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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Children born extremely prematurely are at risk for a variety of problems with motion analysis, including problems with motion-defined (MD) form recognition [Downie, A. L. S., Jakobson, L. S., Frisk, V., & Ushycky, I. (2003). Periventricular brain injury, visual motion processing, and reading and spelling abilities in children who were extremely-low-birthweight. Journal of the International Neuropsychological Society, 9, 440-449]. The aims of the present study were (1) to examine the impact of retinopathy of prematurity (ROP) and mild periventricular brain injury (PVBI) on MD form processing in this population; (2) to assess relationships between MD form recognition in these children and their performance in several other areas of visual competence. To this end, a battery of visual and visuomotor tests was administered to 43, 5- and 6-year old, extremely premature children, all of whom had escaped severe PVBI. A group of full-term controls was also studied. Relative to controls, premature children displayed clear deficits in MD form recognition and these deficits were related to the presence of ROP and/or mild PVBI, rather than to a history of prematurity per se. Regression analyses revealed significant associations in premature children between MD form processing deficits and problems with visual search, stereopsis, visuoconstructive and graphomotor skills, motor development, and Performance IQ. The results suggest that assessment of sensitivity to MD forms may be useful in the early identification of preterm children at greatest risk for visual problems associated with dorsal stream dysfunction.
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PMID:Motion-defined form processing in extremely premature children. 1662 43

High oxygen tension is a major factor in the genesis of retinopathy of prematurity (ROP). However, clinical and experimental evidence suggests a significant role for high carbon dioxide (CO(2)) tension as well. Along these lines, although ischemia is often considered to be synonymous with an oxygen deficit, it is also associated with a concomitant local elevation of CO(2) that can lead to impaired developmental and ischemic neovascularization. The mechanisms by which hypercapnia induces retinal microvascular degeneration, a critical step which precedes the subsequent proliferative preretinal neovascularization, are not known. Nitrative stress has an important role in microvascular degeneration leading to ischemia in conditions such as ROP. Hypercapnia is a facilitator of nitration in vitro. We hereby present evidence that prolonged exposure to CO(2) impairs developmental retinal neovascularization through a mechanism involving increased endothelial nitric oxide synthase and induction of a nitrative stress; effects of hypercapnia are independent of its hyperaemic effects. Moreover, we demonstrate that an in vivo nitrative stress associated with retinal vasoobliteration results in nitration of arachidonic acids into trans-arachidonic acids (TAAs), which can act as mediators of nitrative stress by causing microvascular degeneration by inducing expression of the antiangiogenic factor thrombospondin-1. These recent findings establish a previously unexplored means by which hypercapnia hinders efficient neovascularization and provide new insight into the molecular mechanisms of nitrative stress on microvascular injury involving TAA, and suggest new therapeutic avenues in the management of nitrative stress disorders such as in ischemic retinopathies (of prematurity and of diabetes) and encephalopathies.
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PMID:Hypercapnia- and trans-arachidonic acid-induced retinal microvascular degeneration: implications in the genesis of retinopathy of prematurity. 1681 71

As survival of preterm infants improves, the long-term care of consequent ophthalmic problems is an expanding field. Preterm birth can inflict a host of challenges on the developing ocular system, resulting in the visual manifestations of varied significance and pathological scope. The ophthalmic condition most commonly associated with preterm birth is retinopathy of prematurity, which has the potential to result in devastating vision loss. However, the visual compromise from increased incidence of refractive errors, strabismus, and cerebral vision impairment has significant impact on visual function, which also has influence on other developmental aspects including psychological and educational. In this review, the normal ocular development is discussed, aiming to exemplify the impact of early exteriorisation on one of the more naive organs of prematurity. This is then related to the incidence and visual consequences of many types of deficit, including refractive error, strabismus, and loss of visual function in preterm populations, with comparisons to term infant studies. Often these conditions are linked with causal and resultant factors being impossible to segregate, but the common factor of increased rates of all types of ophthalmic deficits demonstrates that children born prematurely are indeed premature for life.
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PMID:Ophthalmological problems associated with preterm birth. 1791 27

