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.

Vitamin E - The Next 100 Years.

α-Tocopherol is the only tocopherol that has been shown to prevent the human deficiency disease Ataxia with Isolated Vitamin E Deficiency (AVED), and thus it is the only one that, for humans, can be called vitamin E. Vitamin E in addition to preventing AVED has documented immune boosting properties and an activity against nonalcoholic hepatosteatosis and low-grade inflammation. Epidemiological studies indicating that vitamin E could prevent cardiovascular events, neurodegenerative disease, macular degeneration, and cancer were in general not confirmed by clinical intervention studies. Vitamin E and some of its metabolites modulate cell signaling and gene transcription. Future research is needed to achieve a better understanding of the molecular events leading to gene regulation by vitamin E, especially in its phosphorylated form. Isolation and characterization of the vitamin E kinase and vitamin E phosphate phosphatase will help in the understanding of cell regulation processes modulated by vitamin E. A clarification of the pathogenesis of AVED remains an important goal to be achieved. © 2018 IUBMB Life, 71(4):411-415, 2019.

Vitamin E: Mechanism of transport and regulation in the CNS.

Although vitamin E has been recognized as a critical micronutrient to neuronal health for more than half a century, vitamin E transport and regulation in the brain remain a mystery. Currently, the majority of what is known about vitamin E transport has been delineated in the liver. However, clues from the pathogenesis of neurological-related vitamin E deficient diseases point to compromised neuronal integrity and function, underlining the critical need to understand vitamin E regulation in the CNS. Additionally, most of the same molecular players involved in vitamin E transport in the liver are also found in CNS, including sterol SRB1, TTP, and ABCA/ABCG, suggesting similar intracellular pathways between these organ systems. Finally, based on chemical similarities, intracellular CNS shuttling of vitamin E likely resembles cholesterol's use of ApoE particles. Utilizing this information, this review will address what is currently known about trafficking vitamin E across the blood brain barrier in order to ensure an adequate supply of the essential nutrient to the brain. Although debatable, the health of the brain in relation to vitamin E levels has been demonstrated, most notably in oxidative stress-related conditions such as ataxias, Alzheimer's disease, and Parkinson's disease. Future vitamin E research is vital in understanding how the regulation of the vitamin can aid in the prevention, treatment, and curing of neurological diseases. © 2018 IUBMB Life, 71(4):424-429, 2019.

Fat soluble vitamin levels in children with newly diagnosed celiac disease, a case control study.

BACKGROUND: In children diagnosed with celiac disease, fat soluble vitamin levels were aimed to be evaluated and it was intended to determine whether fat soluble vitamin levels were needed to be assessed routinely in these patients during diagnosis. METHODS: Between May 2015-May 2016, diagnosis symptoms of celiac patients (CD) in newly diagnosed pediatric group were questioned, fat soluble vitamin levels simultaneous with intestinal biopsies were evaluated. Vitamin levels were compared with those of healthy control group. RESULTS: A total of 52 patients involving 27 female (51.9%), 25 male (48.1%); and a total of 50 healthy control group including 25 female (50%), 25 male (50%) were evaluated. The average age of patients was 9 ± 4.3 years, and their average weight was determined as 16.2 ± 6.3 kg. Growth retardation was the most frequent symptom in our patients (61.5%). Abdominal pain (51.9%) and diarrhea (11.5%) are among the other most commonly seen symptoms. In the histological examination of patients, Marsh 3B n = 23 (45.1%) was mostly established. Vitamin A and vitamin D levels of patients were determined significantly lower compared to those of control group. Vitamin A and vitamin D deficiencies were identified significantly higher compared to those of healthy control group. Vitamin D insufficiency was observed in 48 patients (92.3%) and vitamin D deficiency was determined in 32 (61.5%) out of 48. Vitamin A deficiency was established in 17 (32.7%) patients. Vitamin E and vitamin K1 deficiency were determined in no patients. In the healthy control group, vitamin D deficiency was seen in 2 (4%) patients, vitamin D insufficiency was determined in 9 (18%) patients. Other vitamin levels were identified at normal levels in the healthy group. CONCLUSIONS: In newly diagnosed children with CD, a significant lowness was established in vitamin D and A. The evaluation of vitamin A and D levels will be helpful in the course of diagnosis in these patients.

