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

17 babies suffering from haemolytic disease or "hyperbilirubinaemia of prematurity" underwent exchange transfusion in the first 4 days of life. In 14 babies, including all those who had abnormally low pre-exchange serum vitamin E levels (<0.5 mg/100 ml), the vitamin E concentration rose as a result of exchange transfusion. In 3 babies the serum vitamin E concentration fell as result of exchange transfusion, but in no case was the post-exchange level below 0.5 mg/100 ml. The normal range of plasma vitamin E in stored ACD blood was 0.44--1.24 mg/100 ml. It was concluded that although vitamin E deficiency might be a factor in the aetiology of the anaemia of prematurity, prior subjection to exchange transfusion is unlikely to make a significant contribution to the vitamin E deficiency.
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PMID:Exchange transfusion and serum vitamin E (tocopherol) concentration in the newborn. 57 29

A refined classification of the stages of the retinopathy of prematurity (RLF) based on the experience of over 7500 examinations during the past decade is presented. We have been using the basic elements of this classification since 1972 in order to evaluate the influence of vitamin E on retrolental fibroplasia (RLF). It is our impression that it provides a more accurate clinical method of following the course of the retinopathy and a tool for assessing the factors other than prematurity and hyperoxia that may play a subtle role in the development of RLF.
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PMID:A classification of retrolental fibroplasia to evaluate vitamin E therapy. 58 96

Fetal hypotrophy or intrauterine growth retardation is an important cause of fetal and neonatal mortality and a real cause of iatrogenic prematurity. When pregnancy is progressing normally there are histological changes in the spiral arteries with an equilibrium between the endothelial prostacyclin and platelet thromboxane on the one part and peroxides and Vitamin E on the other part. This allows uteroplacental circulation to flow rapidly and at a low pressure. Furthermore immunological tolerance of the mother's system in the relationship to her embryo plays a part in bringing about this special haemodynamic state. The physiopathology of retarded growth stemming from the blood vessels brings into play multiple mechanisms. The first cause is a defect in placentation which is shown up as insufficient trophoblastic invasion in the second stage. This brings about endothelial dysfunction with disappearance of the normal equilibrium of the prostaglandins and an alteration in the physiological equilibrium between the peroxides and a natural antagonist, which is vitamin E. Immunological disturbances have also been considered following studies on the immunohistochemistry and with the frequent association of obstetrical vascular complications together with phospholipid specific autoantibodies.
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PMID:[Fetal growth retardation: physiopathology. Review of the literature]. 149 Nov 29

The essential effects of Tocopherol are based on its antioxidative capacity. Tocopherol, however, is just one in a group of antioxidants, which are important for the organism. Established indication for therapeutical application of vitamin E in infancy is only vitamin-E-malabsorption in connection with chronic cholestasis, pancreatic insufficiency (cystic fibrosis) and short bowel syndrome. In emergency therapy vitamin E is suggested with high dosage in case of shock lung and haemolytic-uraemic syndrome. Positive effects of daily vitamin E application in connection with prophylaxis of retinopathy prematurity, bronchopulmonary dysplasia and intraventricular encephalorrhagia of premature infants of severe underweight are not established. Very questionable therapeutic or prophylactic efficiency is opposed to the risk of higher incidence of severe complications in caring for premature infants of severe underweight, such as enterocolitis necroticans and neonatal septicaemia.
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PMID:[The use of vitamin E in childhood]. 209 6