The role of the pancreas and insulin secretion in utero is to support fetal growth and preparation of the fetus with the nutritional reserves to maintain glucose homeostasis after birth. Adaptation at birth includes dramatic endocrine changes, up-regulation of enzymes critical for gluconeogenesis and preparation for the infant to regulate glucose control in the setting of an intermittent enteral supply of nutrition. Disorders of glucose homeostasis are not uncommon at this time, particularly in the setting of prematurity and very low birth weight (VLBW<1,500 g). Although historically hypoglycaemia has been the clinical concern, hyperglycaemia is also a well-documented problem, particularly during the first week in VLBW infants. This hyperglycaemia is a marker of insulin resistance and relative insulin deficiency and may reflect the prolonged catabolism observed in VLBW infants. Reduced insulin levels may also contribute to reduced insulin-like growth factor 1 (IGF-1) generation, and an increased risk of retinopathy of prematurity. Pilot studies of insulin replacement in VLBW infants demonstrate improved glucose control, and increased circulating IGF-1 bioactivity. This suggests that, along with nutritional support, restoration of the normal hormonal balance may be important in promoting anabolism in the VLBW infant.
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PMID:The physiology and clinical management of glucose metabolism in the newborn. 1792 75

Fifteen years of evidence have established that the cytokine erythropoietin offers promise as a treatment for brain injury. In particular, neonatal brain injury may be reduced or prevented by early treatment with recombinant erythropoietin. Extreme prematurity and perinatal asphyxia are common conditions associated with poor neurodevelopmental outcomes including cerebral palsy, mental retardation, hearing or visual impairment, and attention deficit hyperactivity disorder. When high doses of erythropoietin are administered systemically, a small proportion crosses the blood-brain barrier and can protect against hypoxic-ischemic brain injury. In addition to other protective effects, erythropoietin can specifically protect dopaminergic neurons. Since reduced dopamine neurotransmission contributes to attention deficit hyperactivity disorder, this condition may be amenable to erythropoietin treatment. This review focuses on the potential application of erythropoietin as a neuroprotectant with regard to neurologic complications of extreme prematurity, including attention deficit hyperactivity disorder. Recent concerns that early erythropoietin might exacerbate the pathologic neovascularization associated with retinopathy of prematurity are addressed.
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PMID:Recent trends in erythropoietin-mediated neuroprotection. 1793 39

The objective of this article is to review the role of matrix metalloproteinases (MMPs) in fetomaternal/neonatal complications of preterm birth. The function of MMPs as proteolytic enzymes involved in tissue remodeling/destruction is reviewed in preterm labor, preeclampsia, premature rupture of membranes, intrauterine growth restriction, chronic lung disease, necrotizing enterocolitis, intraventricular hemorrhage, cystic periventricular leukomalacia, and retinopathy of prematurity. Cytokines, steroid hormones, and reactive oxygen species all regulate MMP labor and expression/activity. In labor, activation follows an inflammatory response, which results in fetal membrane rupture and cervical dilation/ripening, particularly when premature. Expression/activation is elevated during parturition, particularly when premature. While fetal membrane rupture is preceded by increases in tissue-specific MMPs, neonatal complications also ensue from an imbalance between MMPs and their tissue inhibitors. These e fects implicate environmental triggers and a genetic predisposition. MMPs are involved in the perinatal complications of prematurity and are potential targets for therapeutic intervention. Functional MMP genetic polymorphisms may assist in identifying patients at risk of complications.
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PMID:Matrix metalloproteinases and their tissue inhibitors in preterm perinatal complications. 1800 Feb 25

