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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The major benefits arising from elevated dosages of vitamin E have been the relief of symptoms of vitamin E deficiency in humans with abetalipoproteinemia and chronic cholestasis. In addition, supplements of vitamin E prevent the isolated vitamin E deficiency that has recently been associated with spinocerebellar symptoms. In keeping with the view that newborn infants, and especially premature infants, suffer from vitamin E deficiency, elevated dosages of vitamin E have been administered to prevent the anemia of premature infants, retrolental fibroplasia, bronchopulmonary dysplasia, and intraventricular hemorrhage. However, the results have been conflicting. Furthermore, some infants treated with vitamin E die unexpectedly. The life-threatening hazard of such treatments has been attributed mainly to polysorbates that are used as detergents in preparations of vitamin E for intravenous use rather than to vitamin E itself. The possibility that vitamin E, in its action as an antioxidant, inhibits the generation of superoxide anion in leukocytes is examined in this paper.
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PMID:Clinical uses and abuses of vitamin E in children. 131 69

Several intellectual "autopsies" have recently reviewed errors in clinical epidemiologic studies of causation, such as the original claim that amyl nitrite "poppers" caused AIDS. The current autopsy was done to determine why it took more than a decade--1942 to 1954--to end an iatrogenic epidemic in which high-dose oxygen therapy led to retrolental fibroplasia (RLF) in premature infants, blinding about 10,000 of them. The autopsy revealed a museum of diverse intellectual pathology. When first noted, RLF was regarded as neither a new disease nor a postnatal effect. In early investigations, the ophthalmologists did not establish explicit criteria for diagnosis and confused RLF with malformations previously seen in full-term infants. Because the patients were not referred until months after birth, the ophthalmologists assumed that the lesion, which resembled an embryologic structure, must have occurred prenatally. Other events suggesting a prenatal cause for RLF were its strong statistical associations with fetal anomalies, multiple gestations, and maternal infections. Although these events were also associated with prematurity, it was ignored when the RLF cases were compared with controls who were mainly full-term infants. The postnatal timing of RLF was eventually recognized when investigators did cohort studies in premature infants and found that RLF could develop in eyes that were normal at birth. As the search for a cause turned to events occurring after birth, statistical associations were produced for agents such as light, vitamins, iron, vitamin E deficiency, and hypoadrenalism. Each study had its own methodologic flaws: controls were missing for light; co-maneuvers were ignored for vitamins and iron; objective diagnosis was not used for vitamin E deficiency; and the research on hypoadrenalism contained biases in susceptibility and detection as well as problems of a competing outcome event. When the role of oxygen administration was first considered, the statistical association with RLF was stronger for vitamin- and iron-therapy than for oxygen. In addition, many investigators were dissuaded by contradictory evidence from institutions in which RLF was either absent despite high-dose oxygen or persistent despite reduced dosage. The contradictory evidence was later regarded as erroneous because of unsatisfactory delivery systems for the oxygen or failure to check the actual oxygen concentrations. An alternative explanatory hypothesis, rejecting the role of high-dose and long-duration oxygen, was the idea that RLF was due to "relative hypoxia", produced by overly rapid weaning from oxygen therapy rather than the duration of oxygen treatment itself.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oxygen as a cause of blindness in premature infants: "autopsy" of a decade of errors in clinical epidemiologic research. 143 8

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

Vitamin E was discovered by Evans and Bishop in 1922. Work in the 1930s revealed the chemical structure and the biological function of alpha-tocopherol. In the 1940s Filer and others demonstrated that vitamin E protects tissue unsaturated fatty acids against oxidation. The 1940s and the 1950s marked the beginning of interest in the role of vitamin E in infant nutrition. During this period, investigators examined the intestinal absorption of vitamin E in infants and its use for the prevention of hemolysis, retrolental fibroplasia, intracranial hemorrhage, and pulmonary oxygen toxicity. These studies were the forerunners of more recent studies examining possible benefits of vitamin E therapy in premature infants. Recent studies confirmed earlier reports indicating that enteral administration of vitamin E is the safest and most effective route in infants. Although preventing vitamin E deficiency is clearly necessary, neither earlier nor more recent work has shown any benefit from high-dose vitamin E therapy (greater than 20 IU X kg-1 X d-1) for premature infants.
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PMID:History of vitamin E in infant nutrition. 330 Feb 57