Maternal supplementation with a megadose of vitamin A reduces colostrum level of α-tocopherol: a randomised controlled trial.

BACKGROUND: Maternal supplementation with vitamin A is one of the strategies for controlling its deficiency in the mother-child dyad, although studies with animals showed that supplementation with high doses of vitamin A reduces the levels of α-tocopherol (vitamin E) in the mother's serum and milk. The objective of the present study was to assess the influence of maternal supplementation with vitamin A on the concentration of retinol and α-tocopherol in human milk. METHODS: Healthy puerperal women were randomly distributed into a control group (n = 44) and a supplemented group (n = 44). Blood and colostrum samples were collected after delivery, and mature milk samples were collected 30 days later. The supplemented group received 200 000 IU of retinyl palmitate after the first colostrum collection. The retinol and α-tocopherol levels in the samples were determined by high-performance liquid chromatography. RESULTS: The mean (SD) retinol and α-tocopherol levels in the maternal serum were considered adequate at 46.4 (15.9) and 1023.6 (380.4) µg dL(-1) , respectively. The colostrum retinol levels of the supplemented group increased significantly 24 h after the intervention (P < 0.001). However, the retinol levels in the mature milk of both groups did not differ (P > 0.05). Moreover, after maternal supplementation with vitamin A, the colostrum α-tocopherol level decreased by 16.4%, which is a significant reduction (P < 0.05). However, vitamin A supplementation did not affect the α-tocopherol level of mature milk (P > 0.05). CONCLUSIONS: Maternal supplementation with high doses of vitamin A increased the colostrum level of this nutrient but reduced the bioavailability of α-tocopherol, which may harm the newborn's health because newborns have limited vitamin E reserves.

Vitamin E intake, α-tocopherol levels and pulmonary function in children and adolescents with cystic fibrosis.

Pancreatic insufficiency cystic fibrosis (CF) patients receive vitamin E supplementation according to CF-specific recommendations in order to prevent deficiencies. It has been suggested that higher serum α-tocopherol levels could have protective effects on pulmonary function (PF) in patients with CF. Whether current recommendations are indeed optimal for preventing deficiency and whether vitamin E has therapeutic benefits are subjects of debate. Therefore, we studied vitamin E intake as well as the long-term effects of vitamin E intake, the coefficient of fat absorption (CFA) and IgG on α-tocopherol levels. We also examined the long-term effects of serum α-tocopherol and serum IgG on forced expiratory volume in 1 s expressed as percentage of predicted (FEV1% pred.) in paediatric CF patients during a 7-year follow-up period. We found that CF patients failed to meet the CF-specific vitamin E recommendations, but serum α-tocopherol below the 2·5th percentile was found in only twenty-three of the 1022 measurements (2 %). Furthermore, no clear effect of vitamin E intake or the CFA on serum α-tocopherol was found (both P≥ 0·103). FEV1% pred. was longitudinally inversely associated with age (P< 0·001) and serum IgG (P= 0·003), but it was not related to serum α-tocopherol levels. We concluded that in the present large sample of children and adolescents with CF, vitamin E intake was lower than recommended, but serum α-tocopherol deficiency was rare. We found no evidence that higher serum α-tocopherol levels had protective effects on PF. Adjustment of the recommendations to the real-life intake of these patients may be considered.

Associations between low consumption of fruits and vegetables and nutritional deficiencies in Brazilian schoolchildren.