High oxygen tension is a major factor in the genesis of retinopathy of prematurity (ROP). However, clinical and experimental evidence also suggest a significant role for high levels of carbon dioxide (CO(2)). Hypercapnia is a facilitator of nitration in vitro, and nitrative stress is known to have an important role in microvascular degeneration leading to ischemia in conditions such as ROP. We hereby present evidence that prolonged exposure to CO(2) impairs developmental retinal neovascularisation through a mechanism involving increased endothelial nitric oxide synthase and induction of a nitrative stress; effects of hypercapnia are independent of its hyperaemic effects. Moreover, in a model of oxygen-induced retinopathy, we demonstrate that an in vivo nitrative stress associated with retinal vasoobliteration results in nitration of cis-arachidonic acids into trans-arachidonic acids (TAAs). TAAs act in turn as mediators of nitrative stress by causing microvascular degeneration by inducing expression of the anti-angiogenic factor thrombospondin-1. These recent findings establish a previously unexplored means by which hypercapnia hinders efficient neovascularisation and provide new insight into the molecular mechanisms of nitrative stress on microvascular injury involving TAA, therefore opening new therapeutic avenues in the management of nitrative stress disorders such as in ischemic retinopathies (of prematurity and of diabetes) and encephalopathies.
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PMID:[Hypercapnia- and trans-arachidonic acid-induced retinal microvascular degeneration: implications in the genesis of retinopathy of prematurity]. 1802 4

With improved survival of very low birth infants in India, Retinopathy of Prematurity (ROP) is emerging as a significant problem. The most important risk factor in the pathogenesis of ROP is prematurity. Other factors like, problems with oxygenation frequent blood transfusions, sepsis and apnea have also been implicated in the causation of ROP. Essentially asymptomatic in the initial stages, a good screening program is essential for the early detection and treatment of this condition. Description of the various stages of ROP has been included in the protocol. Guidelines regarding the procedure of dilatation, ophthalmic examination and treatment (if required) have been provided. Close co-operation between the ophthalmologist and neonatologist is essential for a successful outcome.
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PMID:Retinopathy of prematurity. 1824 40

The goal of this study was to determine whether there was an association between perinatal risk factors of prematurity and vestibular evoked myogenic potentials (VEMPs). A prospective case-control trial was designed. Fifty preterm newborns (100 ears) with a gestational age <37 weeks were included. The control group consisted of 20 healthy term infants (40 ears). VEMP recordings were performed, and mean latencies of p13 were calculated in all study subjects. Multivariable logistic regression was used to investigate the influence of perinatal variables on abnormal VEMP responses. VEMPs were elicited in all term infants (40 ears). In preterm infants, the responses were normal in 71 ears, delayed in 24 and absent in 5. There was a significant difference between abnormal VEMP rates for preterm and term infants (p < 0.001). Asphyxia (OR = 13.985, p = 0.048) and time of VEMP test (OR = 0.865, p = 0.038) were related to abnormal VEMP responses. There was no association between delayed VEMPs and gestational age, birth weight, hemoglobin and bilirubin levels, phototherapy, intracranial hemorrhage, convulsions, sepsis, ototoxic drugs, transfusion, mechanical ventilation, retinopathy of prematurity, bronchopulmonary dysplasia and respiratory distress syndrome. These results suggest a delay in the maturation of VEMPs in premature infants. Asphyxia was the most important risk factor for abnormal VEMP responses in preterm infants.
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PMID:Vestibular evoked myogenic potentials in preterm infants. 1866 93

There is growing support for the role of genetic factors in the development of retinopathy of prematurity (ROP), a serious visual morbidity resulting from preterm birth. We used both candidate gene and data-mining approaches to investigate the role of genetic polymorphisms in the development of ROP. Our study population consisted of 330 infants, less than 32 wk gestation, and their parents. We initially studied 24 single nucleotide polymorphisms (SNPs) in 11 candidate genes. Using a family-based analysis strategy, we found an association between SNPs in the EPAS1 gene and the development of ROP (p = 0.007). Logistic regression analysis showed three SNPs associated with development of ROP, two in the CFH gene (p = 0.01) and one in the EPAS1 gene (p = 0.001). Extending this analysis to include genotyping data from a larger genetic study of prematurity (455 SNPs in 153 genes), we found SNPs in five genes associated with the development of ROP: IHH (p = 0.003), AGTR1 (p = 0.005), TBX5 (p = 0.003), CETP (p = 0.004), and GP1BA (p = 0.005). Our data suggest that genetic risk factors contribute to the development of ROP.
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PMID:Genetic contributions to the development of retinopathy of prematurity. 1878 2


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