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Vitamin E therapy

In bronchitics, there have been reports of elevated serum-conjugated dienes, hydroperoxides and aldehydes, and a claim of clinical eflicacy as well as normalization of these parameters after vitamin E therapy (Kleiner et al., 1990). However, these patients were given combined therapy including steroids and thus the effect of vitamin E alone cannot be assessed. N-Acetylcysteine administered to chronic bronchitics increased plasma cysteine from a below-normal baseline but it has not been shown that this intervention had any effect on the disease process, the dosing being of short duration, nor were there short-term effects of the release of ROS from blood neutrophils (reviewed by MacNee et al., 1991). A... [Pg.226]

Today s healthcare policy-makers, including government officials, health insurance companies and managed-care organizations, are faced with the reality of limited resources for healthcare and the knowledge that much medical care is of uncertain value. The value of vitamin E therapy in Alzheimer s disease, for example, is still unclear, but some physicians have recommended it for years without any real measures of its effect on the disease. [Pg.302]

Liu, S.-L., Esposti, S.D., Yao, T., Diehl, A.M. Zern, M.A. (1995) Vitamin E therapy of acute CCl4-induced hepatic injury in mice is associated with inhibition of nuclear factor kappa B binding. Hepatology, 22, 1474-1481... [Pg.428]

Knowledge of the chemical structures of the major vitamins was acquired during the 30 years after 1920, and some were identified as known compounds. They were classified as fat-soluble and water-soluble vitamins. The only heterocyclic compounds in the former class are the tocopherols (vitamin E). They were discovered through their action in preventing sterility in rats, but they appear to play an important part in the metabolism of skeletal muscle. Vitamin E deficiency appears to occur rarely in man, but vitamin E therapy is tried in a number of clinical disorders. The tocopherols may be isolated from vegetable oils, and synthetic a-tocopherol (61) is made by condensing trimethylhydroquinone with phytol or phytyl halides (Scheme 2). For medicinal use they may be converted into their acetates or succinates. [Pg.155]

An increased incidence of infection, even sepsis after intramuscular injection, as an adverse effect of megadose vitamin E therapy in very low birth weight infants was first reported in Japan in 1986 (SEDA-12, 330). In a review of the literature in 1992 it was concluded that pharmacological serum concentrations of vitamin E might predispose premature infants to infectious complications, possibly caused by an inhibitory effect of vitamin E on the formation of superoxide anion in leukocytes (27). [Pg.3678]

Vitamin E therapy in vitamin K-deficient subjects and subjects taking anticoagulants reduces active plasma prothrombin concentrations (44). [Pg.3679]

Desferrioxamine and glutathione have some protective effects against mercury-induced lipid peroxidation vitamin E therapy has also been suggested as a possible protectant against membrane oxidation. Use of antioxidants in general may reduce some of the long-term chronic symptoms of mercury poisoning. [Pg.184]

Reduced chronic hemolysis in Mediterranean glucose-6-phosphate dehydrogenase deficiency after vitamin E therapy. [Pg.46]

When compared with the other trials there are three major differences the type of drug used, the dose administered, and the duration of vitamin E therapy. [Pg.581]

In the early 1970s, megadose vitamin E therapy was promoted as the cure for a variety of ailments, from acne and allergy to infertility and impotence. Many of these claims were loosely based on animal studies that were not backed by scientifc evidence in humans. Vitamin E has suffered from a somewhat tarnished image in recent years. [Pg.166]

Due to bleeding risk, individuals on anticoagulant therapy or individuals who are vitamin K-deficient should not take vitamin E supplementation without close medical supervision. Absent of that, vitamin E is a well-tolerated relatively non-toxic nutrient. A tolerable upper intake level of 1,000 mg daily of a-tocopherol of any form (equivalent to 1,500 IU of RRR a-tocopherol or 1,100 IU of all-rac-a-tocopherol) would be, according to the Food and Nutrition Board of the Institute of Medicine, the highest dose unlikely to result in haemorrhage in almost all adults. [Pg.1298]

Patients with abetalipoproteinaemia, a rare inborn disorder of lipoprotein metabolism, are totally deficient in vitamin E fiom birth and, if untreated, invariably develop a characteristic pigmentary retinopathy similar to that seen in retinitis pigmentosa and peroxisomal disorders. The same retinopathy has been observed in other patients with severe and chronic vitamin E deficiency. A essive vitamin E replacement therapy in all these patients has been shown either to prevent, to halt the progression of, or in some cases, to improve the characteristic visual abnormalities (Muller and Lloyd, 1982). [Pg.136]

Attempts to counteract tolerance development include the use of thiols such as N-acetylcysteine, antioxidants such as vitamin C and vitamin E, and angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists. Other approaches to decreasing the development of tolerance include intermittent therapy... [Pg.294]

Vitamin E may be indicated in some rare forms of anemia such as macrocytic, megaloblastic anemia observed in children with severe malnutrition and the hemolytic anemia seen in premature infants on a diet rich in polyunsaturated fatty acids. Also anemia s in malabsorption syndromes have shown to be responsive to vitamin E treatment. Finally, hemolysis in patients with the acanthocytosis syndrome, a rare genetic disorder where there is a lack of plasma jS-lipoprotein and consequently no circulating alpha tocopherol, responds to vitamin E treatment. In neonates requiring oxygen therapy vitamin E has been used for its antioxidant properties to prevent the development retrolental fibroplasia. It should be noted that high dose vitamin E supplements are associated with an increased risk in allcause mortality. [Pg.476]

The importance of cell death mediated by oxidative damage has led to the popularity of antioxidants as potential therapeutics. A variety of naturally occurring (vitamin C, vitamin E) and synthetic (lazaroids) antioxidants have been smdied as possible remedies for a wide variety of ailments. Large doses of vitamin E have been studied as a putative therapy in Alzheimer s disease, functioning through the inhibition of amyloid-induced oxidative destruction of neuronal membranes within the brain. [Pg.411]

Albright F, Butler AM, Bloom E. Rickets resistant to vitamin D therapy. Am J Dis Child 1937 54 529 14. [Pg.684]


See other pages where Vitamin E therapy is mentioned: [Pg.267]    [Pg.279]    [Pg.634]    [Pg.204]    [Pg.636]    [Pg.267]    [Pg.279]    [Pg.634]    [Pg.204]    [Pg.636]    [Pg.148]    [Pg.1298]    [Pg.108]    [Pg.132]    [Pg.521]    [Pg.459]    [Pg.199]    [Pg.852]    [Pg.920]    [Pg.933]    [Pg.942]    [Pg.213]    [Pg.218]    [Pg.210]    [Pg.513]    [Pg.1363]    [Pg.1364]    [Pg.853]    [Pg.921]    [Pg.934]    [Pg.943]    [Pg.1706]    [Pg.130]   


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