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Готові списки джерел за темами / Fetal growth retardation / Статті в журналах

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Статті в журналах з теми "Fetal growth retardation"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 30 липня 2024

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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 (March 15, 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, no. 12 (December 2001): 1124–27. http://dx.doi.org/10.1007/s001290101082.

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3

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 (December 15, 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.

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4

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

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5

Kempley, S. "Doppler and fetal growth retardation." Archives of Disease in Childhood - Fetal and Neonatal Edition 70, no. 2 (March 1, 1994): F160. http://dx.doi.org/10.1136/fn.70.2.f160-a.

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6

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

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7

Beattie, R. B., and M. J. Whittle. "Doppler and fetal growth retardation." Archives of Disease in Childhood 69, no. 3 Spec No (September 1, 1993): 271–73. http://dx.doi.org/10.1136/adc.69.3_spec_no.271.

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8

Warshaw, Joseph B. "Intrauterine Growth Retardation." Pediatrics In Review 8, no. 4 (October 1, 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.

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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 (February 7, 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.

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10

ZHELEZOVA, M. E., B. K. BEKTUR, L. I. MALTSEVA, T. V. GRIGORYEVA, E. A. BOULYGINA, D. R. KHUSNUTDINOVA, and E. A. ZIATDINOVA. "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 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.

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11

Fox, H. "Placentation in intrauterine growth retardation." Fetal and Maternal Medicine Review 9, no. 2 (May 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.

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12

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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13

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

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14

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

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15

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

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16

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

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17

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 (May 1985): 330. http://dx.doi.org/10.1016/0028-2243(85)90052-8.

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18

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

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19

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

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20

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

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21

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 (January 14, 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.

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22

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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23

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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24

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

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25

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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26

Maršál, Karel. "Antenatal Diagnosis of Intrauterine Growth Retardation by Ultrasound." International Journal of Technology Assessment in Health Care 8, S1 (January 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.

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27

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 (July 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 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.

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28

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 (July 24, 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: Diagnostic tests validation study, with a universe of pregnant patients who attended the outpatient clinic of Hospital General Machala, El Oro-Ecuador, for prenatal control, between 32 and 38 weeks of gestation. The following variables were obtained: gestational dating; ultrasound fetal biometry of all the necessary parameters for the described indices calculation; fetal weight estimated by ultrasound, with cut-off point ≤ P° 10. The LH/CA and TCD/CA Indices were calculated, with cut-off points for fetal growth retardation diagnosis of ≥ 23.5 and ≥16.1 respectively. The index proposed by the authors HCF/CA was also applied, taking as cut-off point the 90th percentile: ≥ 1.063. RESULTS: The prevalence of fetal weight less P° 10 in the present study was 12.22%. The biometric index with the highest sensitivity was the HCF CA index with 70.3%; however, the highest specificity was obtained for the LF CA index with 84%. The positive predictive value of the DTC CA index was 24.7%, of the LF CA index: 27.9%, and of the HCF CA index: 31.1%. The negative predictive values found were, DTC CA: 93.9%; LF CA: 91.6% and HCF CA: 95.0%. The positive likelihood ratios obtained were: DTC CA: 2.352; LF CA: 2.781 and HCF CA: 3.25. The negative likelihood ratios were, HCF CA: 0.378, DTC CA: 0.465, LF CA: 0.661. CONCLUSION:The biometric indices for prediction of fetal growth retardation have limited positive predictive accuracy. All indices have high negative predictive accuracy. To confirm the presence of condition disease the HCF CA index has better results, as well as to confirm the absence of the condition disease; the addition of the HCF CA Index increases the predictive results; the Odds Rate obtained indicates that there is 8.595 times higher probability of a positive response, when the condition"fetus in percentile ≤ 10" is present.

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29

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 (June 15, 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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30

Fay, Roger A., and David A. Ellwood. "Categories of intrauterine growth retardation." Fetal and Maternal Medicine Review 5, no. 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.

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31

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 (December 29, 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.

