Equine neuroaxonal dystrophy/degenerative myeloencephalopathy in Gypsy Vanner horses.

BACKGROUND: Equine neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD/EDM) is a neurodegenerative disease that primarily affects young, genetically predisposed horses that are deficient in vitamin E. Equine NAD/EDM has not previously been documented in Gypsy Vanner horses (GVs). OBJECTIVES: To evaluate: (1) the clinical phenotype, blood vitamin E concentrations before and after supplementation and pedigree in a cohort of GV horses with a high prevalence of neurologic disease suspicious for eNAD/EDM and (2) to confirm eNAD/EDM in GVs through postmortem evaluation. ANIMALS: Twenty-six GVs from 1 farm in California and 2 cases from the Midwestern U.S. METHODS: Prospective observational study on Californian horses; all 26 GVs underwent neurologic examination. Pre-supplementation blood vitamin E concentration was assessed in 17- GVs. Twenty-three were supplemented orally with 10 IU/kg of liquid RRR-alpha-tocopherol once daily for 28 days. Vitamin E concentration was measured in 23 GVs after supplementation, of which 15 (65%) had pre-supplementation measurements. Two clinically affected GVs from California and the 2 Midwestern cases had necropsy confirmation of eNAD/EDM. RESULTS: Pre-supplementation blood vitamin E concentration was ≤2.0 µg/mL in 16/17 (94%) of GVs from California. Post-supplementation concentration varied, with a median of 3.39 µg/mL (range, 1.23-13.87 µg/mL), but only 12/23 (52%) were normal (≥3.0 µg/mL). Normalization of vitamin E was significantly associated with increasing age (P = .02). Euthanized horses (n = 4) had eNAD/EDM confirmed at necropsy. CONCLUSIONS AND CLINICAL IMPORTANCE: GVs could have a genetic predisposition to eNAD/EDM. Vitamin E supplementation should be considered and monitored in young GVs.

Atypical retinopathy in ataxia with vitamin E deficiency: report of a sibship.

Typical retinitis pigmentosa (RP) may not be the only retinal phenotype encountered in ataxia with vitamin E deficiency (AVED). The following short case series describes a novel form of retinopathy in AVED. We describe two patients with AVED belonging to the same consanguineous sibship. Both presented an unusual retinopathy consisting of scattered, multifocal, nummular, hyperautofluorescent atrophic retinal patches. The retinopathy remained stable under vitamin E supplementation. We hypothesize these changes to be the result of arrested AVED-related RP following early supplementation with α-tocopherol acetate.

Vitamin E deficiency in childhood: a narrative review.

Vitamin E is an important nutrient from the earliest stages of life. It plays key roles as an antioxidant and in the maintenance of the immune system, among others. Vitamin E deficiency (VED), which occurs more frequently in children, is rarely addressed in the literature. This narrative review aims to summarise the chemistry, biology, serum indicators and clinical trials that have evaluated the impact of fortification and other relevant aspects of vitamin E, in addition to the prevalence of its deficiency, in children worldwide. Vitamin E intake in recommended amounts is essential for this nutrient to perform its functions in the body. Serum α-tocopherol is the most widely used biochemical indicator to assess the prevalence of VED. VED has been associated with symptoms secondary to fat malabsorption and may lead to peripheral neuropathy and increased erythrocyte haemolysis. Reduced concentrations of α-tocopherol may be caused by the combination of diets with low amounts of vitamin E and inadequate consumption of fats, proteins and calories. The lowest prevalence of VED was found in Asia and the highest in North America and Brazil. High proportions of VED provide evidence that this nutritional deficiency is a public health problem in children and still little addressed in the international scientific literature. The planning, evaluation and implementation of health policies aimed at combatting VED in the paediatric population are extremely important.

The Role of Vitamin Deficiency in Liver Disease: To Supplement or Not Supplement?

