34. http://dx.doi.org/10.1111/j.1471-0528.1989.tb03204.x.

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34

Avni, F. „Fetal renal hyperechogenicity in intrauterine growth retardation“. Pediatric Nephrology 17, Nr. 3 (März 2002): 222. http://dx.doi.org/10.1007/s00467-001-0772-3.

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35

Rizzo, Giuseppe, und Domenico Arduini. „Fetal cardiac function in intrauterine growth retardation“. American Journal of Obstetrics and Gynecology 165, Nr. 4 (Oktober 1991): 876–82. http://dx.doi.org/10.1016/0002-9378(91)90431-p.

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36

Goryunova, Aleksandra G., M. S. Simonova und A. V. Murashko. „Fetal growth retardation syndrome and adaptation of the placenta“. V.F.Snegirev Archives of Obstetrics and Gynecology 3, Nr. 2 (15.06.2016): 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.

37

Degtyareva, E. A., O. A. Zakharova, M. A. Kufa, M. G. Kantemirova und 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, Nr. 6 (29.12.2018): 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 interest: The authors of this article confirmed the lack of conflict of interest and financial support, which should be reported.

38

Naeem, Muhammad Ahmad, Humaira Rauf, Sayeda Kiran Aftab, Fatima Mahrukh, Akash John und Warda Kiran. „Prevalence of Intrauterine Growth Retardation on Antenatal Ultrasound Scan in Lahore, Pakistan“. Lahore Garrison University Journal of Life Sciences 6, Nr. 04 (15.11.2022): 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 of 9% of pregnancies resulted in intrauterine growth retardation at 5% level of significance at 5% margin of error. The study included pregnant females in third trimesters of pregnancy. The data was analyzed using SPSS version 20. A total of 87 obstetric ultrasounds were performed during the study period. The mean age of the patients was 28.69 ±4.46 years with age range 20-42. The 87 included patients showed mean gestational age 35.29 ±2.50 weeks. The mean biparietal diameter was 8.69±0.57 cm and abdominal circumference was 29.72±3.03 cm. The mean fetal body weight is 2.52±0.59 kg. The frequency of intrauterine growth retardation was 10.3%. Fetal biometry, biophysical profile and Doppler studies were helpful in the diagnosis of intrauterine growth retardation and evaluation of ultrasound parameters in third trimester.

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Parkes, M. J., und D. J. Hill. „Lack of growth hormone-dependent somatomedins or growth retardation in hypophysectomized fetal lambs“. Journal of Endocrinology 104, Nr. 2 (Februar 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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Orudzhova, E. A., N. A. Samburova, E. V. Anichkova, K. E. Gotsiridze und V. O. Bitsadze. „Thrombophilia in the pathogenesis of fetal growth retardation“. Obstetrics, Gynecology and Reproduction 15, Nr. 2 (05.05.2021): 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 (placental, maternal, and fetal). Special attention is paid to genetic and acquired thrombophilia (due to the circulation of antiphospholipid antibodies) and their role in development of such complication of pregnancy.

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Gulyaeva, Olga N., Anastasiya S. Kazitskaya, Olga A. Zagorodnikova, Lyudmila V. Renge und 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, Nr. 6 (07.08.2021): 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. The aim of the study was to determine the relationship between the polymorphism of the genes of the I and II phases of the xenobiotic biotransformation system with the intrauterine fetal growth retardation in women living in the South of the Kemerovo region and working under harmful labor conditions. A survey of 39 women of reproductive age living in the territory of Novokuznetsk was carried out, 20 of them worked at various enterprises of the city. The study group included 14 women who gave birth to children with intrauterine growth retardation of varying severity. The comparison group (control) consisted of 25 women. They did not have spontaneous miscarriages and they carried a child without the intrauterine growth retardation. The work investigated the frequency of occurrence of polymorphisms of genes of the xenobiotic biotransformation system - CYP1A2*1F, GSTM1 (they determine the activity of detoxification enzymes), as well as their combinations - in a group of working women and housewives who gave birth to children with intrauterine growth retardation. The forms of genes associated with the intrauterine fetal growth retardation, as well as genes associated with the resistance to this pathology, were identified. Combinations of gene forms of different phases of the xenobiotic biotransformation and their relationship with intrauterine fetal growth retardation were shown. There were no statistically reliable differences between various cohorts of women. A positive association of a high risk of the intrauterine fetal growth retardation in women with A/A CYP1A2*1F genotype and deletion polymorphism of the GSTM1 "-" gene has been shown. The heterozygous form of the C/A CYP1A2*1F gene polymorphism is statistically reliably associated with the resistance to this pathology, as well as the normally functioning GSTM1 "+" gene. Genotype A/A CYP1A2*1F in the combination with the deletion polymorphism of GSTM1 "-" gene is statistically reliably associated with intrauterine fetal growth retardation, and C/A CYP1A2*1F genotype in the combination with normally functioning GSTM1 "+" gene is associated with a low risk of the intrauterine fetal growth retardation. Comparative analysis of the relationship of the studied forms of genes of the xenobiotic biotransformation system with the intrauterine fetal growth retardation in the groups of female workers and housewives did not show statistically reliable differences.