OBJECTIVE: We examined associations between the frequency of fruit and vegetable (F&V) consumption and nutritional deficiencies among Brazilian schoolchildren. DESIGN: A cross-sectional, population-based study was performed. A short FFQ was used to assess consumption of fruits and vegetables (F&V) over the past month. The prevalence ratios (PR) and 95 % confidence intervals for stunting, obesity, anaemia, vitamin A and folate deficiencies, vitamin E and vitamin D insufficiencies were estimated for low F&V consumption frequency (vegetables ≤ 3 times/month and fruits ≤ 3 times/week) and compared with children with usual F&V consumption frequency (vegetables ≥ 1 time/week and fruits ≥ 4 times/week). SETTING: Acrelândia, Western Brazilian Amazon. SUBJECTS: A total of 702 children aged 4-10 years. RESULTS: Only 5 % of children consumed F&V ≥ 5 times/d. Prevalence of deficiency was 31 %, 15 %, 9 % and 2 % for vitamins D, A, E and folate, respectively. Overall, 6.3% of children were anaemic, 3.3% were stunted, 2.7% were obese and 33 % had multiple nutritional deficiencies. Low frequency of F&V consumption was associated with lower plasma concentrations of carotenoids and vitamin E. Nutritional deficiencies were higher among non-consumers of F&V when compared with usual consumers: anaemia (PR=1.9; 95 % CI 1.0, 3.7), vitamin E insufficiency (PR=2.5; 95% CI 1.5, 4.2), vitamin D insufficiency (PR=1.5; 95% CI 1.1, 1.9) and stunting (PR=2.6; 95% CI 1.1, 6.1). CONCLUSIONS: In our study, the occurrence of nutritional deficiencies in children with low F&V consumption was twice as high as in children with usual F&V consumption, reinforcing the importance of effective actions to promote the consumption of F&V.

Vitamin E trafficking in neurologic health and disease.

Vitamin E was identified almost a century ago as a botanical compound necessary for rodent reproduction. Decades of research since then established that of all members of the vitamin E family, α-tocopherol is selectively enriched in human tissues, and it is essential for human health. The major function of α-tocopherol is thought to be that of a lipid-soluble antioxidant that prevents oxidative damage to biological components. As such, α-tocopherol is necessary for numerous physiological processes such as permeability of lipid bilayers, cell adhesion, and gene expression. Inadequate levels of α-tocopherol interfere with cellular function and precipitate diseases, notably ones that affect the central nervous system. The extreme hydrophobicity of α-tocopherol poses a serious thermodynamic barrier for proper distribution of the vitamin to target tissues and cells. Although transport of the vitamin shares some steps with that of other lipids, selected tissues evolved dedicated transport mechanisms involving the α-tocopherol transfer protein (αTTP). The critical roles of this protein and its ligand are underscored by the debilitating pathologies that characterize human carriers of mutations in the TTPA gene.

Brown bowel syndrome: a rare complication in diseases associated with long-standing malabsorption.

BACKGROUND/AIMS: Longtime chronic malabsorption may among other things cause a lack of liposoluble vitamins. Vitamin E deficiency can lead to formation of lipofuscin aggregates. Its deficiency is also associated with an increased lipofuscinosis of the bowel, i.e. brown bowel syndrome. METHODS: Systematic research via Medline on brown bowel syndrome, lipofuscinosis, and vitamin E deficiency was performed. We combined our own clinical experience and a review of the literature for this paper. Its goal is to inform about the possible consequences of severe malabsorption and brown bowel syndrome. RESULTS: Systematic data about the occurrence of severe malabsorption and brown bowel syndrome are rare. Only about 27 scientific reports can be found on this subject. Brown bowel syndrome is found mostly in conjunction with vitamin E deficiency and lipofuscinosis of the bowel. The clinical findings are caused by both malabsorption and lipofuscinosis. Case reports show a therapeutic effect of vitamin E. CONCLUSION: Vitamin deficiency caused by longtime chronic malabsorption can lead to the development of brown bowel syndrome, which is seen as the expression of lipofuscinosis of the bowel, and can cause further clinical disorders. Patients with malabsorption should therefore be monitored regarding their vitamin E levels.