Over the past few years, growing interest has been shown for the impact of dietary requirements and nutritional factors on chronic diseases. As a result, nutritional programs have been reinforced by public health policies. The precise role of micronutrients in chronic liver disease is currently receiving particular attention since abnormalities in vitamin levels are often detected. At present, treatment programs are focused on correcting vitamin deficiencies, which are frequently correlated to higher rates of comorbidities with poor outcomes. The literature reviewed here indicates that liver diseases are often related to vitamin disorders, due to both liver impairment and abnormal intake. More specific knowledge about the role of vitamins in liver disease is currently emerging from various results and recent evidence. The most significant benefits in this area may be observed when improved vitamin intake is combined with a pharmacological treatment that may also affect the progression of the liver disease, especially in the case of liver tumors. However, further studies are needed.

Vitamin E: How much is enough, too much and why!

α-Tocopherol (α-T) is a required dietary nutrient for humans and thus is a vitamin. This narrative review focuses on vitamin E structures, functions, biological determinants and its deficiency symptoms in humans. The mechanisms for the preferential α-T tissue enrichment in the human body include the α-T transfer protein (TTPA) and the preferential metabolism of non-α-T forms. Potential new α-T biomarkers, pharmacokinetic data, and whether there are better approaches to evaluate and set the α-T dietary requirement are discussed. Finally, the possible role of α-T supplements in delay of chronic diseases and the evaluation of vitamin E safety are considered.

Hidden Hunger of Vitamin E among Healthy College Students: A Cross- Sectional Study.

BACKGROUND: College students may have a risk of fat-soluble vitamin deficiencies due to unhealthy dietary habits, especially for vitamin A and E. They are important members of the human antioxidant network; deficiencies of these vitamins may increase the risk of many critical diseases. OBJECTIVE: The current study was undertaken to determine the status of vitamin A and E in college students. METHODS: Healthy college students were recruited, and fasting blood samples of them were collected and used for determining serum levels of retinol and α-tocopherol by the HPLC method. RESULTS: We found that there was no vitamin A deficiency in college students. However, vitamin E deficiency existed in 34.5% of college students, especially in males. All the students had no vitamin E adequacy. In addition, our findings showed that BMI was inversely associated with serum α-- tocopherol, but not serum retinol. CONCLUSION: These results suggest that vitamin E deficiency in college students should be given more attention, and it is necessary to consider using vitamin E supplements.

Increased anxiety-like behaviour is an early symptom of vitamin E deficiency that is suppressed by adrenalectomy in rats.

We previously reported that dietary vitamin E deficiency increased anxiety-like behaviour in rats exposed to social isolation. Here, we performed a detailed investigation of this phenomenon and its underlying mechanism. First, we fed Wistar rats with a vitamin E-free diet for 3 d, 1 week or 2 weeks and found an increase in anxiety-like behaviour after 1 and 2 weeks of vitamin E deficiency based on behavioural indicators. Next, we examined the effect of a control diet (150 mg all-racemic α-tocopheryl acetate/kg) on anxiety-like behaviours in rats that received a 4-week vitamin E-free diet. We found that increased anxiety-like behaviour was reversed to control levels after refeeding vitamin E for 7 d but not for 1 or 3 d. Further, anxiety-like behaviour increased or decreased gradually based on the amount of vitamin E intake; however, it had a quicker progression than physical symptoms of vitamin E deficiency. Moreover, rats fed with excess vitamin E (500 mg all-racemic α-tocopherol/kg diet) showed less anxiety-like behaviour than control rats, indicating that vitamin E supplementation is effective for preventing anxiety increase under social isolation stress. Since plasma corticosterone levels were higher in vitamin E-deficient rats, we investigated the effect of adrenalectomy on anxiety-like behaviour and found that adrenal hormones played an essential role in the increased anxiety-like behaviour induced by vitamin E deficiency. In conclusion, increased anxiety-like behaviour is a symptom that emerges earlier than physical vitamin E deficiency and is caused by adrenal hormone-dependent mechanisms.

