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Background: The causal relationship between familial hypercholesterolemia (FH) and various vitamin deficiencies has not yet been elucidated. Therefore, this study investigated the cause-and-effect relationship between FH and the risk of multiple vitamin deficiencies in humans., Methods: Mendelian randomization (MR) analysis was performed by extracting six datasets for FH, FH with ischemic heart disease (IHD), and vitamin deficiency (vitamin A, thiamine, other B-group vitamins, and vitamin D) from the FinnGen study, covering a total of 329,115; 316,290; 354,932; 354,949; 355,411 and 355,238 individuals, respectively., Results: FH was suggestively associated with higher odds of thiamine deficiency [inverse variance weighted odds ratio (OR IVW ) 95% confidence interval (CI): 1.62 (1.03, 2.55), P = 0.036] and vitamin D deficiencies [OR IVW CI: 1.35 (1.04, 1.75), P = 0.024], low-density lipoprotein receptor ( LDLR ) rs112898275 variant, rs11591147 and rs499883 in proprotein convertase subtilisin/kexin 9 ( PCSK9 ), rs9644862 in cyclin-dependent kinase inhibitor 2 B antisense RNA1 ( CDKN2B-AS1 ), and rs142834163 in dedicator of cytokinesis 6 ( DOCK6 ) and rs115478735 in ABO blood group ( ABO ) strongly influenced the risk of thiamine deficiency, while the rs7412 variant in apolipoprotein E ( APOE ) mostly influenced the risk of vitamin D deficiency. FH with IHD was suggestively associated with higher odds of vitamin D deficiency (OR IVW, weighted median [WM][95%CI]: 1.31 [1.05, 1.64]; 1.47 [1.10, 1.97]) ( P = 0.018; 0.010) without any single significant SNPs observed., Conclusion: FH was positively associated with increased risks of thiamine and vitamin D deficiencies, revealing a prospective and unfortunate complication of FH., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhang, Wei, Zhou and Liu.)

The deficiency of vitamins, a condition known as "hidden hunger", causes comprehensive pathological states. Research over the years has identified a relationship between liver diseases and hypovitaminosis or defects in vitamin metabolism. The exact mechanisms remain elusive; however, the crucial involvement of specific vitamins in metabolic functions, alongside the reclassification of liver disease as metabolic dysfunction-associated steatotic liver disease (MASLD), has prompted researchers to investigate the potential cause-effect dynamics between vitamin deficiency and liver disease. Moreover, scientists are increasingly investigating how the deficiency of vitamins might disrupt specific organ crosstalk, potentially contributing to liver disease. Although the concept of a dysmetabolic circuit linking adipose tissue and the liver, leading to liver disease, has been discussed, the possible involvement of vitamin deficiency in this axis is a relatively recent area of study, with numerous critical aspects yet to be fully understood. In this review, we examine research from 2019 to July 2024 focusing on the possible link between liver-adipose tissue crosstalk and vitamin deficiency involved in the onset and progression of non-alcoholic fatty liver disease (NAFLD). Studies report that vitamin deficiency can affect the liver-adipose tissue axis, mainly affecting the regulation of systemic energy balance and inflammation.

Background and Aims: Water-soluble vitamins play an essential coenzyme role in the nervous system. Acquired vitamin deficiencies are easily treatable, however, without treatment, they can lead to irreversible complications. This study aimed to provide clinical, laboratory parameters and neuroimaging data on vitamin deficiencies in an attempt to facilitate early diagnosis and prompt supplementation., Methods: From July 1998 to July 2023, patients at Necker-Enfants-Malades Hospital presenting with acute neurological symptoms attributed to acquired vitamin deficiency were included. Clinical data were extracted from Dr Warehouse database. Neuroimaging, biochemical and electrophysiological data were reviewed., Results: Patients with vitamin B1 deficiency exhibited abnormal eye movements (n = 4/4), fluctuations in consciousness (n = 3/4), and ataxia (n = 3/4). Brain MRI showed alterations of fourth ventricle region (n = 4/4), periaqueductal region (n = 4/4), tectum (n = 3/4), and median thalami (n = 3/4). Patients with vitamin B2 deficiency presented with early onset hypotonia (n = 3/4), hyperlactatemia (n = 4/4), and hyperammonemia (n = 4/4). Plasma acylcarnitines revealed a multiple acyl-coA dehydrogenase deficiency-like profile (n = 4/4). In vitamin B12 deficiency, young children presented with developmental delay (n = 7/7) and older children with proprioceptive ataxia (n = 3/3). Brain MRI revealed atrophy (n = 7/7) and spinal MRI hyperintensity in posterior cervical columns (n = 3/3). Metabolic findings showed elevated methylmalonic acid (n = 6/7) and hyperhomocysteinemia (n = 6/7). Patients with vitamin C deficiency exhibited gait disturbances and muscle weakness (n = 2/2)., Conclusions: Acquired vitamin deficiencies may display reversible clinical symptoms mimicking inherited metabolic disorders. Some situations raise suspicion for diagnosis: concordant clinical presentation, suggestive neuroimaging findings, and/or biochemical evidence. Any acute neurological condition should be treated without waiting for definitive biochemical confirmation., Competing Interests: Declaration of competing interest The authors declare no conflicts of interest., (© 2024 Published by Elsevier Ltd on behalf of European Paediatric Neurology Society.)