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Alsat, E., C. Marcotty, R. Gabriel, A. Igout, F. Frankenne, G. Hennen und D. Evain-Brion. „Molecular approach to intrauterine growth retardation: an overview of recent data“. Reproduction, Fertility and Development 7, Nr. 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 hormones in fetal growth is to mediate utilization of available substrate. Fetal growth seems to be regulated by fetal insulin, IGF-1 and certainly IGF-2, while growth hormone has only a secondary role to play. In late gestation, placental size and fetal growth rate are well correlated, pointing to a key role of the placenta in the regulation of fetal growth. It is therefore of importance to understand the molecular mechanisms involved in regulating placental development and endocrine functions. TGF alpha and EGF might play a major role as suggested by the modulation of their receptors with placental development, and by the specific alterations of epidermal growth factor receptors in intrauterine growth retardation. In addition, human placenta secretes specifically placental growth hormone. The concentration of placental growth hormone is significantly decreased in sera of pregnant women bearing a fetus with intrauterine growth retardation.

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Thureen, P. J., K. A. Trembler, G. Meschia, E. L. Makowski und R. B. Wilkening. „Placental glucose transport in heat-induced fetal growth retardation“. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, Nr. 3 (01.09.1992): 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 (3.2 vs. 5.6 mg.min-1.kg fetus-1, P less than 0.05). Differences in placental perfusion and glucose consumption could not account for this result, thus indicating a reduced placental glucose transport capacity. In state A, fetal hypoglycemia enlarged significantly (P less than 0.01) the delta to 56.7 mg/dl and increased Rf,UP approximately 50% over the Rf,UP at a normal delta. In heat-induced fetal growth retardation, fetal hypoglycemia increases the flux of maternal glucose across a placenta with reduced glucose transport capacity.

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Chareonsirisuthigul, Takol, Suchin Worawichawong, Rachanee Parinayok, Patama Promsonthi und 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 demonstrated trisomy 16 that was found 100% in placenta and only 16% in the fetal heart while other organs had normal karyotype. In addition, cardiac and other internal organs examination revealed normal morphology.

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Spinillo, Arsenio, Ezio Capuzzo, Sabrina Nicola, Laura Colonna, Angela Iasci und Carlo Zara. „Interaction between fetal gender and risk factors for fetal growth retardation“. American Journal of Obstetrics and Gynecology 171, Nr. 5 (November 1994): 1273–77. http://dx.doi.org/10.1016/0002-9378(94)90146-5.

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Rizzo, G., D. Arduini, F. Pennestri, C. Romanini und S. Mancuso. „Fetal behaviour in growth retardation: Its relationship to fetal blood flow“. Prenatal Diagnosis 7, Nr. 4 (Mai 1987): 229–38. http://dx.doi.org/10.1002/pd.1970070402.

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Orudzhova, E. A. „Antiphospholipid antibodies, genetic thrombophilia and fetal growth retardation“. Obstetrics, Gynecology and Reproduction 15, Nr. 6 (12.01.2022): 695–704. http://dx.doi.org/10.17749/2313-7347/ob.gyn.rep.2021.278.