Effect of Fat-Soluble Vitamins A, D, E and K on Vitamin Status and Metabolic Profile in Patients with Fat Malabsorption with and without Urolithiasis.

Patients with intestinal fat malabsorption and urolithiasis are particularly at risk of acquiring fat-soluble vitamin deficiencies. The aim of the study was to evaluate the vitamin status and metabolic profile before and after the supplementation of fat-soluble vitamins A, D, E and K (ADEK) in 51 patients with fat malabsorption due to different intestinal diseases both with and without urolithiasis. Anthropometric, clinical, blood and 24-h urinary parameters and dietary intake were assessed at baseline and after ADEK supplementation for two weeks. At baseline, serum aspartate aminotransferase (AST) activity was higher in stone formers (SF; n = 10) than in non-stone formers (NSF; n = 41) but decreased significantly in SF patients after supplementation. Plasma vitamin D and E concentrations increased significantly and to a similar extent in both groups during intervention. While plasma vitamin D concentrations did not differ between the groups, vitamin E concentrations were significantly lower in the SF group than the NSF group before and after ADEK supplementation. Although vitamin D concentration increased significantly in both groups, urinary calcium excretion was not affected by ADEK supplementation. The decline in plasma AST activity in patients with urolithiasis might be attributed to the supplementation of ADEK. Patients with fat malabsorption may benefit from the supplementation of fat-soluble vitamins ADEK.

Vitamin E supplementation in people with cystic fibrosis.

BACKGROUND: People with cystic fibrosis are at an increased risk of fat-soluble vitamin deficiency, including vitamin E. Vitamin E deficiency can cause a host of conditions such as haemolytic anaemia, cerebellar ataxia and cognitive difficulties. Vitamin E supplementation is widely recommended for people with cystic fibrosis and aims to ameliorate this deficiency. This is an updated version of the review. OBJECTIVES: To determine the effects of any level of vitamin E supplementation on the frequency of vitamin E deficiency disorders in people with cystic fibrosis. SEARCH METHODS: We searched the Cochrane Group's Cystic Fibrosis Trials Register and also searched international online trial registries for any ongoing clinical trials that were not identified during our register search. Date of last search of the Register: 11 August 2020. Date of last search of international online trial registries: 20 July 2020. SELECTION CRITERIA: Randomised controlled trials and quasi-randomised controlled trials comparing any preparation of vitamin E supplementation to placebo or no supplement, regardless of dosage or duration. DATA COLLECTION AND ANALYSIS: Two authors extracted outcome data from each study (published information) and assessed the risk of bias of each included study. They assessed the quality of the evidence using GRADE. MAIN RESULTS: Four studies with a total of 141 participants were included in the review, two of these were in children (aged six months to 14.5 years), and two did not specify participants' age. All studies used different formulations and doses of vitamin E for various durations of treatment (10 days to six months). Two studies compared the supplementation of fat-soluble as well as water-soluble formulations to no supplementation in different arms of the same study. A third study compared a water-soluble formulation to a placebo; and in the fourth study a fat-soluble formulation of vitamin E was assessed against placebo. There was limited detail about randomisation and blinding in the included studies which compromises the quality of the evidence base for the review. The heterogeneous mix of the formulations with differing biovailabilities among these studies also limits the generalisability of the data to the wider cystic fibrosis population. None of the studies in either comparison report the review's primary outcomes of vitamin E total lipid ratio or the incidence of vitamin E-specific deficiency disorders, or the secondary outcomes lung function or quality of life. Water-soluble vitamin E Water-soluble vitamin E may improve serum vitamin E levels compared with control at six months, one study (45 participants), mean difference (MD) 19.74 umol/L (95% confidence interval (CI) 13.48 to 26.00) (low-quality evidence). Similar results were also seen at one month, two studies (32 participants), MD 17.66 umol/L (95% CI 10.59 to 24.74) and at three months, one study (45 participants), MD 11.61 umol/L (95% CI 4.77 to 18.45). Only one study (45 participants) reported weight (secondary outcome of growth and nutritional status) at one and six months, but showed no difference between treatment and control at either time point. Fat-soluble vitamin E Two studies (36 participants) reported higher levels of serum vitamin E at one month with fat-soluble vitamin E compared with control, MD 13.59 umol/L (95% CI 9.52 to 17.66); however, at three months one study (36 participants) showed no difference between treatment and control. No studies in this comparison reported on growth or nutritional status. AUTHORS' CONCLUSIONS: Vitamin E supplementation may lead to an improvement in vitamin E levels in people with cystic fibrosis, although evidence we assessed was low quality. No data on other outcomes of interest were available to allow conclusions about any other benefits of this therapy. In future, larger studies are needed, especially in people already being treated with enteric-coated pancreatic enzymes and supplemented with vitamin E, to look at more specific outcome measures such as vitamin E status, lung function and nutritional status. Future studies could also look at the optimal dose of vitamin E required to achieve maximal clinical effectiveness.