All vitamins play essential roles in various aspects of body function and systems. Patients with chronic kidney disease (CKD), including those receiving dialysis, may be at increased risk of developing vitamin deficiencies due to anorexia, poor dietary intake, protein energy wasting, restricted diet, dialysis loss, or inadequate sun exposure for vitamin D. However, clinical manifestations of most vitamin deficiencies are usually subtle or undetected in this population. Testing for circulating levels is not undertaken for most vitamins except folate, B 12 , and 25-hydroxyvitamin D because assays may not be available or may be costly to perform and do not always correlate with body stores. The last systematic review through 2016 was performed for the Kidney Disease Outcome Quality Initiative (KDOQI) 2020 Nutrition Guideline update, so this article summarizes the more recent evidence. We review the use of vitamins supplementation in the CKD population. To date there have been no randomized trials to support the benefits of any vitamin supplementation for kidney, cardiovascular, or patient-centered outcomes. The decision to supplement water-soluble vitamins should be individualized, taking account the patient's dietary intake, nutritional status, risk of vitamins deficiency/insufficiency, CKD stage, comorbid status, and dialysis loss. Nutritional vitamin D deficiency should be corrected, but the supplementation dose and formulation need to be personalized, taking into consideration the degree of 25-hydroxyvitamin D deficiency, parathyroid hormone levels, CKD stage, and local formulation. Routine supplementation of vitamins A and E is not supported due to potential toxicity. Although more trial data are required to elucidate the roles of vitamin supplementation, all patients with CKD should undergo periodic assessment of dietary intake and aim to receive various vitamins through natural food sources and a healthy eating pattern that includes vitamin-dense foods., (Copyright © 2023 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Chronic pancreatitis (CP) is often associated with exocrine pancreatic insufficiency (EPI), which may increase risk for fat-soluble vitamin depletion. Although vitamin D deficiency is widespread among the general population, vitamins A, E, and K deficiencies may more uniquely present in patients with CP. Yet, it is unclear whether fat-soluble vitamin status should be routinely monitored in all patients with CP or limited to those with EPI. The purpose of this review is to describe the laboratory status of vitamins A, E, and K in adult patients with CP and their association with exocrine pancreatic function. Five primary, observational studies met the inclusion criteria for qualitative synthesis. Biochemical deficiencies in fat-soluble vitamins were observed across trials but results varied with respect to whether EPI increased risk. Challenges related to the diagnosis and treatment of EPI along with potential confounders may contribute to the heterogeneity among study results. Although more studies are needed to determine the influence of pancreatic enzyme replacement therapy on fat-soluble vitamin status as well as effective vitamin repletion strategies, clinicians should consider periodically screening for deficiencies in all patients with CP regardless of EPI to avoid associated health effects of vitamin depletion., (© 2023 American Society for Parenteral and Enteral Nutrition.)

Nutritional peripheral neuropathies are a global problem, heavily influenced by geopolitical, cultural and socioeconomic factors. Peripheral neuropathy occurs most frequently secondary to B-vitamin deficiencies, which is suspected to increase in years to come due to the popularity of vegan and vegetarian diets and increased use of bariatric surgery.This review will focus on the common B-vitamins for which a causal link to peripheral neuropathy is more established (vitamins B 1 , B 2 , B 6 , B 9 and B 12 ). We will review the historical human and animal data on which much of the clinical descriptions of vitamin deficiencies are based and summarise current available tools for accurately diagnosing a nutritional deficiency. We will also review recently described genetic diseases due to pathogenic variants in genes involved in B-vitamin metabolism that have helped to inform the phenotypes and potential causality of certain B-vitamins in peripheral neuropathy (B 2 and B 9 ).Endemic outbreaks of peripheral neuropathy over the last two centuries have been linked to food shortages and nutritional deficiency. These include outbreaks in Jamaican sugar plantation workers in the nineteenth century (Strachan's syndrome), World War two prisoners of war, Cuban endemic neuropathy and also Tanzanian endemic optic neuropathy, which remains a significant public health burden today. An improved understanding of lack of which vitamins cause peripheral neuropathy and how to identify specific deficiencies may lead to prevention of significant and irreversible disability in vulnerable populations., Competing Interests: Competing interests: CK is supported by a UCL Queen Square Institute of Neurology and Cleveland Clinic London MPhil/PhD Neuroscience fellowship., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: This review aims to identify the current indications and gaps in the management of fat-soluble vitamins in pediatric patients with cholestasis., Methods: A comprehensive review of the literature using PubMed, Scopus, Web of Science and Embase was performed. Two authors independently identified the most relevant studies published over the past 20 years up to February 2022, including original papers, narrative reviews, observational studies, clinical trials, systematic reviews and meta-analyses. The literature was screened, and preclinical studies about pathogenetic mechanisms were also included. Keywords searched for each fat-soluble vitamin (A, D, E and K), alone or in combination, were "cholestasis", "chronic liver disease", "biliary atresia", "malnutrition" and "nutritional needs". Studies published prior to the selected time range were searched manually and, when considered relevant, included within the list of references., Results: Eight hundred twenty-six articles were initially screened. From these, 48 studies were selected. A comparison of the recommended methods of supplementation for fat-soluble vitamins was then carried out. The causes of malabsorption were explained and current methods for defining deficiency and monitoring complications were summarized., Conclusions: According to the literature, children with cholestasis are at a higher risk of fat-soluble vitamin deficiency. Although there are general recommendations, the treatment for vitamin deficiency is not uniformly validated.