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Aim: to study the role of antiphospholipid antibodies (AРA) and genetic thrombophilia as a potential cause of the development or a component in the pathogenesis of early and late fetal growth retardation (FGR).Materials and Methods. There was conducted a prospective randomized controlled trial with 118 women enrolled. The main group consisted of 83 patients, whose pregnancy was complicated by FGR degrees II and III, stratified into two groups: group 1 – 36 pregnant women with early FGR, group 2 – 47 pregnant women with late FGR. Women were subdivided into subgroups according to the FGR severity. The control group consisted of 35 pregnant women with a physiological course of pregnancy. АРА were determined according to the Sydney antiphospholipid syndrome criteria by enzyme immunoassay (ELISA): against cardiolipin, β2 -glycoprotein 1, annexin V, prothrombin, etc. (IgG/IgM isotypes); lupus anticoagulant – by the three-stage method with Russell's viper venom; antithrombin III and protein C levels – by chromogenic method; prothrombin gene polymorphisms G20210A and factor V Leiden – by polymerase chain reaction; homocysteine level – by ELISA.Results. AРA circulation (medium and high titers), genetic thrombophilic defects and/or hyperhomocysteinemia were detected in 40 (48.2 %) patients with FGR, which was significantly higher than that in the control group (p < 0.05): in group 1 (41.7 % of women) AРA (30.6 %) and AРA with genetic thrombophilia or hyperhomocysteinemia (11.1 %) were revealed; in group 2 (51.1 % of women) AРA (21.3 %), AРA with hyperhomocysteinemia (4.3 %), genetic thrombophilia (25.5 %), and due to hyperhomocysteinemia (2.1 %) were found. No differences in prevalence of thrombophilia rate in patients were observed related to FGR severity, but a correlation between the FGR severity and AРA titers was found.Conclusion. Testing for the presence of AРA, genetic thrombophilia and hyperhomocysteinemia should be recommended for patients with FGR (including those with FGR in medical history), especially in the case of its early onset. It is recommended to determine the full AРA spectrum.

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Alirzayeva, Kh. „Assessment of risk factors for fetal growth retardation“. HEALTH OF WOMAN, Nr. 9-10(155-156) (30.12.2020): 50–53. http://dx.doi.org/10.15574/hw.2020.155-156.50.

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The objective: to determine the risk factors for the development of ESRD in pregnant women with preeclampsia and anemia. Materials and methods. 97 pregnant women with preeclampsia with iron-deficiency anemia were monitored. The first group included 46 pregnant women with diagnosed ZRD, the second group-51 pregnant women who gave birth to children with normal body weight. Criteria of FGR is to reduce body weight and length of newborn at birth (less than 10 percentile of assessment tables in comparison with due to gestational age), morphological maturity index (a lag of 2 weeks or more from the true gestational age), disproportionate body, the signs of malnutrition and trophic disorders of the skin and mucous membranes. Results. A step-by-step elimination of the factors that contributed the least to the development of ARI in a combination of preeclampsia and anemia was performed. The results of multivariate analysis showed that in General, the following factors had the strongest influence on the development of RR in preeclampsia and anemia: arterial hypertension (RR= 2.055 [95% CI 1.31-3.20]), overweight/obesity (RR=1.646 [95% CI 1.03-2.62]), anemia in the anamnesis (RR=2.591[95% CI 1.56-4.28]),complicated labor in the anamnesis (RR=1.886 [95% CI 1.29-2.74]), habitual miscarriage (RR=1.850 [95% CI 1.21-2.82]), a history of preeclampsia (RR= 1.922 [95% CI 1.31-2.80]), a history of RR (RR=3.502 [CI 2.37-5.16]). Conclusions. The most significant clinical and anamnestic risk factors for the development of RRT are: arterial hypertension, overweight/obesity, anemia in the anamnesis, pre-eclampsia in the anamnesis, complicated labor in the anamnesis, habitual miscarriage, RRT in the anamnesis. Keywords: pregnancy, preeclampsia, anemia, fetal growth retardation, risk factors.

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Chard, T., A. Yoong und M. Macintosh. „The myth of fetal growth retardation at term“. BJOG: An International Journal of Obstetrics and Gynaecology 100, Nr. 12 (Dezember 1993): 1076–81. http://dx.doi.org/10.1111/j.1471-0528.1993.tb15169.x.

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Blair, Eve. „The myth of fetal growth retardation at term“. BJOG: An International Journal of Obstetrics and Gynaecology 101, Nr. 9 (September 1994): 830–31. http://dx.doi.org/10.1111/j.1471-0528.1994.tb11965.x.

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