Multifunctional activity of vitamin E in animal and animal products: A review.

Vitamin E is an essential nontoxic fat-soluble micronutrient whose effects on livestock performance and products can be attributed to its antioxidant and nonantioxidant properties. Although it is needed in small quantity in the diet, its roles in livestock production are indispensable as it is required in boosting performance, nutritional qualities, and yield of animal and animal products. The dietary or oral supplementation of vitamin E is essential in reducing lipid oxidation in muscle, egg, and dairy products as well as lowering cholesterol concentrations and improving antioxidant status of livestock. Evidence has shown that bioavailability of vitamin E-enriched animal products could serve as an invaluable nutritional benefit to consumers; especially those in regions of limited resources where vitamin E deficiencies pose a risk that may be detrimental to some cellular activities of the body and on human health. It is therefore important to redirect research on the impact of vitamin E supplementation as antioxidant on livestock performance and animal products.

Aspectos epidemiológicos e clínico-patológicos de um surto de miopatia nutricional em potros ˗ relato de caso / [Epidemiological and clinical-pathological aspects of an outbreak of nutritional myopathy in young horses ˗ case report]

A miopatia nutricional é uma doença degenerativa que pode afetar os músculos esqueléticos e cardíaco, causada pela deficiência dietética de selênio e/ou vitamina E. Objetivou-se relatar a ocorrência de miopatia nutricional em dois potros Puro Sangue Inglês, criados de forma extensiva, com baixa disponibilidade de forragem e sem suplementação mineral. De um lote de nove animais de diferentes idades (cinco éguas adultas, uma potra lactente de três meses,uma mula e dois potros de 16 e 17 meses), apenas os dois últimos foram afetados. Clinicamente, havia decúbito lateral ou esternal, taquicardia, taquipneia, desidratação e dor à palpação muscular na região dos glúteos.O diagnóstico presuntivo de miopatia nutricional foi realizado por meio da associação dos sinais clínicos aos dados epidemiológicos.O animal 1 foi eutanasiado cinco dias após o atendimento devido à piora gradativa do quadro, e o animal 2 recuperou-se com o tratamento adotado. O diagnóstico foi confirmado com base nos exames complementares, nos achados de necropsia e na dosagem da concentração hepática de selênio. Este relato de caso alerta para o risco da ocorrência de miopatia nutricional em equinos, sobretudo jovens, sem acesso a pastagens ou feno de boa qualidade e sem suplementação mineral adequada.(AU)