Purpose: Chronic pancreatitis (CP) leads to diabetes and pancreatic exocrine insufficiency (PEI). PEI may lead to maldigestion and malnutrition, which may cause fat-soluble vitamin deficiency, sarcopenia and abnormal bone density. We aim to study the prevalence of osteoporosis, sarcopenia and vitamin deficiency among CP patients., Methods: Long-term (4-5 years) follow-up was implemented on CP patients. We recorded CP duration, BMI, smoking, alcohol consumption and medication. We determined the serum values for A, D and E vitamins, albumin, creatinine, haemoglobin, calcium and magnesium. Bone density measurement was taken from the proximal femur and lumbar spine. CT/MRI scans were used to measure for psoas muscle area., Results: A total of 33 patients (median age 62 [39-81] years, 61% male) were included. None of these patients had earlier diagnosis of osteopathy, and none of them had known vitamin deficiency or were sarcopenic. Nineteen patients (57%) had pancreatic exocrine insufficiency and of these seven patients (37%) had no pancreatic enzyme replacement therapy (PERT) and one (5%) had inadequate enzyme therapy. During the study, osteoporosis was diagnosed in 20% and possible sarcopenia in 48% of patients. PEI and inadequate PERT was associated with low E vitamin levels (75% vs. 0%, p = 0.012), higher risk of osteoporosis (43% vs. 5.6%, p = 0.013) and sarcopenia (80% vs. 36%, p = 0.044)., Conclusion: This study demonstrates that chronic pancreatitis is associated with osteoporosis, sarcopenia and vitamin deficiency. If untreated, pancreatic exocrine insufficiency is associated with increased risk of these outcomes. This highlights the importance of identifying and treating PEI in CP patients., (© 2023. The Author(s).)

Patients with cystic fibrosis (CF) are at high risk of fat-soluble vitamin deficiencies, even with supplementation. The contribution of a suboptimal vitamin K status to respiratory and endocrine pathophysiology in CF has been inadequately characterized. This is a cross-sectional study in adult CF patients (≥18 years old) from the Montreal Cystic Fibrosis Cohort. Vitamin K 1  (VK1) was measured with high-performance liquid chromatography, using fasted serum samples collected during an oral glucose tolerance test (OGTT: 2 h with plasma glucose and insulin every 30 min) ( n  = 168). Patients were categorized according to VK1 status (suboptimal defined as <0.30 nmol/L). Suboptimal VK1 levels were observed in 66% of patients. Patients with a suboptimal VK1 status have a higher risk of colonization with Pseudomonas aeruginosa  ( p  = 0.001), have lower body mass index (BMI) ( p  = 0.003), and were more likely to have exocrine pancreatic insufficiency ( p  = 0.002). Using an established threshold for VK1, we did show significantly reduced OGTT-derived measures of insulin secretion in patients with a VK1 status below 0.30 nmol/L (first- and second-phase area under the curve (AUC) INS/GLU  ( p  = 0.002 and p  = 0.006), AUC INS  ( p  = 0.012) and AUC INS/GLU  ( p  = 0.004)). Subclinical vitamin K deficiency is more common than other fat-soluble vitamin deficiencies in patients with CF. We demonstrate an association between a suboptimal VK1 status and measures of insulin secretion. We highlight the potential associations of mild vitamin K deficiency with pseudomonal colonization and lower BMI, although these need to be validated in prospective studies.

Background: Anemia is a common extraintestinal manifestation of inflammatory bowel disease (IBD), with a 6% to 74% prevalence and a negative impact on patient survival and quality of life, although the prevalence is apparently declining due to improved disease treatment. We aimed to investigate the prevalence, pathogenesis, and clinical correlates of anemia in Italian patients with IBD., Methods: A multicenter, prospective, observational study, involving 28 Italian gastroenterology centers, was conducted to investigate the epidemiology and consequences of IBD-associated anemia. Clinical and laboratory data of anemic patients were obtained at study enrolment., Results: Anemia was diagnosed in 737 of 5416 adult IBD outpatients (prevalence 13.6%); females were more commonly affected than males (odds ratio, 1.5; 95% confidence interval [CI], 1.2-1.7) and had more severe anemia. In the majority of cases, anemia was due to iron deficiency (62.5% of cases; 95% CI, 58.3%-66.6%), either isolated or in association with inflammation and/or vitamin deficiencies; anemia of inflammation accounted for only 8.3% of cases. More severe anemia was associated with increasing fatigue and worse quality of life. Only 68.9% of anemic patients with iron deficiency (95% CI, 63.4%-73.8%) and 34.6% of those with vitamin deficiencies (95% CI, 26.2%-44.2%) were properly treated with supplementation therapy., Conclusions: In Italy, the prevalence of IBD-associated anemia is lower than previously reported. Anemia of IBD is most commonly due to iron deficiency and contributes to fatigue and poor quality of life, but remains untreated in a large proportion of patients with iron and/or vitamin deficiencies. This study is registered at clinicaltrials.gov as NCT02872376., (© The Author(s) 2022. Published by Oxford University Press on behalf of Crohn’s & Colitis Foundation. All rights reserved. 
For permissions, please e-mail: journals.permissions@oup.com.)

Vitamin deficiencies are an emerging concern in the management of children with autism spectrum disorder (ASD). Particular attention is required for recognizing the variable signs caused by unbalanced food intakes. We herein report two patients with multiple vitamin deficiencies who needed critical care showing different prognoses. Patient 1 with 'Shoshin' beriberi presenting with cardiac arrest had thiamine deficiency developed severe neurological sequelae despite rapid vitamin supplementation. Patient 2, who had leg pain and a limping gait, showed a rapid recovery with intravenous infusion and tube feeding after being diagnosed with scurvy. A literature search revealed several children with ASD with critically ill thiamine deficiency, but few reports documented a life-threatening condition in the form of cardiac arrest at the onset. Considering the high observation rate of food selectivity in children with ASD, early intervention is required to prevent the exacerbation of vitamin deficiencies to severe neurological disabilities., (© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)

Vitamin deficiencies and excesses are known to cause various types of brain or peripheral nerve injuries. Improved nutritional status and dietary patterns have led to reduced prevalence, and at least some of these conditions are rare in recent times. However, delayed diagnosis (For example, in patients with Wernicke's encephalopathy) may worsen patient prognosis even in current times. Recent studies have reported an association between cognitive function and some vitamins. In this article, we summarize past and present research focused on neurological symptoms that occur secondary to vitamin deficiencies and excesses.

