Current concepts of fetal growth restriction: part I. Causes, classification, and pathophysiology

Lin, Chin-Chu; Santolaya-Forgas, Joaquín

doi:10.1016/s0029-7844(98)00328-7

Cited by 107 publications

(98 citation statements)

References 95 publications

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“…[29][30][31][32] Common infections accounts for FGR foetuses are viral (rubella, cmv, herpes, varicella, herpes zoster, HIV) parasitic infections (toxoplasmosis, syphilis, malaria) and bacterial infections (chlamydia, mycoplasma, listeria, and tuberculosis). 33,34 Other viral, parasitic, and bacterial infections are associated with direct cell damage, or transplacental passage causing foetal infection, or placental vascular insufficiency.…”

Section: Foetal Factorsmentioning

confidence: 99%

Fetal growth restriction: aetiology, screening, diagnosis and management

Augusthy

2015

Int J Reprod Contracept Obstet Gynecol

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Foetal growth restriction (FGR) is a pathological condition that refers to a foetus that fails to reach his/her genetically predetermined growth potential. FGR remains a leading contributor to perinatal mortality and morbidity and metabolic syndrome in later life. The purpose of this review is to provide the summary statements of the aetiology of FGR and to establish a framework for screening, diagnosis, and management of pregnancies affected with foetal growth restriction. For this study, published literature was retrieved through searches of PubMed (Medline), Highwire, Google Scholar, Scopus, Cochrane Database of Systematic Reviews. Conference/Seminar proceedings, textbooks, previously published systematic reviews, controlled clinical trials, high quality prospective and retrospective observational studies, research articles and unpublished studies were also used for this study. The identification of FGR begins with assessment of maternal, foetal, placental and environmental risk factors and the diagnosis is made by Ultrasound biometry examination. Functional assessment of placental and foetal circulation by Doppler velocimetry and blood flow volume, together with computerized assessment of foetal heart rate variability, are key examinations in early and late FGR to assess severity of the disease and monitor foetal wellbeing. Appropriate timing of delivery in early FGR might change the outcome, and appropriate monitoring in late and term FGR might avoid unnecessary interventions.

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Section: Foetal Factorsmentioning

confidence: 99%

Fetal growth restriction: aetiology, screening, diagnosis and management

Augusthy

2015

Int J Reprod Contracept Obstet Gynecol

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“…Embryo/placental-disk ratios, however, which are typically elevated in placental insufficiency, were comparable between genotypes (Hs3st1 +/+ and Hs3st1 -/-ratios were 19.7 ± 0.8 versus 20.8 ± 1.1, respectively). IUGR from placental insufficiency also usually shows sparing of head growth (asymmetric IUGR) (46,47). Yet Hs3st1 -/-embryos, compared with Hs3st1 +/+ gestation mates, showed a significant reduction in the biparietal diameter (Figure 5b) -an established parameter of embryonic head growth (48).…”

Section: Figurementioning

confidence: 99%

Normal levels of anticoagulant heparan sulfate are not essential for normal hemostasis

Hajmohammadi¹,

Enjyoji²,

Princivalle³

et al. 2003

J. Clin. Invest.

125

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Endothelial cell production of anticoagulant heparan sulfate (HSact) is controlled by the Hs3st1 gene, which encodes the rate-limiting enzyme heparan sulfate 3-O-sulfotransferase-1 (3-OST-1). In vitro, HSact dramatically enhances the neutralization of coagulation proteases by antithrombin. The in vivo role of HSact was evaluated by generating Hs3st1–/– knockout mice. Hs3st1–/– animals were devoid of 3-OST-1 enzyme activity in plasma and tissue extracts. Nulls showed dramatic reductions in tissue levels of HSact but maintained wild-type levels of tissue fibrin accumulation under both normoxic and hypoxic conditions. Given that vascular HSact predominantly occurs in the subendothelial matrix, mice were subjected to a carotid artery injury assay in which ferric chloride administration induces de-endothelialization and occlusive thrombosis. Hs3st1–/– and Hs3st1+/+ mice yielded indistinguishable occlusion times and comparable levels of thrombin•antithrombin complexes. Thus, Hs3st1–/– mice did not show an obvious procoagulant phenotype. Instead, Hs3st1–/– mice exhibited genetic background–specific lethality and intrauterine growth retardation, without evidence of a gross coagulopathy. Our results demonstrate that the 3-OST-1 enzyme produces the majority of tissue HSact. Surprisingly, this bulk of HSact is not essential for normal hemostasis in mice. Instead, 3-OST-1–deficient mice exhibited unanticipated phenotypes suggesting that HSact or additional 3-OST-1–derived structures may serve alternate biologic roles

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“…One theory suggests that anemia (leading to hypoxia) and iron deficiency (which increases serum nor-epinephrine concentrations) induces maternal and fetal stress, ultimately leading to stimulation of the production of corticotropin-releasing hormone (CRH) (Allen, 2001;Dallman, 1987;Emanuel et al, 1994). Elevated CRH is a major risk factor for preterm labour, pregnancy-induced hypertension, eclampsia, premature rupture of the membranes, maternal infection (leading to yet more CRH synthesis), and increased fetal cortisol production (inhibiting longitudinal growth of the fetus) (Allen, 2001;Falkenberg et al, 1999;Lin et al, 1998;Linton et al, 1990, McLean et al, 1995. A second theory suggests that iron deficiency may increase oxidative damage to erythrocytes and the fetal-placental unit (Cester et al, 1994;Poranen et al, 1996).…”

Section: Preterm Delivery and Growthmentioning

confidence: 99%

Iron Deficiency Anemia: A Public Health Problem of Global Proportions

Charles¹

2012

Public Health - Methodology, Environmental and Systems Issues

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Current concepts of fetal growth restriction: part I. Causes, classification, and pathophysiology

Cited by 107 publications

References 95 publications

Fetal growth restriction: aetiology, screening, diagnosis and management

Fetal growth restriction: aetiology, screening, diagnosis and management

Normal levels of anticoagulant heparan sulfate are not essential for normal hemostasis

Iron Deficiency Anemia: A Public Health Problem of Global Proportions

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