Nutritional myopathy is a degenerative disease caused by the dietary deficiency of selenium and/or vitamin E that can affect skeletal and cardiac muscles. The objective of this study was to report the occurrence of nutritional myopathy in two Thoroughbred young horses, raised in pastures with low forage availability and no mineral supplementation. From a herd of nine animals of different ages (five adult mares, one three-month-old nursing foal, one mule and two 16- and 17-month-old horses), only the last two were affected. Clinical signs were lateral or sternal recumbency, tachycardia, tachypnea, dehydration and muscle pain. Presumptive diagnosis of nutritional myopathy was made associating clinical signs and epidemiological data. Animal 1 was euthanized five days after the first evaluation due to clinical signs gets worse, and animal 2 recovered with the established treatment. Diagnosis was confirmed with complementary exams, necropsy findings and levels of hepatic selenium. This paper alerts to the risk of nutritional myopathy occurrence in horses, mainly young animals, which are not ingesting good quality hay or green forage and do not receive appropriate mineral supplementation.(AU)

Mulberry Heart Disease and Hepatosis Dietetica in Farm Pigs (Sus scrofa domesticus) in a Research Setting.

Perioperative complications and deaths occurred while developing a novel surgical model of pediatric kyphosis in 10 to 12 kg male farm-raised Yorkshire piglets. All piglets appeared clinically normal preoperatively. Intraoperative complications included tachycardia, respiratory acidosis, and death. Postoperatively, clinical signs included posterior paresis, head pressing, prolonged anesthetic recovery, difficulty rising, and sudden death. Necropsies were performed on all piglets. Some morbidity and mortality were accurately attributed to the spinal surgery. However, the index piglet for this report died suddenly approximately 16 to 18 h after surgery. Necropsy of this animal revealed clear, serosanguineous pleural and pericardial effusions along with myocardial hemorrhage and hepatic lesions, consistent with mulberry heart disease and hepatosis dietetica, respectively. Serum vitamin E and selenium levels from this animal were below age-specific lab reference ranges. Clinical signs of vitamin E and selenium deficiency are most common in fast-growing weaner piglets. The added stress of major surgery may exacerbate the condition in young piglets. Resolution of morbidity and mortality in both juvenile and adult pigs occurred upon the use of an alternate vendor able to provide feed analyses meeting industry standards, although serum levels of vitamin E and selenium in similar ages and breed of swine were still occasionally slightly below reference ranges.

First Recognized Patient with Genetic Vitamin E Deficiency Stable after 36 Years of Controlled Supplement Therapy.

INTRODUCTION: Familial isolated deficiency of vitamin E (VED or AVED; MIM #277460) is a progressive neurodegenerative disorder resembling Friedreich ataxia. It is caused by the deficiency of α-tocopherol transfer protein that prevents patients from retaining vitamin E. Oral vitamin E supplements are an accepted treatment, but detailed dosage recommendations and reports on long-term therapeutic results are scarce. METHODS: The first patient with VED was discovered at our institution at the age of 12 years and has since been followed with clinical, neurophysiological, neuroradiological, and biochemical investigations to his present age of 52 years. For the last 36 years, the patient has scrupulously followed a custom-made high-dose vitamin E supplement regimen that we devised on the basis of studies of his metabolism of vitamin E. RESULTS: Over the long period of observation, the patient has remained in good general health and has not shown progression of neurological symptoms and signs. His vitamin E plasma levels were always moderately above the normal range. During short interruptions of vitamin E supplements, vitamin E levels fell rapidly, even after years of massive supplementation. DISCUSSION: In this VED patient, a specified and carefully controlled high-dose vitamin E therapy has prevented any recognizable progression of the neurodegenerative process over more than 3 decades of observation.

Influence of specific management practices on blood selenium, vitamin E, and beta-carotene concentrations in horses and risk of nutritional deficiency.