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is currently an increasing contributor to cancer-related mortality. Despite advances in cancer treatment, PDAC survival rates have remained roughly unchanged over the years. Specifically, late diagnosis and insensitivity to currently available therapeutic regimens have been identified as the main causes for its poor survival. Pancreatic exocrine insufficiency (PEI) is a typical complication associated with PDAC diagnosis and pancreatic surgery. Pancreatic exocrine insufficiency, a major contributor to maldigestion in PDAC, is often not treated because it remains undetected because of lack of overt signs and symptoms. In this review, we will focus on the major consequences of PEI, including the inadequacy of lipase excretion, which results in deficiency of fat-soluble vitamins. Because PDAC is known for its immune-high jacking mechanisms, we describe key features in which deficiencies of fat-soluble vitamins may contribute to the aggressive biological behavior and immune evasion in PDAC. Because PEI has been shown to worsen survival rates in patients with PDAC, detecting PEI and the related fat-soluble vitamin deficits at the time of PDAC diagnosis is critical. Moreover, timely supplementation of pancreatic enzymes and fat-soluble vitamins may improve outcomes for PDAC patients., Competing Interests: The authors declare no conflict of interest., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity., Methods: In this review, we have compiled various reports collected from PubMed, Scholar Google, Research gate, and Science direct. The findings were evaluated, compiled, and represented in this manuscript., Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer's disease, Parkinson's disease, Huntington's disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer's disease, there is a lack of vitamin- B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson's disease, vitamin- D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, vitamin-C and vitamin-D deficiency causes demyelination of neurons. In Huntington's disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. vitamin B5 deficiency in Huntington's disease disrupts the synthesis of acetylcholine and hormones in the brain., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

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.

Vitamins are an indispensable food source and important owing to the enzyme cofactor and catalytic roles they play in the body. Fat-soluble vitamins A, D, E, K, and B12, are stored in the body and can cause problems with their excessive accumulation. Other vitamins rarely accumulate in the body because they dissolve in water and are excreted through the kidneys. Alcoholism, strict diets, insufficient parental nutrition, and gastrointestinal absorption problems may be included in the causes of vitamin deficiencies. Although clinical findings of vitamin deficiencies display different characteristics depending on the vitamins, the signs that generally occur are cutaneous pigmentation, pigmentation on mucous membranes, palmoplantar keratoderma characterized by fissures, palmar streaking, yellow streaking on the nails, nail layering, and intranail hemorrhage., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Objectives: Inappropriate vitamin supply is a public health problem and is related to abnormalities in brain development, immune response and, more recently, in changes of gut microbial composition. It is known that low levels of vitamin in early life are linked to increased susceptibility to neurodevelopmental disorders, such as Autism Spectrum Disorders (ASD). Unfortunately, the possible peripheral influences of vitamin deficiency that leads to alterations in the gut microbiota-immune-brain axis, one important modulator of the ASD pathology, remain unclear. This narrative review discusses how the impact of vitamin deficiency results in changes in the immune regulation and in the gut microbiota composition, trying to understand how these changes may contribute for the development and severity of ASD., Methods: The papers were selected using Pubmed and other databases. This review discusses the following topics: (1) vitamin deficiency in alterations of central nervous system in autism, (2) the impact of low levels of vitamins in immunomodulation and how it can favor imbalance in gut microbiota composition and gastrointestinal (GI) disturbances, (3) gut microbiota imbalance/inflammation associated with the ASD pathophysiology, and (4) possible evidences of the role of vitamin deficiency in dysfunctional gut microbiota-immune-brain axis in ASD., Results: Studies indicate that hypovitaminosis A, B12, D, and K have been co-related with the ASD neuropathology. Furthermore, it was shown that low levels of these vitamins favor the Th1/Th17 environment in the gut, as well as the growth of enteropathogens linked to GI disorders., Discussion: GI disorders and alterations in the gut microbiota-immune-brain axis seems to be linked with ASD severity. Although unclear, hypovitaminosis appears to regulate peripherally the ASD pathophysiology by modulating the gut microbiota-immune-brain axis, however, more research is still necessary to confirm this hypothesis.

Background and purpose - There is growing evidence that hypoproteinemia is an important risk factor for adverse events after surgery. Less is known about the impact of vitamin deficiency on postoperative outcome. Therefore we evaluated the prevalence and impact of malnutrition and vitamin deficiency in geriatric patients undergoing elective orthopedic surgery.Patients and methods - In a retrospective analysis of 599 geriatric patients who had undergone elective orthopedic surgery in 2018 and 2019, hypoproteinemia, and deficiency of vitamin D, vitamin B12, and folate were assessed. Reoperation rates, readmission rates, complication rates, and transfusion rates were compared between malnourished patients and patients with normal parameters. Multivariable logistic regression models were used to assess the relationship between malnutrition and postoperative adverse events, controlling for confounding factors such as age, sex, diabetes mellitus, and frailty.Results - Patients with malnutrition showed a higher rate of reoperation (13% vs. 5.5%; p = 0.01) and exhibited more wound-healing disorders (7.4% vs. 1.3%, p = 0.001) as well as Clavien-Dindo IV° complications (7.4% vs. 2.4%; p = 0.03). Deficiency of vitamin D led to a higher rate of falls (8.4% vs. 2.9%, p = 0.006). Deficiency of vitamin B12 and folate did not affect postoperative adverse events. Although correlated to frailty (p = 0.004), multivariable regression analysis identified malnutrition as independent risk factor for reoperation (OR 2.6, 95% CI 1.1-6.2) and wound healing disorders (OR 7.1, CI 1.9-26).Interpretation - Malnutrition is common among geriatric patients undergoing elective orthopedic surgery and represents an independent risk factor for postoperative adverse events.

