scholarly journals OP01.06: Short and long-term impact of intrauterine growth restriction on neurobehavior, white matter diffusion and connectivity in a rabbit model

2012 ◽  
Vol 40 (S1) ◽  
pp. 56-56
Author(s):  
M. Illa ◽  
E. Eixarch ◽  
D. Batalle ◽  
E. Muñoz-Moreno ◽  
A. Arbat-Plana ◽  
...  
Obesity ◽  
2013 ◽  
Vol 22 (2) ◽  
pp. 608-615 ◽  
Author(s):  
Tessa L. Crume ◽  
Ann Scherzinger ◽  
Elizabeth Stamm ◽  
Robert McDuffie ◽  
Kimberly J. Bischoff ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Erich Cosmi ◽  
Tiziana Fanelli ◽  
Silvia Visentin ◽  
Daniele Trevisanuto ◽  
Vincenzo Zanardo

Intrauterine growth restriction is a condition fetus does not reach its growth potential and associated with perinatal mobility and mortality. Intrauterine growth restriction is caused by placental insufficiency, which determines cardiovascular abnormalities in the fetus. This condition, moreover, should prompt intensive antenatal surveillance of the fetus as well as follow-up of infants that had intrauterine growth restriction as short and long-term sequele should be considered.


NeuroImage ◽  
2014 ◽  
Vol 100 ◽  
pp. 24-38 ◽  
Author(s):  
Dafnis Batalle ◽  
Emma Muñoz-Moreno ◽  
Ariadna Arbat-Plana ◽  
Miriam Illa ◽  
Francesc Figueras ◽  
...  

Metabolites ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 267 ◽  
Author(s):  
Elena Priante ◽  
Giovanna Verlato ◽  
Giuseppe Giordano ◽  
Matteo Stocchero ◽  
Silvia Visentin ◽  
...  

Recognizing intrauterine growth restriction (IUGR) is a matter of great concern because this condition can significantly affect the newborn’s short- and long-term health. Ever since the first suggestion of the “thrifty phenotype hypothesis” in the last decade of the 20th century, a number of studies have confirmed the association between low birth weight and cardiometabolic syndrome later in life. During intrauterine life, the growth-restricted fetus makes a number of hemodynamic, metabolic, and hormonal adjustments to cope with the adverse uterine environment, and these changes may become permanent and irreversible. Despite advances in our knowledge of IUGR newborns, biomarkers capable of identifying this condition early on, and stratifying its severity both pre- and postnatally, are still lacking. We are also still unsure about these babies’ trajectory of postnatal growth and their specific nutritional requirements with a view to preventing, or at least limiting, long-term complications. In this setting, untargeted metabolomics—a relatively new field of ‘-omics’ research—can be a good way to investigate the metabolic perturbations typically associated with IUGR. The aim of this narrative review is to provide a general overview of the pathophysiological and clinical aspects of IUGR, focusing on evidence emerging from metabolomic studies. Though still only preliminary, the reports emerging so far suggest an “early” pattern of glucose intolerance, insulin resistance, catabolite accumulation, and altered amino acid metabolism in IUGR neonates. Further, larger studies are needed to confirm these results and judge their applicability to clinical practice.