Vitamin E deficiency begins within 6 months after gastrectomy for gastric cancer.

BACKGROUND: To clarify factors related to vitamin E malabsorption after gastric surgery, we evaluated serum vitamin E levels in patients who had undergone gastrectomy for gastric cancer. METHODS: We studied 39 patients (26 men, 13 women; mean age, 61.7 years) who underwent gastrectomy for early gastric cancer. Surgical procedures included 24 subtotal gastrectomies and 15 total gastrectomies. We measured serum levels of vitamin E before and 3, 6, 9, and 12 months after gastrectomy. A level of less than 0.75 mg/dl was defined as a low vitamin E level. RESULTS: Serum vitamin E levels decreased to less than 0.75 mg/dl in 6 (15.4%) of the 39 patients within 6 months after gastrectomy and in 7 (17.9%) of the 39 patients within 1 year after gastrectomy. The proportion of patients with a low serum vitamin E level was significantly higher in the total gastrectomy group (p = 0.002). A low vitamin E level was significantly associated with a low total cholesterol level. Total cholesterol levels in low vitamin E levels patients were lower than normal vitamin E levels patients. None of the patients with a low vitamin E level had neuropathy. CONCLUSIONS: The type of operation performed (total vs. subtotal gastrectomy) may be the major cause of vitamin E malabsorption after gastrectomy for gastric cancer. Vitamin E deficiency probably begins within 6 months after gastrectomy for gastric cancer.

The prevalence of fat-soluble vitamin deficiencies and a decreased bone mass in patients with chronic pancreatitis.

BACKGROUND/OBJECTIVES: In chronic pancreatitis, malabsorption of fat is common due to loss of exocrine function. Consequently, these patients are at risk to acquire deficiencies of the fat-soluble vitamins, which may result in a decreased bone mineral density (BMD) and the development of osteopenia and osteoporosis. METHODS: We prospectively enrolled all patients diagnosed with chronic pancreatitis, who visited our outpatient clinic between March and November 2011. Data were collected regarding demographic characteristics, symptoms, and pancreatic function. Serum concentrations of vitamins A, E, K, and D were determined, and BMD was assessed by means of bone densitometry. Results were analyzed according to pancreatic function status and enzyme use, and compared to reference data, when available. RESULTS: Forty patients were included (43% female; mean age of 52). Alcohol abuse was the major cause of pancreatitis (50%). Twenty-eight patients were exocrine insufficient (70%), of whom 19 used pancreatic enzymes. Vitamin A, D, E, and K deficiencies were present in 3, 53, 10, and 63% of patients, respectively. Osteopenia and osteoporosis were observed in 45% and 10% of patients. A decreased BMD was more frequently observed than expected, based on reference data, even in exocrine sufficient patients. CONCLUSIONS: Deficiencies of fat-soluble vitamins and a decreased BMD are frequently present in chronic pancreatitis, even in exocrine sufficient patients. Consequently, all patients with chronic pancreatitis should be routinely screened for fat-soluble vitamin deficiencies and a decreased BMD.

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.

Malnutrition in morbidly obese patients: fact or fiction?

Reports of nutritional deficiencies after Bariatric surgery have lead investigators to inquire about the preoperative nutritional status of morbidly obese patients. Interestingly, numerous reports demonstrated a pattern of low levels of various micronutrients among overweight and obese patients, even in comparison with normal weight population. In this article we reviewed the literature for micronutrient deficiencies in obese patients prior to weight reduction surgery.

Brown bowel syndrome: a rare malnutrition-related complication of bariatric surgery.