Aim: To evaluate the status of vitamin D in women with rheumatoid arthritis (RA) and establish its associations with comorbidity, disease activity, and body composition components., Materials and Methods: 86 women with RA (average age 58.18.5 years) were enrolled in the study. We analyzed the relationship of vitamin D levels with clinical and laboratory parameters and with the results of two-energy x-ray absorptiometry. MannWhitney or KruskalWallis, 2 and Spearman tests were performed using Statistica for Windows 10.0 (StatSoft Inc., USA)., Results: Vitamin D level was 22.4 [17.8; 27.3] ng/ml: deficiency was detected in 33%, and insufficiency in 46% of women with RA. Only 41% of patients with low vitamin D levels received supplements of cholecalciferol, while only 9% in a sufficient dose. 25(OH)D level was significantly lower in RA patients with sarcopenia, obesity, high activity according to DAS28 and in those who did not receive vitamin D supplements. There werent differences in 25(OH)D levels among subgroups of patient according to age, fertility, BMD status, comorbidity index, RA duration, ESR and CRP levels, medical therapy performed., Conclusion: 79% of patients with RA had low levels of vitamin D, while less than half of them received additional cholecalciferol supplements. Low vitamin D levels in RA patients were associated with high disease activity, sarcopenia, and obesity.

Purpose: The purpose of this study was to determine whether deficiencies of water-soluble vitamin intake predicted health-related quality of life (HRQOL) and the composite end point of all-cause mortality or cardiac- or heart failure (HF)-related hospitalization in HF patients. Patients with HF may be at risk for inadequate consumption of water-soluble vitamins due to poor appetite and dietary sodium restriction. Because water-soluble vitamins are important in metabolic processes, inadequate dietary intake of these vitamins may negatively affect health outcomes., Methods: We consecutively recruited patients with HF from outpatient clinics affiliated with academic medical centers. Patients were referred by providers to investigators who verified their eligibility. Patients with HF completed a four-day food diary to determine dietary deficiencies of water-soluble vitamins and the Minnesota Living with HF questionnaire to assess HRQOL at baseline. Patients were followed to determine an event., Results: A total of 216 patients were included. Patients with a higher number of dietary deficiencies of water-soluble vitamins had poorer HRQOL (unstandardized coefficient = 4.92, 95% confidence interval 2.20-7.27). Cox regression showed that for each additional deficiency of a water-soluble vitamin intake, there was a 30% increase in risk for an event (95% confidence interval 1.03-1.75), controlling for demographic and clinical variables., Conclusion: Inadequate dietary consumption of water-soluble vitamins was associated with poor HRQOL and prognosis and in HF. Our findings highlight that clinicians should understand the importance of encouraging patients to consume water-soluble vitamin-rich foods, which may result in enhancing outcomes in HF.

A 57-year-old man, known with severe malnutrition, vitamin E deficiency and peripheral neuropathies, presented with vomiting and abdominal tenderness. There was a suspicion of ileus and small bowel obstruction. During the exploratory laparotomy a complete brown colored bowel without peristalsis was seen.

Progressive familial intrahepatic cholestasis (PFIC) is a rare disease of impaired bile acid excretion which can lead to nutritional deficiencies. Vitamin deficiencies during pregnancy can result in adverse maternal and fetal outcomes. A 20-year-old primiparous woman at 30 4/7 weeks with PFIC type 2 presented with worsening cholestasis, coagulopathy and fat-soluble vitamin deficiency. She developed visual deficits and was found to have severe vitamin A deficiency. Her coagulopathy and visual deficits improved following vitamin K and A supplementation, respectively. She delivered at 32 2/7 weeks following preterm labour. This case highlights several unique aspects in the care of pregnant women with liver disease. These patients are at risk for fat-soluble vitamin deficiencies which can result in significant coagulopathy and rarely, visual deficits due to vitamin A deficiency. Prompt treatment is necessary to prevent permanent sequelae., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Polycystic ovary syndrome (PCOS) is an increasingly common problem for women in the reproductive age throughout the entire world. A reduction diet with a low glycaemic index (GI) has proved to support the treatment of PCOS. The aim of the study was to analyse the influence of the diet on the level of vitamins soluble in water. The study included 55 women, 40 of which suffered from PCOS (identified by means of the Rotterdam Criteria) and 15 healthy women of the Caucasian race. The level of vitamins before and after the dietary intervention was measured. The diet was a reduction diet with a reduced glycaemic index (GI). Biochemical analyses were made on the basis of liquid chromatography-Infinity 1260 Binary liquid chromatography (LC) Agilent Technology. The level of vitamins in the serum was analysed together with the consumption before and after the dietary intervention. A higher level of vitamin C in the plasma was observed before and after the dietary intervention in the PCOS group in comparison to the control group despite the lower intake of this vitamin in the PCOS group. The remaining vitamins were at a comparable or lower level (B1, B3, B5, B6 and B12). After the dietary intervention, only B1 and B9 were at a clearly lower level (a trend of p = 0.093 and p = 0.085). A properly balanced reduction diet with reduced GI improves the supply of vitamins in women with PCOS. An additional recommendation should be the additional supplementation of B1, niacinamide and the combination of folates with inositol. The level of vitamin C in the plasma may not be a good marker of its supply in the PCOS group.