BACKGROUND: Selenium or alpha-tocopherol deficiency can cause neuromuscular disease. Beta-carotene has limited documentation in horses. OBJECTIVE: To evaluate the effect of owner practices on plasma beta-carotene concentration and risk of selenium and alpha-tocopherol deficiencies. ANIMALS: Three-hundred and forty-nine adult (≥1 year), university and privately owned horses and mules. METHODS: Cross-sectional study. Whole blood selenium, plasma alpha-tocopherol, and plasma beta-carotene concentrations were measured once. Estimates of daily selenium and vitamin E intake, pasture access, and exercise load were determined by owner questionnaire. Data were analyzed using t tests, Mann-Whitney tests, parametric or nonparametric analysis of variance (ANOVA), Kruskal-Wallis test, Spearman's correlation and contingency tables (P < .05). RESULTS: Nearly 88% of the horses received supplemental selenium; 71.3% received ≥1 mg/d. Low blood selenium concentration (<80 ng/mL) was identified in 3.3% of horses, and 13.6% had marginal concentrations (80-159 ng/mL). Non-supplemented horses were much more likely to have low blood selenium (odds ratio [OR], 20.2; 95% confidence interval [CI], 9.26-42.7; P < .001). Supplemental vitamin E was provided to 87.3% of horses; 57.7% received ≥500 IU/d. Deficient (<1.5 µg/mL) and marginal (1.5-2.0 µg/mL) plasma (alpha-tocopherol) occurred in 15.4% and 19.9% of horses, respectively. Pasture access (>6 h/d) and daily provision of ≥500 IU of vitamin E was associated (P < .001) with higher plasma alpha-tocopherol concentrations. Plasma beta-carotene concentration was higher in horses with pasture access (0.26 ± 0.43 versus 0.12 ± 0.13 µg/mL, P = .003). CONCLUSIONS AND CLINICAL IMPORTANCE: Suboptimal blood selenium and plasma alpha-tocopherol concentrations occurred in 16.7% and 35.5% of horses, respectively, despite most owners providing supplementation. Inadequate pasture access was associated with alpha-tocopherol deficiency, and reliance on selenium-containing salt blocks was associated with selenium deficiency.

Vitamin A deficiency exacerbates extrinsic atopic dermatitis development by potentiating type 2 helper T cell-type inflammation and mast cell activation.

BACKGROUND: Vitamin A deficiency (VAD) has been hypothesized to play a role in the pathophysiology of atopic dermatitis (AD). OBJECTIVE: We sought to verify whether VAD can exacerbate AD development, and explore the possible pathophysiologic mechanism. METHODS: We detected serum vitamin A (VA) concentration in different phenotypes of AD infants (intrinsic AD, iAD and extrinsic AD, eAD), and established ovalbumin (OVA) percutaneous sensitized AD model and passive cutaneous anaphylaxis (PCA) model on VAD and vitamin A supplementation (VAS) model in wild-type mice (C57BL/6) and established AD model on both normal VA (VAN) and VAD feeding mast cell deficiency mice (ckitw-sh/w-sh ). RESULTS: The average serum VA concentration of eAD was significantly lower than that of iAD, as well as healthy controls. In OVA-induced C57BL/6 mouse AD model, compared with VAN group, VAD mice manifested significantly more mast cells accumulation in the skin lesions, more severe Th2-mediated inflammation, including higher serum IgG1 and IgE levels, more IL-4, IL-13 mRNA expression in OVA-sensitized skin, and lower Th1 immune response, including lower serum IgG2a and IFN-γ mRNA expression in the skin. But there was no significant difference in the expression of IL-17 mRNA between OVA-treated skin of VAN and VAD mice. However, in OVA-induced ckitw-sh/w-sh mouse AD model, we did not find any significant differences in the above measurements between VAD and VAN group. In PCA model, VAD mice showed remarkable more blue dye leakage than that in VAN mice. Compared with VAD group, the above-mentioned inflammatory measurements in VAS group and VAN group were similar in OVA-induced AD model mice. CONCLUSIONS AND CLINICAL RELEVANCE: VAD can exacerbate extrinsic AD by augmenting Th2-mediated inflammation and mast cell activation. Therapeutic VAS can rescue VAD-aggravated eAD. It may provide a new strategy for future prevention or treatment of atopic dermatitis.