INTRODUCTION: Case report: we present the case of a 44-year-old male who presented with uncontrollable diarrhea, severe protein-calorie malnutrition and multiple vitamin deficiencies, along with peripheral neuropathy ten years after classic biliopancreatic diversion (BPD). He underwent nutritional support and had the surgery converted to a Roux-en-Y gastric bypass, with an uneventful outcome. The histopathology of the resected bowel revealed lipofuscinosis of the muscular layer compatible with brown bowel syndrome. Discussion: brown bowel syndrome is a rare complication of malnutrition that can be observed after BPD. It is associated with vitamin E deficiency. After recovery with nutritional support, a reoperation that elongates the common channel, and thus minimizes the degree of malabsorption, should be indicated in these cases.

INTRODUCCIÓN: Caso clínico: presentamos el caso de un paciente varón de 44 años que presentó diarrea incontrolable, desnutrición proteica-calórica severa y deficiencias de múltiples vitaminas, junto con neuropatía periférica diez años después de derivación biliopancreatica clásica (DBP). Se sometió a soporte nutricional y la cirugía se convirtió en un bypass gástrico en Y de Roux, con un resultado sin complicaciones. La histopatología del intestino resecado reveló una lipofuscinosis de la capa muscular compatible con el síndrome del intestino marrón. Discusión: el síndrome de intestino marrón es una complicación rara de la desnutrición que se puede observar después de la DBP. Se asocia a deficiencia de vitamina E. Después de la recuperación con soporte nutricional, se debe indicar una reoperación que alargue el canal común y, por lo tanto, minimice el grado de malabsorción en estos casos.

Chronic Complications of Cholestasis: Evaluation and Management.

Patients with primary biliary cholangitis (PBC) are at risk for various harmful consequences of chronic cholestasis. These include fat-soluble vitamin deficiency, even in the setting of macronutrient sufficiency, as well as metabolic bone disease, including osteoporosis with fractures. Hyperlipidemia is often present and less commonly associated with risk of cardiovascular event; however, the long-term effect of new emerging therapies for PBC remains to be determined. Patients with PBC also have infrequent but notable risk of portal hypertension despite early-stage disease. This review discusses the background, evaluation, and practical management of these complications of chronic cholestasis.

Burn and smoke inhalation injury in sheep depletes vitamin E: kinetic studies using deuterated tocopherols.

To test the hypothesis that burn and smoke injury will deplete tissue alpha-tocopherol and cause its faster plasma disappearance, deuterium-labeled vitamin E was administered to sheep exposed to both surface skin burn and smoke insufflation, which cause injuries similar to those of human victims of fire accidents. Two different protocols were used: (1) deuterated vitamin E was administered orally with food at time 0 (just before injury) or (2) the labeled vitamin E was administered orally with food the day before injury. The animals, which had been operatively prepared seven days before, were anesthetized and then received both 40% body surface area third-degree burn and 48 breaths of cotton smoke or sham injuries. All were resuscitated with Ringer's lactate solution (4 ml/kg/% BSA burn/24 h) and mechanically ventilated. Blood samples were collected at various times after vitamin E dosing. In both studies the depletion of plasma alpha-tocopherol was faster in the injured sheep. The sheep given deuterated vitamin E 24 h before injury had similar maximum alpha-tocopherol concentrations at similar times. The exponential rates of alpha-tocopherol disappearance were 1.5 times greater and half-lives were 12 h shorter (p < 0.05) in the injured sheep. In separate studies, various tissues were obtained from sheep that were sacrificed from 4 to 48 h after injury. The liver alpha-tocopherol concentrations in sheep killed at various times after injury seem to show a linear decrease at a rate of 0.1 nmol alpha-tocopherol/g liver per hour, suggesting that the liver is supplying alpha-tocopherol to maintain the plasma and lung alpha-tocopherol concentrations, but that this injury is so severe the liver is unable to maintain lung alpha-tocopherol concentrations. These findings suggest that alpha-tocopherol should be administered to burn patients to prevent vitamin E depletion and to protect against oxidative stress from burn injury.

Deficiency of vitamin E in the alveolar fluid of cigarette smokers. Influence on alveolar macrophage cytotoxicity.