Objective: In 2019, an infection provoked by SARS-CoV-2 virus arose in Wuhan, China. Currently, there is still no definite and efficacious therapy for SARS-CoV-2 infection. Moreover, our understanding of the physiopathology of the infection, and risk elements for severity and mortality, is incomplete., Patients and Methods: One largely neglected element that could affect prognosis of SARS-CoV-2 infection is the vitamin status of population. The purpose of this review is to evaluate whether a vitamin insufficiency could provoke an augmented risk of SARS-CoV-2 infection or the appearance of major complications. In particular, we evaluated the presence of studies related to the state and effects of vitamin D, C, B, and A in subjects with SARS-CoV-2 disease., Results: Although, actually, the interest in a possible use for vitamin supplementation in SARS-CoV-2 patients is essentially based on indirect data, we tried to examine the evidence about a favorable effect of vitamin supplementation in the therapy of the infection and its complications., Conclusions: Supplements with vitamin A, B, C, D, and E could represent an inexpensive and sufficiently safe approach, and a useful therapeutic complement. However, solid clinical research data are expected to support such claim.

Idiopathic pulmonary fibrosis (IPF) is a chronic disease mainly associated with aging and, to date, its causes are still largely unknown. It has been shown that dietary habits can accelerate or delay the occurrence of aging-related diseases; however, their potential role in IPF development has been underestimated so far. The present review summarizes the evidence regarding the relationship between diet and IPF in humans, and in animal models of pulmonary fibrosis, in which we discuss the bioactivity of specific dietary food ingredients, including fatty acids, peptides, amino acids, carbohydrates, vitamins, minerals and phytochemicals. Interestingly, many animal studies reveal preventive and therapeutic effects of particular compounds. Furthermore, it has been recently suggested that the lung and gut microbiota could be involved in IPF, a relationship which may be linked to changes in immunological and inflammatory factors. Thus, all the evidence so far puts forward the idea that the gut-lung axis could be modulated by dietary factors, which in turn have an influence on IPF development. Overall, the data reviewed here support the notion of identifying food ingredients with potential benefits in IPF, with the ultimate aim of designing nutritional approaches as an adjuvant therapeutic strategy.

Recently, connections have been made between feeding and eating problems and autism spectrum disorder (ASD) and between autism pathophysiology and diet issues. These could explain some of the mechanisms which have not yet been discovered or are not sufficiently characterized. Moreover, there is an increased awareness for micronutrients in ASD due to the presence of gastrointestinal (GI) problems that can be related to feeding issues. For example, levels of vitamins B 1 , B 6 , B 12 , A and D are often reported to be low in ASD children. Thus, in the present mini review we focused on describing the impact of some vitamins deficiencies and their relevance in ASD patients., Competing Interests: The authors declare no conflict of interest.

In critical illness, homeostatic corrections representing the culmination of hundreds of millions of years of evolution, are modulated by the activated glucocorticoid receptor alpha (GRα) and are associated with an enormous bioenergetic and metabolic cost. Appreciation of how homeostatic corrections work and how they evolved provides a conceptual framework to understand the complex pathobiology of critical illness. Emerging literature place the activated GRα at the center of all phases of disease development and resolution, including activation and re-enforcement of innate immunity, downregulation of pro-inflammatory transcription factors, and restoration of anatomy and function. By the time critically ill patients necessitate vital organ support for survival, they have reached near exhaustion or exhaustion of neuroendocrine homeostatic compensation, cell bio-energetic and adaptation functions, and reserves of vital micronutrients. We review how critical illness-related corticosteroid insufficiency, mitochondrial dysfunction/damage, and hypovitaminosis collectively interact to accelerate an anti-homeostatic active process of natural selection. Importantly, the allostatic overload imposed by these homeostatic corrections impacts negatively on both acute and long-term morbidity and mortality. Since the bioenergetic and metabolic reserves to support homeostatic corrections are time-limited, early interventions should be directed at increasing GRα and mitochondria number and function. Present understanding of the activated GC-GRα's role in immunomodulation and disease resolution should be taken into account when re-evaluating how to administer glucocorticoid treatment and co-interventions to improve cellular responsiveness. The activated GRα interdependence with functional mitochondria and three vitamin reserves (B1, C, and D) provides a rationale for co-interventions that include prolonged glucocorticoid treatment in association with rapid correction of hypovitaminosis., (Copyright © 2020 Meduri and Chrousos.)

Megaloblastic anemia causes macrocytic anemia from ineffective red blood cell production and intramedullary hemolysis. The most common causes are folate (vitamin B 9 ) deficiency and cobalamin (vitamin B 12 ) deficiency. Megaloblastic anemia can be diagnosed based on characteristic morphologic and laboratory findings. However, other benign and neoplastic diseases need to be considered, particularly in severe cases. Therapy involves treating the underlying cause-eg, with vitamin supplementation in cases of deficiency, or with discontinuation of a suspected medication., (Copyright © 2020 The Cleveland Clinic Foundation. All Rights Reserved.)