Genome-Wide Association Study and Subsequent Exclusion of ATCAY as a Candidate Gene Involved in Equine Neuroaxonal Dystrophy Using Two Animal Models.

Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM) is an inherited neurodegenerative disorder of unknown etiology. Clinical signs of neurological deficits develop within the first year of life in vitamin E (vitE) deficient horses. A genome-wide association study (GWAS) was carried out using 670,000 SNP markers in 27 case and 42 control Quarter Horses. Two markers, encompassing a 2.5 Mb region on ECA7, were associated with the phenotype (p = 2.05 × 10-7 and 4.72 × 10-6). Within this region, caytaxin (ATCAY) was identified as a candidate gene due to its known role in Cayman Ataxia and ataxic/dystonic phenotypes in mouse models. Whole-genome sequence data in four eNAD/EDM and five unaffected horses identified 199 associated variants within the ECA7 region. MassARRAY® genotyping was performed on these variants within the GWAS population. The three variants within ATCAY were not concordant with the disease phenotype. No difference in expression or alternative splicing was identified using qRT-PCR in brainstem across the ATCAY transcript. Atcayji-hes mice were then used to conduct functional analysis in a second animal model. Histologic lesions were not identified in the central nervous system of Atcayji-hes mice. Additionally, supplementation of homozygous Atcayji-hes mice with 600 IU/day of dl-α-tocopheryl acetate (vitE) during gestation, lactation, and adulthood did not improve the phenotype. ATCAY has therefore been excluded as a candidate gene for eNAD/EDM.

Association Between Fat-soluble Vitamins and Lipid Profile in the Overweight Population.

BACKGROUND & AIMS: It is well-known that the coronary artery stenosis is related to lipid profile. This is a descriptive cross-sectional study to investigate the relationship between the serum fat-soluble vitamins (A, E and D), circulating proprotein convertase subtilisin/kexin type 9 (PCSK9), and lipid profile in the study population. METHODS: A total of 120 overweight subjects were participated in this study. The circulating PCSK9 and vitamin D were measured by ELISA technique. The serum vitamin A and vitamin E amounts were simultaneously measured by the HPLC method. The Serum Small Dense LDLCholesterol (sdLDL-C) values were evaluated using heparin-Mg2+ precipitation technique. The lipid profile was measured by routine laboratory techniques. RESULTS: The serum vitamin E values correlated significantly to vitamin A (r= 0.47, P= 0.0001), VLDL-C (r= 0.30, P= 0.002), total cholesterol (r= 0.309, P= 0.001), PCSK9 (r= 0.233, P= 0.01) and total triglyceride (r= 0.61, P= 0.0001) values. The circulating PCSK9 values correlated significantly to LDL-C (r= 0.17, P= 0.05) and total cholesterol (r= 0.23, P= 0.009) values. However, there were not correlations between the levels of serum D and A vitamins, the serum LDL-C, sdLDL-C and total cholesterol values. CONCLUSION: The data showed the correlations between serum vitamin E and PCSK9-related LDLC values lower than the normal range. Furthermore, the results suggested a nutritional need on the patents considering supplementation or fortification of vitamin E for the overweight subjects with higher LDL-C levels.

Multiple Micronutrient Powder Reduces Vitamin E Deficiency in Brazilian Children: A Pragmatic, Controlled Clinical Trial.