Cigarette smoking produces oxidant-mediated changes in the lung important to the pathogenesis of emphysema. Since vitamin E can neutralize reactive oxygen species and prevent peroxidation of unsaturated lipids, it may constitute an important component of the lung's defense against oxidant injury. To better characterize the antioxidant protective role of vitamin E, young asymptomatic smokers and nonsmokers were evaluated by bronchoalveolar lavage before and immediately after a 3-wk course of oral vitamin E (2,400 IU/d). Smoker alveolar fluid at baseline was relatively deficient in vitamin E compared with nonsmoker fluid (3.1 +/- 0.7 ng/ml vs. 20.7 +/- 2.4 ng/ml, P less than 0.005). Although smoker alveolar fluid vitamin E levels increased to 9.3 +/- 2.3 ng/ml after supplementation, the levels remained significantly lower than nonsmoker baseline levels (P less than 0.01). This deficiency was explained, in part, by the increased oxidative metabolism of vitamin E to the quinone form in the lungs of smokers compared with nonsmokers. Although the significance of a lower concentration of alveolar fluid vitamin E is unclear, it may compromise the antioxidant protection afforded by the alveolar fluid as it coats the lung's epithelial surface. The protective role of vitamin E was assessed by cytotoxicity experiments, which demonstrated that the killing of normal rat lung parenchymal cells by smoker alveolar macrophages was inversely related to the vitamin E content of the parenchymal cells. These findings suggest that vitamin E may be an important lower respiratory tract antioxidant, and that the deficiency seen in young smokers may predispose them to an enhanced oxidant attack on their lung parenchymal cells.

The risk of plasma vitamin A, C, E and D deficiency in patients with metabolic syndrome: A case-control study.

BACKGROUND: The increasing incidence of metabolic diseases such as obesity or diabetes have made them a major public health problem. Increasing oxidative stress induced by reactive oxygen species, which initiate the oxidative adverse changes in the cell, is mentioned, among other risk factors, to underlie these diseases. Vitamin A, C and E are listed among the non-enzymatic mechanisms counteracting this phenomenon. Vitamin D deficiency is also associated with cardiovascular diseases. OBJECTIVES: The aim of the study was to assess the risk of vitamin A, C, E and D deficit in the plasma of metabolic syndrome (MS) patients. MATERIAL AND METHODS: The study included 191 patients with MS and 98 subjects without MS. Loglinear analysis was used in the assessment of mutual interactions between the vitamin concentration and the analysis of classification by ROC curves to predict the frequency of vitamin deficiency in MS patients. RESULTS: A correlation was found between the plasma level of vitamins in the group of MS patients. Vitamin A concentration correlated with that of vitamin C (r = 0.51, p = 0.0000), vitamin D (r = 0.49, p = 0.0000) and E (r = 0.32, p = 0.0001). The plasma level of vitamin D correlated with the level of vitamin E (r = 0.46, p = 0.00000) and vitamin C (r = 0.37, p = 0.0000). Regression analysis showed a correlation between the concentration of the tested vitamins in patients with MS. Interactions were observed between vitamins C and A and between C and D. HDL cholesterol level was lower in patients with vitamin A deficiency compared to patients with its normal level. CONCLUSIONS: The plasma levels of vitamin A, C, E and D were significantly lower in patients with MS than in healthy subjects and they mutually correlated with each other. The normalization of glucose and HDL level may contribute to the regulation of the concentration of vitamin A in patients with MS.

Fat-soluble vitamin deficiency in pregnancy: a case report and review of abetalipoproteinemia.

BACKGROUND: Abetalipoproteinemia (ABL) is a metabolic disorder resulting in poor absorption of fat-soluble vitamins. CASE: Two pregnancies in a woman with ABL are reported, contrasting outcomes with subtherapeutic and normal vitamin levels. CONCLUSION: Fat-soluble vitamin levels in pregnancy are critical for many aspects of fetal development. This report details a congenital ophthalmologic finding that may be associated with vitamin A deficiency.