Vitamins are indispensable nutrients for metabolism. Adequate vitamin intake plays vital role in physiological processes including embryonic development, cellular and immunity proliferation and differentiation, DNA synthesis and oxidative response. In contrast, insufficient vitamin levels usually lead to a large number of clinical manifestations including xerophthalmia, nyctalopia, hyperpigmentation, vitiligo, jaundice, megaloblastic anemia, glossitis, scurvy, stroke, cancer, coronary heart disease, Alzheimer's disease, multiple sclerosis and Parkinson's disease. In recent years, more and more researches have focused on the relationship between vitamin family and otorhinolaryngologic diseases. This review will summarize the current knowledge of vitamin family and vitamin-mediated regulating role in those related otorhinolaryngologic diseases., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2019. Published by Elsevier Ltd.)

Heart failure (HF) is a chronic condition with many imbalances, including nutritional issues. Next to sarcopenia and cachexia which are clinically evident, micronutrient deficiency is also present in HF. It is involved in HF pathophysiology and has prognostic implications. In general, most widely known micronutrients are depleted in HF, which is associated with symptoms and adverse outcomes. Nutritional intake is important but is not the only factor reducing the micronutrient availability for bodily processes, because absorption, distribution, and patient comorbidity may play a major role. In this context, interventional studies with parenteral micronutrient supplementation provide evidence that normalization of micronutrients is associated with improvement in physical performance and quality of life. Outcome studies are underway and should be reported in the following years.

Obesity and nutrients intake deficiencies may contribute to the clinical manifestations and inflammatory processes in systemic lupus erythematosus (SLE). The aim of this study was to assess the relationship between nutritional status and dietary intake with clinical variables in Mexican-mestizo SLE patients. A cross-sectional study was conducted in 130 female SLE patients, classified by the 1997 SLE American College of Rheumatology (ACR) criteria; the clinical activity was evaluated by the Mexican-Systemic Lupus Erythematosus-Disease Activity Index (Mex-SLEDAI); body mass index (BMI) by the World Health Organization (WHO) criteria; the energy calculation and nutritional intake were performed by Nutritionist Pro Diet software. SLE patients with excess weight (BMI > 25 kg/m 2 ) showed a higher score of clinical activity (Mex-SLEDAI = 2; p = 0.003), higher clinical activity prevalence (40.9%; p = 0.039) and a significant association for high clinical activity (odds ratio (OR) = 2.52; 95% confidence interval (CI) = 1.08-5.9; p = 0.033), in comparison with patients without excess weight (BMI < 25 kg/m 2 ). In particular, the excess weight increased the Mex-SLEDAI score (β coefficient = 1.82; R 2 = 0.05; p = 0.005). Also, the SLE patients presented a high prevalence (%) of deficient consumption (cut-off point: <67% of dietary adequacy) of vitamin E (100%), iodine (96%), omega 3 (93.44%), biotin (78%), vitamin K (73.33%), iron (67%), vitamin D (63.3%), potassium (59%), folic acid (56.67%), pantothenic acid (43.3%), vitamin A (41.67%) and zinc (32%). In conclusion, in SLE patients the excess weight was associated with increased clinical activity and to the presence of deficiencies in some essential nutrients ingested.

We investigate the long-term effect of very-low dose exposure to a mixture of six pesticides associated with hydrophilic vitamin deficiency on the neurobehavioral outcomes of rats. Two hundred Wistar rats were divided into four groups, two control groups, a vitamin sufficient control group and a vitamin deficiency control group and 2 test groups, a vitamin sufficient test group, and a vitamin deficiency group. The test groups were exposed for 9 months to a mixture of diquat, imazamox, imazethapyr, tepraloxydin, bentazone and acifluorfen in doses of 0.01xNOAEL (mg/kg bw/day). After 9 months of exposure, the behavior changes were evaluated by open field test and elevated plus maze test and the memory was assessed by passive avoidance test. Chronic vitamin deficiency decreased locomotor and special orientation activity and increased anxiety-like behavior in rats. Exposure to very low doses of a mixture of 6 pesticides caused central nervous effects, manifested as decreased locomotor activity, and increased anxiety levels. Vitamin deficiency and low dose chronic pesticides mixture exposure thus affected the central nervous system, especially long-term memory., (Copyright © 2019 Elsevier B.V. All rights reserved.)

This report describes the post-bariatric-surgery evolution of an obese patient who had low adherence to the diet and micronutrient supplementation. Four years after two bariatric surgeries, the patient was admitted due to transient loss of consciousness, slow thinking, anasarca, severe hypoalbuminemia, in addition to vitamin and mineral deficiencies. She had subcutaneous foot abscess but did not present fever. Received antibiotics, vitamins A, D, B12, thiamine, calcium, and parenteral nutrition. After hospitalization (twenty-eight days), there was a significant body weight reduction probably due to the disappearance of clinical anasarca. Parenteral nutrition was suspended after twenty-five days, and the oral diet was kept fractional. After hospitalization (weekly outpatient care), there was a gradual laboratory data improvement, which was now close to the reference values. Such outcome shows the need for specialized care in preventing and treating nutritional complications after bariatric surgeries as well as clinical manifestations of infection in previously undernourished patients.

