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At least 217 records · Page 12Linked to original sources
PubMed2000

Vitamin E for neuroleptic-induced tardive dyskinesia.

BACKGROUND: Neuroleptic (antipsychotic) medication is used extensively to treat people with chronic mental illnesses. However, it is associated with a wide range of adverse effects, including movement disorders such as tardive dyskinesia (TD). Vitamin E has been proposed as a treatment to prevent or decrease the severity of TD. OBJECTIVES: To determine the clinical effects of vitamin E for people with schizophrenia or other chronic mental illnesses who also developed neuroleptic-induced tardive dyskinesia. SEARCH STRATEGY: Electronic searches of Biological Abstracts (1982-1998), The Cochrane Schizophrenia Group's Register (September 1998), EMBASE (1980-98), LILACS (1982-96), MEDLINE (1966-98), PsycLIT (1974-98), SCISEARCH, handsearching the references of all identified studies and contacting the first author of each included trial. SELECTION CRITERIA: Reports identified in the search were included if they were controlled trials dealing with people with neuroleptic-induced TD and schizophrenia or other chronic mental illness who had been randomly allocated to either vitamin E or to a placebo or no intervention. DATA COLLECTION AND ANALYSIS: Data were independently extracted from these trials by each reviewer and Peto odds ratios (OR) or average differences, with the 95% confidence intervals (CI) were estimated. The reviewers assumed that people who dropped out had no improvement. MAIN RESULTS: Eight studies were included, and another three are currently awaiting further data from authors. The overall results for both, 'clinically relevant improvement' and 'any improvement' of TD symptoms, were in favour of vitamin E (OR 0.16, CI 0.04-0.7, NNT 5 CI 2.-32 and OR 0.23, CI 0.10-0.55, NNT 4 CI 2. 5-12 respectively). People who had not used vitamin E showed more deterioration of their symptoms (OR 0.20, CI 0.04-0.93). No difference could be found regarding the presence of adverse effects or leaving the study early before the end of study. There is no trial-based information regarding the effect of vitamin E for those with early onset of TD. REVIEWER'S CONCLUSIONS: Small trials with uncertain quality of randomisation, tend to suggest that vitamin E improves the symptoms of TD. Methodological problems such as small sample size, short term interventions, and inappropriate use of crossover design need to be dealt with in any future studies. The results of a recently completed trial involving 158 participants are eagerly awaited.

Antipsychotic Agents↗
PubMed1988

Plasma concentrations of vitamin K1 and PIVKA-II in bottle-fed and breast-fed infants with and without vitamin K prophylaxis at birth.

Plasma vitamin K1 and proteins induced by vitamin K absence (PIVKA) were assayed simultaneously 1-4 days and 29-35 days after delivery in three groups of infants: breast-fed not receiving vitamin K at birth (n = 12), bottle-fed without vitamin K administration at birth (n = 7) and breast-fed receiving 1 mg vitamin K1 administered by intramuscular injection at birth (n = 13). The bottle-fed infants had a significantly higher vitamin K1 plasma level than breast-fed infants who did not receive vitamin K1 at birth. Extremely high levels of vitamin K were obtained 1-4 days after intramuscular administration. At the age of 1 month, breast-fed infants had the same plasma vitamin K1 concentration whether or not they had received vitamin K1 supplements. Decarboxy prothrombin (PIVKA-II) a reliable indicator of biochemical vitamin K deficiency, was found in 5 out of 12 breast-fed and in 2 out of 6 bottle-fed infants who had not received supplemental vitamin K1 after birth. In a separate study, we followed up to 90 days after birth a larger group if infants. PIVKA-II was found with significantly greater frequency in breast-fed infants receiving no vitamin K than in breast-fed infants receiving 1 mg vitamin K intramuscularly at birth, or in bottle-fed infants without extra vitamin K1. These data form a strong argument for routine vitamin K prophylaxis after birth for all breast-fed infants. The optimum dose and manner of administration require further study.

Biomarkers↗
PubMed1996

Supplemental vitamin A enhances the recovery from iron deficiency in rats with chronic vitamin A deficiency.