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32

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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33

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

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34

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 (May 1985): 108–10. http://dx.doi.org/10.1111/j.1479-828x.1985.tb00619.x.

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35

James, D. "Diagnosis and management of fetal growth retardation." Archives of Disease in Childhood 65, no. 4 Spec No (April 1, 1990): 390–94. http://dx.doi.org/10.1136/adc.65.4_spec_no.390.

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36

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

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37

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 (October 1989): 1233–34. http://dx.doi.org/10.1111/j.1471-0528.1989.tb03204.x.

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38

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

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39

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

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40

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 (August 7, 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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41

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 (November 15, 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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42

Alsat, E., C. Marcotty, R. Gabriel, A. Igout, F. Frankenne, G. Hennen, and D. Evain-Brion. "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 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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43

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 (February 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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44

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 (May 5, 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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45

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 (September 1, 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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46

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 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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47

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 of delivery histories was performed in 116 (8.95%) cases in pregnant women with hypertensive disorders. Hypertensive disorders included: gestational hypertension - 27 (23.2%), chronic arterial hypertension combined with preeclampsia - 18 (15.5%), severe preeclampsia - 35 (30.2%), moderate preeclampsia - 36 (31.1%) cases. Early fetal growth retardation (up to 32 weeks of gestation) was in 32 (26.8%) cases, late fetal growth retardation - in 84 (73.2%) cases. Perinatal losses occurred in 4 (34.4%o) cases in pregnant women with early FGR. Results. Pregnant women with hypertensive disorders most often had concomitant kidney disease, hypertension, obesity of II-III degree, and varicose veins. The highest percentage of newborns with FGR as in pregnant women with chronic arterial hypertension of 2-3 grades (38.9%) and in women with severe preeclampsia (31.4%). The lowest average body weight (1260±52 g) was in newborns whose mothers had blood pressure above 200/130 mm Hg. The highest average body weight (1485±85 g) was in newborns whose mothers had blood pressure up to 160/100 mm Hg. Conclusions. Thus, pregnant women with hypertensive disorders are at high risk of developing a serious complication - early fetal growth retardation. The highest risk of uteroplacental circulation disorders is in pregnant women with chronic hypertension of 2-3 grades and severe preeclampsia.

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Pickard, MR, AJ Leonard, LM Ogilvie, PR Edwards, IM Evans, AK Sinha, and RP Ekins. "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 (February 1, 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 weight at 16, 19 and 21 days gestation (d.g.) was related to pre-mating maternal serum total thyroxine (TT(4)) levels; permanent fetal growth retardation occurred in severely (TX(s); pre-mating maternal serum TT(4) 16.19 nM) - but not in moderately (TX(m)) - hypothyroid dams. In TX(s) dams, glycogen concentration was elevated in maternal liver and in the fetal side of the placenta at 16 and 19 d.g., and in the maternal side of the placenta at 19 and 21 d.g., despite maternal euglycemia. In contrast, fetal liver glycogen concentration was deficient in TX(m) dams at 19 d.g. and in TX(s) dams at 19 and 21 d.g., and fetal hypoglycemia occurred in TX(s) dams at 21 d.g. Multiple regression analyses indicate that these fetal deficits are strongly associated with the retardation in fetal growth, while the elevated maternal liver and placental glycogen concentrations have no impact on fetal growth near term. The mechanisms by which severe maternal hypothyroidism permanently retards rat fetal growth remain to be determined.

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Spinillo, Arsenio, Ezio Capuzzo, Sabrina Nicola, Laura Colonna, Angela Iasci, and Carlo Zara. "Interaction between fetal gender and risk factors for fetal growth retardation." American Journal of Obstetrics and Gynecology 171, no. 5 (November 1994): 1273–77. http://dx.doi.org/10.1016/0002-9378(94)90146-5.

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50

Rizzo, G., D. Arduini, F. Pennestri, C. Romanini, and S. Mancuso. "Fetal behaviour in growth retardation: Its relationship to fetal blood flow." Prenatal Diagnosis 7, no. 4 (May 1987): 229–38. http://dx.doi.org/10.1002/pd.1970070402.

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