The use of elevated dosages of vitamin E in humans has led to the discovery of vitamin E deficiency syndromes in neurological areas. This evidence comes from careful clinical studies in which elevated vitamin E dosages were applied. In long-term studies it has now been established that retinal and neurological abnormalities are due to vitamin E deficiency and can be ameliorated by therapy with a large amount of the vitamin enterally or parenterally, which can possibly completely prevent the development of clinical manifestations if adequate treatment is given from an early age. It has also become clear that similar neurological and ocular lesions occur in other chronic fat malabsorptive states such as cholestatic liver diseases, cystic fibrosis, and extensive resection of the gut, with respect to an elevated dosage of vitamin E therapy. More recently, several patients with spinocerebellar degeneration from vitamin E deficiency without other evidence of malabsorption have been reported on in whom the progression of the diseases is cessated by the vitamin E therapy. Whether or not the use of elevated dosages of vitamin E should be recommended for certain diseases in premature infants is controversial. Previously, it has been thought that newborn infants, especially premature infants, suffer from vitamin E deficiency, because of their low plasma vitamin E concentrations and high susceptibility of erythrocytes to hydrogen peroxide hemolysis test. Furthermore, tocopherol deficiency has been implicated in four neonatal conditions: anemia of prematurity, retrolental fibroplasia (RLF), bronchopulmonary dysplasia (BPD), and intraventricular hemorrhage (IVH). A hemolytic anemia, associated with thrombocytosis and edema, which is responsive to vitamin E therapy, is not well recognized and occurs in a minority of preterm infants, who were given high amounts of polyunsaturated fatty acids in their formula. However, prophylactic use of an elevated dosage of vitamin E to prevent anemia in the majority of premature infants is controversial. There is no evidence for beneficial effects in BPD. In addition, the prophylactic use of pharmacological dosages of vitamin E for prevention of RLF and IVH has also had conflicting results. In the course of therapy with elevated dosages of vitamin E, administered either orally, intramuscularly, or intravenously, many problems arose in the infants, such as unexpected death, increased frequency of necrotizing enterocolitis (NEC) and sepsis, and the development of unusual symptoms including hepatic injuries.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use and safety of elevated dosages of vitamin E in infants and children. 250 8

We conclude that 5 mg/kg of vitamin E, administered intra-arterially as an 8-hour continuous infusion, significantly and predictably raises serum vitamin E levels into the supraphysiologic range with no apparent side effects. In a group of premature infants whose initial serum vitamin E levels were generally greater than or equal to 0.5 mg/dL, no decrease in bilirubin production was observed. Thus, vitamin E deficiency probably does not play a prominent role in jaundice of prematurity.
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PMID:Continuous parenteral infusion of vitamin E pharmacokinetics and bilirubin production in premature neonates. 262 4

The newborn brain, and even more so the brain of the premature child, can be considered as an authentic target organ for numerous pathological conditions, some of which exist outside the central nervous system (changes involving primarily both respiratory function and cardiocirculatory function with serious repercussions at encephalic level). In the premature, this greater "vulnerability" is related to the reduced or absent capacity for self-regulation of the cerebral blood low (mechanism influenced negatively by hypoxia, hypercapnia and metabolic acidosis conditions) and the important role played by numerous factors in protecting newborns from haemorrhagic damage. Of these the most important are the state of prematurity, the presence of vascular, intravascular and extravascular changes, the effects exerted on cerebral haemodynamics by mechanical ventilation and by certain drugs employed in treatment. In mechanically ventilated newborns and premature, prevention of haemorrhagic damage (periendoventricular) is currently based on the application of clear-cut protocols of intensive and rehabilitative treatment. The following form part of these protocols: low damage ventilation techniques (high frequencies, low PJP, low MAP), curarisation (to avoid fluctuations in cerebral blood flow), neuroprotection (phenobarbital), the use of substances and drugs which, by exploiting different mechanisms, go to reduce the extent of the haemorrhage (vitamin E, indomethacin, ethamosylate, tranexamic acid).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevention of hemorrhagic cerebral injury in newborn and premature infants subjected to mechanical ventilation]. 269 3