Studies with anaemic children and pregnant women from areas where vitamin A deficiency is endemic have shown a beneficial effect on Fe status of supplemental vitamin A in addition to Fe supplementation. This suggests a relationship between vitamin A and Fe status, which we attempted to mimic in rats with anaemia and chronic vitamin A deficiency. Male rats were fed on Fe-adequate diets (35 mg Fe/kg) containing different levels of vitamin A (1200, 450, 150, 75 and 0 retinol equivalent (RE)/kg feed) until they were 5 weeks old. These diets were identical to the diets fed to their mothers. Then the young male rats were transferred to diets containing the same levels of vitamin A but no added Fe. After another 2 weeks the rats were repleted with Fe (35 mg/kg feed) without or with vitamin A to a level of 1200 RE/kg feed. Increased vitamin A intake by the groups previously fed on diets with either 0 or 75 RE/kg produced a reduction in blood haemoglobin concentration, packed cell volume and erythrocyte count. In the group which had been fed on the diet without vitamin A, supplemental vitamin A raised mean cell volume, plasma Fe concentration and total Fe-binding capacity. Vitamin A supplementation during the period of Fe repletion produced a decrease in splenic and tibia Fe concentration, the effect being greater with increasing severity of previous vitamin A deficiency. The paradoxical effect of supplemental vitamin A on haemoglobin, packed cell volume and erythrocyte count can be explained by a decrease in the degree of haemoconcentration. Thus, the positive effect of supplemental vitamin A seen in humans is also observed with rats under controlled experimental conditions. We speculate that supplemental vitamin A during Fe repletion contributes to optimum erythropoiesis and Fe mobilization when baseline vitamin A status is impaired.

Anemia, Iron-Deficiency↗
PubMed2006

The kidney in vitamin B12 and folate homeostasis: characterization of receptors for tubular uptake of vitamins and carrier proteins.

Over the past 10 years, animal studies have uncovered the molecular mechanisms for the renal tubular recovery of filtered vitamin and vitamin carrier proteins. Relatively few endocytic receptors are responsible for the proximal tubule uptake of a number of different vitamins, preventing urinary losses. In addition to vitamin conservation, tubular uptake by endocytosis is important to vitamin metabolism and homeostasis. The present review focuses on the receptors involved in renal tubular recovery of folate, vitamin B12, and their carrier proteins. The multiligand receptor megalin is important for the uptake and tubular accumulation of vitamin B12. During vitamin load, the kidney accumulates large amounts of free vitamin B12, suggesting a possible storage function. In addition, vitamin B12 is metabolized in the kidney, suggesting a role in vitamin homeostasis. The folate receptor is important for the conservation of folate, mediating endocytosis of the vitamin. Interaction between the structurally closely related, soluble folate-binding protein and megalin suggests that megalin plays an additional role in the uptake of folate bound to filtered folate-binding protein. A third endocytic receptor, the intrinsic factor-B12 receptor cubilin-amnionless complex, is essential to the renal tubular uptake of albumin, a carrier of folate. In conclusion, uptake is mediated by interaction with specific endocytic receptors also involved in the renal uptake of other vitamins and vitamin carriers. Little is known about the mechanisms regulating intracellular transport and release of vitamins, and whereas tubular uptake is a constitutive process, this may be regulated, e.g., by vitamin status.

Animals↗
PubMed1996

Effect of vitamins A and E on blood plasma vitamin status and daily body mass gain of different fat-tailed sheep breeds.

Ninety ram lambs of three Iranian fat-tailed sheep breeds including the Shal breed (age: 4-6 months) in one experiment and the Sanjabi and Bakhtiari breeds (6-9 months) in another experiment were assigned to five groups of 5-7 lambs each to receive a basal diet plus different levels of vitamins A and E supplementation. The groups received 0, 50 or 100 IU vitamin A/kg body mass (b.m.) and 0, 15 or 30 IU vitamin E/kg of diet. In the vitamin A groups a constant level of 15 IU vitamin E and in the vitamin E groups a constant level of 50 IU vitamin A supplementation was provided. Blood plasma samples were taken at the beginning and at the end of the experiments and the concentrations of vitamins A and E were determined by high-performance liquid chromatography (HPLC). Vitamin A supplementation of the highest level (100 IU/kg b.m.) significantly increased the retinol content of the blood plasma in the Shal (P < 0.01) and Bakhtiari (P < 0.05) breeds. The mild increase of retinol concentration in the Sanjabi breed was not significant (P > 0.05). Vitamin A supplementation greatly decreased the alpha-tocopherol content of the blood plasma in all three breeds (P < 0.01). It increased the average daily body mass gain of lambs of the Shal breed (P < 0.01) but decreased that of Bakhtiari lambs (P < 0.05). Supplementation of vitamin E mildly decreased the retinol content of the blood plasma in all the breeds and the decrease was statistically significant (P < 0.05) for the Shal breed at the highest dose level. Vitamin E supplementation greatly increased the alpha-tocopherol concentration of the blood plasma in all the breeds (P < 0.01-0.001). It decreased the average daily body mass gain of the Shal breed (P < 0.001) but improved it in the two other breeds. That increase was statistically significant (P < 0.05) in the Bakhtiari breed. It was concluded that the Shal breed gave a better response to vitamin A supplementation while the Sanjabi and Bakhtiari breeds to vitamin E. This indicates that fat-tailed breeds have dissimilar requirements for vitamins A and E supplementation. A higher level of vitamin E intake is required for raising the alpha-tocopherol content of the blood plasma above the level critical for sheep (0.8 microgram/ml).

Animals↗