Plasma Proteomics Characteristics of Subclinical Vitamin E Deficiency of Dairy Cows During Early Lactation

Vitamin E (VE) is an essential fat-soluble nutrient for dairy cows. Vitamin E deficiency leads to immune suppression and oxidative stress and increases the susceptibility of cows to reproductive disorders in the early post-partum period. However, studies on plasma proteomics of VE deficiency have not been reported so far. Therefore, the purpose of this study was to understand the changes of blood protein profile in cows with subclinical VE deficiency in the early post-partum period. In this study, plasma protein levels of 14 healthy cows (>4 μg/ml α-tocopherol) and 13 subclinical VE-deficient cows (2–3 μg/ml α-tocopherol) were analyzed by tandem mass tag (TMT). The results showed that there were 26 differentially expressed proteins (DEPs) in the plasma of cows with subclinical VE deficiency compared with healthy controls. Twenty-one kinds of proteins were downregulated, and five kinds were upregulated, among which eight proteins in protein–protein interactions (PPI) network had direct interaction. These proteins are mainly involved in the MAPK signaling pathway, pantothenic acid and coenzyme A (CoA) biosynthesis, PPAR signaling pathway, and glycosylphosphatidylinositol (GPI)-anchor biosynthesis. The top four DEPs in PPI (APOC3, APOC4, SAA4, PHLD) and one important protein (VNN1) by literature review were further verified by ELISA and Western blot. The expression levels of APOC3, VNN1, and SAA4 were significantly lower than those of healthy controls by ELISA. VNN1 was significantly lower than those of healthy controls by Western blot. VNN1 is closely related to dairy cow subclinical VE deficiency and can be a potential biomarker. It lays a foundation for further research on the lack of pathological mechanism and antioxidative stress of VE.

The Association Between Vitamin E Deficiency and Critically Ill Children With Sepsis and Septic Shock

Background: Literature is scarce on the assessment of vitamin E status in septic children. We aim to investigate the prevalence of vitamin E deficiency in critically ill children with sepsis and septic shock and its association with clinical features and outcomes.Methods: We compared serum vitamin E status between the confirmed or suspected infection and no infection groups, the sepsis shock and no sepsis shock groups upon pediatric intensive care unit admission. Clinical characteristics were compared in subgroup patients with and without vitamin E deficiency. The association between vitamin E deficiency and septic shock were evaluated using univariate and multivariable methods.Results: 182 critically ill children with confirmed or suspected infection and 114 without infection were enrolled. The incidence of vitamin E deficiency was 30.2% in the infection group and 61.9% in the septic shock subgroup (P < 0.001). Thirty-days mortality in critically ill children with vitamin E deficiency was significantly higher than that without vitamin E deficiency (27.3 vs. 14.2%, P < 0.05). Vitamin E levels were inversely associated with higher pediatric risk of mortality (r = − 0.238, P = 0.001) and cardiovascular sequential organ failure assessment (r = −0.249, p < 0.001) scores in critically ill children with infection. In multivariable logistic regression, vitamin E deficiency showed an independent effect on septic shock (adjusted OR: 6.749, 95%CI: 2.449–18.60, P < 0.001).Conclusion: Vitamin E deficiency is highly prevalent in critically ill children with sepsis and contributed to the septic shock.

Role of Vitamin E in Boosting the Immunity from Neonates to Elderly

The vitamin E is a fat-soluble vitamin which occurs as a tocopherol component abundant in humans. The vitamin E supplements in humans and animals have provided numerous health benefits. The vitamin E is rich in antioxidants which slow the aging process and reduce the free radical damage. Vitamin E isoforms play an important role in respiratory health. It is also important in health and well-being of preterm neonates. Vitamin E deficiency in new born includes hemolytic anemia, disease of retina, bronchopulmonary dysplasia. Further, in vitro studies, vitamin E has increased the oxidative resistance and prevents the atherosclerotic plaque. The consumption of vitamin E rich foods reduces coronary heart diseases. This chapter focuses on the treatment of vitamin E deficiency in preterm babies and the role of vitamin E in preventing coronary heart diseases.