Author(s):  
Ronny Geva

Recent data shows that 30 million low-birth-weight (LBW) infants are born annually worldwide (23.8% of all births). Although the global prevalence of such births is gradually decreasing, rates are still as high as 30% in many developing countries (World Health Organization 2008). Low birth weight is due to intrauterine growth restriction (IUGR), rather than or in addition to prematurity, in approximately one-third of these cases. This staggering number of affected children underscores the importance of understanding the short- and long-term cognitive and behavioral complications of IUGR. Intrauterine growth restriction conveys short- and long-term neurodevelopmental risks and thus requires costly long-term investment of medical, cognitive emotional, educational, and economical resources. Nevertheless, if treated aggressively, IUGR more often than not bears a fairly optimistic outlook, once the infant overcomes the initial life-threatening issues (Geva et al. 2006a). Intrauterine growth restriction is frequently detected in a pregnancy with a less-than-expected third trimester weight gain (100–200 g [3.5–7 oz] per week) or as an incidental finding on ultrasound examination when fetal measurements are less than expected for gestational age (GA; Geva et al. 2005). An estimated fetal weight under the 10th percentile, as determined by serial ultrasound examination, strongly correlates with growth restriction (Bernstein and Gabbe 1996; McCormick 1985). The etiologies of IUGR are typically thought of according to three interdependent categories: fetal factors, placental factors, and maternal factors (Kay 2008). Fetal factors include chromosomal events, such as trisomy 18 and 13 and sex chromosome abnormalities, which account for 5%–15% of all IUGR cases. Further exploration of genetic factors is currently under way, with mixed results (Kotzot et al. 2001). Other fetal factors linked to IUGR include congenital anomalies, mostly cardiovascular malformations, gastroschisis and omphalocele; infection, often related to rubella, cytomegalovirus, and toxoplasmosis (see Chapter 25); and multiple gestations, in which uteroplacental blood flow variations and/or twin–twin transfusion develops (Miller et al. 2008). Fetal villus circulation abnormalities are placental factors related to IUGR (Roberts and Post 2008).


2021 ◽  
pp. 088307382199989
Author(s):  
Lijia Wan ◽  
Kaiju Luo ◽  
Pingyang Chen

Intrauterine growth restriction is a condition that prevents normal fetal development, and previous studies have reported that intrauterine growth restriction is caused by adverse intrauterine factors. This condition affects both short- and long-term neurodevelopmental disorders. Studies have revealed that neurodevelopmental disorders can contribute to gray and white matter damage and decrease the brain volume of affected individuals. Further, these disorders are associated with increased risks of mental retardation, cognitive impairment, and cerebral palsy, which seriously affect the quality of life. Although the mechanisms underlying the neurologic injury associated with intrauterine growth restriction are not completely clear, studies have revealed that neuronal apoptosis, neuroinflammation, oxidative stress, excitatory toxicity, disruption of blood-brain barrier, and epigenetics may be involved in this process. This article reviews the manifestations and possible mechanisms underlying neurologic injury in intrauterine growth restriction and provides a theoretical basis for the effective prevention and treatment of this condition.


2021 ◽  
pp. 153537022110035
Author(s):  
Mari Kinoshita ◽  
Fàtima Crispi ◽  
Carla Loreiro ◽  
Eduard Gratacós ◽  
Míriam Illa ◽  
...  

Intrauterine growth restriction affects up to 10% of all pregnancies, leading to fetal programming with detrimental consequences for lifelong health. However, no therapeutic strategies have so far been effective to ameliorate these consequences. Our previous study has demonstrated that a single dose of nutrients administered into the amniotic cavity, bypassing the often dysfunctional placenta via intra-amniotic administration, improved survival at birth but not birthweight in an intrauterine growth restriction rabbit model. The aim of this study was to further develop an effective strategy for intra-amniotic fetal therapy in an animal model. Intrauterine growth restriction was induced by selective ligation of uteroplacental vessels on one uterine horn of pregnant rabbits at gestational day 25, and fetuses were delivered by cesarean section on GD30. During the five days of intrauterine growth restriction development, three different methods of intra-amniotic administration were used: continuous intra-amniotic infusion by osmotic pump, multiple intra-amniotic injections, and single fetal intraperitoneal injection. Technical feasibility, capability to systematically reach the fetus, and survival and birthweight of the derived offspring were evaluated for each technique. Continuous intra-amniotic infusion by osmotic pump was not feasible owing to the high occurrence of catheter displacement and amnion rupture, while methods using two intra-amniotic injections and one fetal intraperitoneal injection were technically feasible but compromised fetal survival. Taking into account all the numerous factors affecting intra-amniotic fetal therapy in the intrauterine growth restriction rabbit model, we conclude that an optimal therapeutic strategy with low technical failure and positive fetal impact on both survival and birthweight still needs to be found.


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