A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
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PMID:A reexamination of the role of oxygen in retrolental fibroplasia. 641 99

Vitamin E (alpha-tocopherol) has been credited with a variety of beneficial effects in the premature newborn infant. It has been thought that deficiency of vitamin E is at least partly responsible for the anemia which often occurs 4 to 6 wk after premature birth, and routine dietary supplementation with vitamin E is frequently recommended. However, critical analysis reveals that published controlled studies of vitamin E supplementation do not agree on the magnitude or even the existence of this protective effect against anemia. Analysis of commonly used feeding practices suggests that the dietary ratio of alpha-tocopherol to polyunsaturated fatty acids is generally sufficient to prevent manifestations of vitamin E deficiency without supplementation. Large parenteral doses of vitamin E have been purported to protect premature infants exposed to oxygen-enriched environments and mechanical ventilation from the complications of retrolental fibroplasia and bronchopulmonary dysplasia. Subsequent studies, however, have not yet substantiated encouraging early reports of these protective effects. At present, there seems to be no clearly established need for supplementing the premature infant's usual dietary intake of vitamin E.
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PMID:The role of vitamin E in the nutrition of premature infants. 678 56

Preterm infants may be susceptible to chronic lung disease and retinopathy of prematurity because of deficient antioxidant mechanisms including deficiency of vitamin E. The aim of this study was to evaluate the status of the antioxidant vitamin E among preterm and term livebirths. Umbilical cord blood samples collected from 40 preterm and 180 term babies were analyzed for vitamin E levels using high performance liquid chromatography. Linear regression analysis was used to examine the relationship of vitamin E with gestational age, birth weight and appropriateness of weight for gestational age. The median vitamin E level of preterm babies (2.61 mg/L) was not significantly different from that of term babies (2.77 mg/L), p = 0.2. Linear regression analysis demonstrated a weak but statistically significant correlation between cord blood vitamin E levels and gestational age (r = 0.14, p = 0.046). Vitamin E levels did not correlate with birth weight or weight for gestational age. Preterm babies had a higher incidence of vitamin E deficiency compared to term babies (38% v 19%, p = 0.02). Our findings lead us to conclude that vitamin E accumulates in the fetus throughout the third trimester so that preterm infants are likely to have vitamin E deficiency.
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PMID:Vitamin E status of infants at birth. 1064 61

Retrolental fibroplasia is today the principal cause of blindness in children of preschool age, exceeding all other causes combined. The disease occurs in infants of low weight at birth, commonly those born prematurely. The incidence of the disease is rising at an alarming rate. Vitamin E deficiency, corticotropin (ACTH) deficiency, the use of cow's milk in place of mother's milk, and improper oxygenation have been suggested as etiologic factors but the cause remains a mystery. Often the incidence is high in institutions in which maximal care is given premature infants.Clinically, the disease advances through an "active" phase during which regression is possible, and a "subsiding" or "cicatricial" phase which terminates with the formation of a disorganized opaque mass behind the lens. The earliest manifestations are noted in the fundi. Hemorrhages, neovascularization, transudation commencing in the periphery, and retinal separation contribute to the formation of the characteristic retrolental membrane. The diagnosis may be made when the retrolental membrane is observed in the eye of an infant whose weight at birth was low. Differential diagnosis is required occasionally. Thus far, no form of therapy has prevented or reversed the pathologic changes successfully. Use of vitamin E, corticotropin and mother's milk has not influenced the incidence of the disease. Avoidance of premature delivery if possible is indicated.
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PMID:Retrolental fibroplasia; blindness in infants of low weight at birth. 1300 70