Serum vitamin E levels are reduced in newborn infants. It has been reported that this deficiency is responsible, in part, for the development of anemia in premature infants during the first 6 weeks of life. The efficacy of vitamin E supplementation for the prevention of anemia in premature infants has been studied in a randomized, controlled, and blinded trial. Premature infants whose birth weights were less than 1,500 g were given, by gavage, 25 IU of dl-alpha-tocopherol or a similar volume of the drug vehicle. Treatment was continued for the first 6 weeks of life. A total of 178 infants were studied. Vitamin E levels were significantly higher in a supplemented group by day 3 and for the remainder of the 6-week period. At 6 weeks of age, there was no significant difference between the supplemented and unsupplemented groups in hemoglobin concentration, reticulocyte and platelet counts, or erythrocyte morphology. It is concluded that there is no evidence to support a policy of administering vitamin E to premature infants to prevent the anemia of prematurity.
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PMID:Oral vitamin E supplementation for the prevention of anemia in premature infants: a controlled trial. 354 Aug 36

To test the efficacy and safety of vitamin E in preventing retinopathy of prematurity, 287 infants with birth weights of less than 1.5 kg or gestational ages of less than 33 weeks were enrolled within 24 hours of birth in a randomized, double-masked trial of IV, followed by oral, placebo v tocopherol (adjusted to plasma levels of 3 to 3.5 mg/dL). In the 196 infants completing ophthalmic follow-up, tocopherol did not prevent retinopathy of prematurity of any stage (28% placebo treated v 26% tocopherol treated) or moderately severe retinopathy of prematurity (8% placebo treated v 11% tocopherol treated). Cicatricial sequelae were not significantly different (1/97 placebo treated v 3/99 tocopherol treated), with one placebo-treated infant and one tocopherol-treated infant having retinal detachments. Among all 232 infants examined, those treated with tocopherol had more retinal hemorrhage than placebo-treated infants (8/121 placebo treated v 16/111 tocopherol treated), and retinal hemorrhage correlated positively (P less than .01) with plasma levels of tocopherol after the first 2 weeks of age. Prospective monitoring of morbidity including late-onset sepsis, necrotizing enterocolitis, etc revealed no differences between groups except that grades 3 and 4 intraventricular hemorrhage occurred more frequently in infants weighing less than 1 kg at birth who had received tocopherol (14/42, 33%) v those who had received placebo (4/43, 9%) (P less than .02). Our data do not support the use of tocopherol for prophylaxis against retinopathy of prematurity in premature infants and suggest that IV tocopherol treatment starting on day 1 may increase the incidence of hemorrhagic complications of prematurity, particularly in infants with birth weights of less than 1 kg.
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PMID:Tocopherol efficacy and safety for preventing retinopathy of prematurity: a randomized, controlled, double-masked trial. 354

1. Studies were made on the vitamin E status of the newborn as judged by cord serum vitamin E and erythrocyte haemolysis in vitro in relation to gestational age, birth weight and maternal vitamin E status in subjects belonging to low (LIG)- and high (HIG)-income groups in urban Baroda. 2. In the case of full-term infants, the mean values for maternal serum vitamin E (mg/l) for LIG (n 73) and HIG (n 43) were 9.9 (SE 0.4) and 11.6 (SE 0.5). The corresponding values for cord serum vitamin E were 3.6 (SE 0.2) and 4.6 (SE 0.2) mg/l. 3. Serum vitamin E levels (mg/l) were lower in premature infants (2.3 (SE 0.2); n 20) and low-birth-weight full-term infants (2.9 (SE 0.2); n 25) than in full-term normal infants (4.2 (SE 0.1); n 91). This was associated with differences in maternal serum vitamin E levels (7.4 (SE 0.5), 8.2 (SE 0.5) and 11.1 (SE 0.3) respectively). The differences were more marked for LIG. 4. A negative correlation was found between serum vitamin E and erythrocyte haemolysis in vitro in the case of maternal blood but not in cord blood. 5. These results suggest that maternal vitamin E deficiency is one of the features associated with prematurity and intra-uterine growth retardation.
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PMID:Vitamin E status of the newborn in relation to gestational age, birth weight and maternal vitamin E status. 367 41


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