Multiple micronutrient powder supplementation is a health promotion strategy, but data on its effectiveness regarding vitamin E are rare. The objective was to evaluate the impact of home fortification with powdered micronutrients on α-tocopherol concentrations, growth, and inflammation in Brazilian children aged 6-15 months. This is a pragmatic, controlled clinical trial, in which the intervention group received micronutrient powder sachets for up to 3 months. Vitamin E deficiency was considered when α-tocopherol was less than 11.6 µmol/L. The Poisson regression model was used to estimate adjusted values for prevalence ratios (PR) for the outcome variable. A total of 224 children participated in the study. The intervention group had a higher median α-tocopherol level (17.2 versus 3.6 µmol/L; p < 0.001) and an 82.0% reduction in the prevalence of vitamin deficiency (PR = 0.18; 95% CI 0.11-0.30) when compared with the control group. Consumption of multiple micronutrients in powder increases serum α-tocopherol concentrations, promotes better linear growth, and reduces morbidity in children.

Impact of alpha-tocopherol deficiency and supplementation on sacrocaudalis and gluteal muscle fiber histopathology and morphology in horses.

BACKGROUND: A subset of horses deficient in alpha-tocopherol (α-TP) develop muscle atrophy and vitamin E-responsive myopathy (VEM) characterized by mitochondrial alterations in the sacrocaudalis dorsalis medialis muscle (SC). OBJECTIVES: To quantify muscle histopathologic abnormalities in subclinical α-TP deficient horses before and after α-TP supplementation and compare with retrospective (r)VEM cases. ANIMALS: Prospective study; 16 healthy α-TP-deficient Quarter Horses. Retrospective study; 10 retrospective vitamin E-responsive myopathy (rVEM) cases . METHODS: Blood, SC, and gluteus medius (GM) biopsy specimens were obtained before (day 0) and 56 days after 5000 IU/450 kg horse/day PO water dispersible liquid α-TP (n = 8) or control (n = 8). Muscle fiber morphology and mitochondrial alterations were compared in samples from days 0 and 56 and in rVEM cases. RESULTS: Mitochondrial alterations more common than our reference range (<2.5% affected fibers) were present in 3/8 control and 4/8 treatment horses on day 0 in SC but not in GM (mean, 2.2; range, 0%-10% of fibers). Supplementation with α-TP for 56 days did not change the percentage of fibers with mitochondrial alterations or anguloid atrophy, or fiber size in GM or SC. Clinical rVEM horses had significantly more mitochondrial alterations (rVEM SC, 13% ± 7%; GM, 3% ± 2%) and anguloid atrophy compared to subclinical day 0 horses. CONCLUSIONS AND CLINICAL IMPORTANCE: Clinically normal α-TP-deficient horses can have mitochondrial alterations in the SC that are less severe than in atrophied VEM cases and do not resolve after 56 days of α-TP supplementation. Preventing α-TP deficiency may be of long-term importance for mitochondrial viability.

Correlation of serum vitamin A, D, and E with recurrent respiratory infection in children.

OBJECTIVE: To investigate the correlation of serum vitamin A, D, and E levels with a recurrent respiratory infection (RRI) in children. PATIENTS AND METHODS: The medical records of 422 children with RRI (a study group) in Cangzhou Central Hospital from January 2015 to December 2018 were retrospectively analyzed (the study group was divided into an active group and a stable group). Further 100 healthy children who underwent physical examination at the same time were enrolled as a control group. High-performance liquid chromatography (HPLC) was used to determine vitamin A, D, and E levels, so as to analyze their differences between the groups. RESULTS: Vitamin A, D, and E in the active and stable groups were significantly lower than those in the control group (p < 0.001); in the active group they were significantly lower than those in the stable group (p < 0.001). According to partial correlation analysis, in children with active RRI, vitamin A was respectively positively correlated with vitamin D (r=0.945, p < 0.001), and vitamin E (r=0.988, p < 0.001). Moreover, vitamin E was positively correlated with vitamin D (r=0.959, p < 0.001). CONCLUSIONS: The deficiency of vitamin A, D, and E is positively correlated with the disease activity of children with RRI. Therefore, the supplement of vitamin A, D, and E through dietary adjustment is beneficial to the rehabilitation of the children.