Vitamin responsive conditions in pediatric neurology

Vitamin responsive conditions can be either due to inherited defects in the metabolic pathways resulting in vitamin dependency or due to acquired deficiency states. Due to widespread malnutrition and predominantly vegetarian population in India, vitamin deficiency state is quite common and early identification is essential. Inherited defects, if treated earlier, lead to reduced morbidity and mortality and improvement in long-term neurocognitive outcomes. Various vitamin responsive conditions in pediatric neurology shall be discussed in this review. Infantile presentation of thiamine deficiency results in beriberi, and in adults, it leads to Wernicke’s encephalopathy and Korsakoff psychosis. Biotin thiamine-responsive basal ganglia disease is a defect of thiamine transporter 2, which leads to neuroregression and characteristic neuroimaging features of basal ganglia involvement, it responds to high doses of biotin and thiamine. Riboflavin is an enzyme involved in mitochondrial energy synthesis and is supplemented in various mitochondrial metabolic conditions. Brown-Vialetto-Van Laere syndrome is progressive pontobulbar palsy caused by defect in riboflavin transporters responsive to high doses of riboflavin. Pyridoxine responsive epilepsy presents with pharmacoresistant seizures in neonatal or early infantile age, biotinidase deficiency also presents with similar neurological manifestations, but typical cutaneous symptoms of rash and seborrheic dermatitis also occur. Both are epileptic encephalopathies and any infant presenting with epilepsy not responding to conventional AEDs must be given a trial of pyridoxine, biotin, and folinic acid. Vitamin B12 responsive conditions can include deficiency states, such as those manifesting with peripheral neuropathy and the syndrome of infantile tremor syndrome (developmental delay or regression, tremors, and megaloblastic anemia) as well as inherited disorders of homocysteine and cobalamin metabolism. These disorders are differentiated on the basis of clinical phenotype and laboratory parameters (serum B12, homocysteine levels, methylmalonic acid levels, etc.). Infantile tremor syndrome responds drastically to mega doses of Vitamin B12 and other multivitamins. Vitamin E deficiency causes ataxia with Vitamin E deficiency, other vitamins which can neurological symptoms include Vitamin C (pseudoparalysis) and Vitamin K (central nervous system bleeds). It is imperative for a practicing pediatrician to be well versed with these conditions, as these are potentially treatable conditions.

Chronic Vitamin E Deficiency in Rural Bangladeshi Women

Objectives Vitamin E deficiency (VED) appears to be common in rural areas of South Asia, with prevalence of ≥ 50% reported among women of reproductive age. Long term deficiency may impart neurological damage, but little information exists about persistence of VED. We provide initial estimates of chronic VED (CVED) in women of reproductive age living in Gaibandha District, a typical rural setting in NW Bangladesh. Methods We assessed α-tocopherol concentrations by HPLC in early pregnancy and 3-month postpartum (PP) plasma samples of women participating in biochemical sub-studies of JiVitA-1 (n = 2,319), a cluster-randomized, placebo-controlled, weekly vitamin A or β-carotene supplementation trial from 2001–7, and JiVitA-3 (N = 2,073), a cluster-randomized, daily multiple micronutrient (MMS) versus iron-folic acid (IFA) supplementation trial from 2008–12. VED was conventionally defined by an α-tocopherol concentration < 12 μmol/L and CVED as α-tocopherol < 12 μmol/L at both early pregnancy and postpartum assessments, an interval spanning a median (IQR) of 9.4 (2.8) months. Results Across both trials combined (N = 4,392), the mean ± SD plasma α-tocopherol concentration and prevalence of VED in early pregnancy and at 3 months post-partum was 11.28 ± 4.07 and 10.86 ± 4.41 μmol/L, and 53.5% and 42.2%, respectively. In JiVitA-3, the post-partum prevalence of VED among women not previously receiving MMS (containing 15 mg of vitamin E as all-rac-α-tocopheryl acetate) was 57.5% (vs 42.5% among MMS recipients, p < 0.001). The prevalence of CVED among women in both trials combined was 32.0% (34.45% in JiVitA-1 and 26.65% in JiVitA-3, IFA group only). Across a maternal age range of 11–43 [median: 20 (IQR: 8) years, risk of CVED decreased comparably per year of age in the JiVitA-1 [OR = 0.94 (95% CI: 0.93–0.95)] and JiVitA-3 [OR = 0.93 (95% CI:0.92–0.95)] trials. Conclusions In rural NW Bangladesh, where over half of women enter pregnancy vitamin E-deficient, about one-third are also deficient postpartum, ∼10 months later, providing a provisional estimate of chronic maternal vitamin E deficiency in a South Asian setting. Funding Sources Bill & Melinda Gates Foundation (Grant GH614, OPP1141435) and US Agency for International Development (AID (HRN-A-00–97-00015–00).

Brown Bowel Syndrome Is a Rare and Commonly Missed Disease: A Case Report and Literature Review

Background. Brown bowel syndrome (BBS) is a rare gastrointestinal condition, and vitamin E deficiency has been considered to be a main contributor. However, vitamin E deficiency has been found in only a few patients throughout the published literature studies and its cutoff lab value for diagnosis is not entirely clarified. Case Presentation. A 56-year-old female patient with a history of congenital bowel obstruction (repaired at birth) presented with bloating, abdominal pain, and chronic diarrhea. Endoscopy identified unremarkable gastrointestinal mucosa except a few small polyps in the colon. A partial obstruction was detected by a small bowel follow-through series and then confirmed by CT scan. The resected small bowel was significantly dilated with a thickened brown wall and extensive serosal adhesion. Microscopic examination revealed unremarkable mucosa, but dense granular brown pigments were identified in the cytoplasm of the smooth muscle cells in the muscularis propria. These deposits resulted to be lipofuscin, and BBS was diagnosed. The patient was asymptomatic at 9-month follow-up after surgery without vitamin E supplement. Conclusion. Mitochondrial damage with lipofuscin deposition is at the root of BBS pathogenesis. Any etiology associated with mitochondrial damage can cause this disease, and vitamin E deficiency is just one of them. Dysmotility from extensive serosal adhesion could be a possible etiology for this patient. Due to overlapping symptoms, lipofuscin deposition primarily in the muscularis propria, and unclear serum value of vitamin E, this syndrome is often missed in routine clinical practice from the superficial biopsy. A transmural biopsy is necessary for a definite diagnosis.