Background: Various antiepileptic drugs can potentially cause psychiatric side effects in patients with epilepsy, but the precise mechanism of these actions remains unknown. In recent years, the common polymorphism C677T in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene has attracted attention for its role in the onset of psychiatric diseases. MTHFR and several vitamins (as cofactors) are crucial for remethylation of homocysteine via folate and homocysteine metabolism. We report a case of a Japanese patient who presented with reversible schizophrenia-like symptoms during antiepileptic drug therapy., Case Presentation: Our patient had frontal lobe epilepsy and had been treated with several antiepileptic drugs since the age of 13 years. He developed auditory hallucinations and multiple personalities at 17 years of age, several months after the initiation of phenytoin and phenobarbital, despite these antiepileptic drugs being used within the therapeutic ranges. Genetic analysis revealed that he was homozygous for the C677T polymorphism of MTHFR. Hyperhomocysteinemia, hypomethionemia, and multiple vitamin deficiencies, including folate, riboflavin, and pyridoxal, were identified at the age of 23 years. Vitamin supplementation and alteration of the antiepileptic drugs improved his psychotic symptoms. Multiple vitamin deficiencies with homozygous MTHFR C677T should be considered in patients presenting with schizophrenia-like symptoms during antiepileptic drug therapy., Conclusions: To the best of our knowledge, this is the first report of antiepileptic drug-induced psychosis associated with homozygous C677T and multiple vitamin deficiencies. Our findings will contribute to the elucidation of the pathogenesis of the psychiatric side effects of antiepileptic drugs and lead to improved medical management for patients with epilepsy.

Objective: The pathophysiology of atopic dermatitis (AD) involves a complex interplay between immune system dysfunction, genetics, and environmental factors. It is well known that nutritional status is essential to a proper functioning immune system, leading to a highly debated question regarding the role of dietary factors in the pathogenesis of AD. Food allergies and elimination diets have been broadly studied in atopy; however, less consideration has been given to how vitamins, minerals, and other micronutrients influence the risk for AD and severity of symptoms. This systematic review discusses evidence on how various micronutrients, including vitamins (C, E, and D) and trace minerals (zinc, selenium, iron, copper, magnesium, and strontium) are associated with AD, and how supplementation influence disease severity. Design: A systematic search was conducted to identify the role that oral micronutrients have on AD. The authors reviewed 49 studies herein. Results: While there are weak associations between vitamins C or E and AD, there is sufficient evidence to suggest that vitamin D supplementation provides benefit in AD patients. Deficiency of selenium and zinc may exacerbate AD. Current reports are not sufficient to confidently discern the role of other vitamins and trace minerals on AD. Conclusions: Though oral micronutrients may play a role in AD, the current literature is limited, and there is a need for more comprehensive randomized controlled trials (RCTs) to truly decipher the role between oral micronutrients and AD.

The review discusses thesteps of vitamin B12 metabolism and its role in maintaining of neurological functions. The term "vitamin B12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the peripherу cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as "holotranscobalamin"). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B12 - only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxyadenosylcobalamin (in mitochondria). The main causes of cobalamin deficiency are related to inadequate intake of animal products, autoimmune gastritis, pancreatic insufficiency, terminal ileum disease, syndrome of intestinal bacterial overgrowth. Relative deficiency may be seen in excessive binding of vitamin B12 to transcobalamin I. Cobalamin deficiency most significantly affects functions of blood, nervous system and inflammatory response. Anemia occurs in 13-15% of cases; macrocytosis is an early sign. The average size of neutrophils and monocytes is the most sensitive marker of megaloblastic hematopoiesis. The demands in vitamin B12 are particularly high in nervous tissue. Hypovitaminosis is accompanied by pathological lesions both in white and gray brain matter. Several types of neurological manifestations are described: subacute combined degeneration of spinal cord (funicular myelinosis), sensomotor polyneuropathy, optic nerve neuropathy, cognitive disorders. The whole range of neuropsychiatric disorders with vitamin B12 deficiency has not been studied well enough. Due to certain diagnostic difficulties they are often regarded as "cryptogenic", "reactive", "vascular» origin. Normal or decreased total plasma cobalamin level could not a reliable marker of vitamin deficiency. In difficult cases the content of holotranscobalamin, methylmalonic acid / homocysteine, and folate in the blood serum should be investigated besides carefully analysis of clinical manifestations.

The associations of multiple vitamin deficiencies on incident fractures were uncertain, the relationships between serum vitamin markers and incident bone fractures were investigated in Japanese postmenopausal women. The number of deficiencies was additively associated with incident fracture after adjustment for possible confounding factors including the treatment of osteoporosis., Introduction: To evaluate the associations of multiple vitamin deficiencies on incident fractures, the relationships between serum vitamin markers and incident bone fractures were investigated in Japanese postmenopausal women., Methods: This analysis used a subset of the ongoing cohort maintained by a primary care institution. Inclusion criteria of the present study were postmenopausal women aged ≥ 50 years, without vitamin supplementation and secondary osteoporosis. Baseline serum concentrations of 25-hydroxyvitamin D (25(OH)D), undercarboxylated osteocalcin (ucOC), and homocysteine (Hcy) were measured to assess vitamin D, vitamin K, and vitamin B, respectively. Since 25(OH) D positively relates to vitamin D, ucOC and Hcy negatively relate to vitamin K and vitamin B nutrients, respectively, the subjects with lower (25(OH)D) or higher (ucOC or Hcy) values than each median value was defined as subjects with the corresponding vitamin deficiency. Subjects were divided into four groups according to the number of deficiency: no deficiency, single deficiency, double deficiencies, and triple deficiencies. Relationships between the vitamin deficiencies and incident fractures were evaluated by Cox regression analysis., Results: A total of 889 subjects were included in this analysis; their mean and SD age was 68.3 ± 9.5 years, and the follow-up period was 6.3 ± 5.1 years. The numbers of subjects in the four groups were 139 (15.6%), 304 (34.2%), 316 (35.5%), and 130 (14.6%) for the groups with no, single, double, and triple deficiencies, respectively. Incident fractures were observed in 264 subjects (29.7%) during the observation period. The number of deficiencies was significantly associated with incident fracture (hazard ratio 1.25, 95% confidence interval 1.04-1.50, P = 0.018) after adjustment for possible confounding factors including the treatment of osteoporosis., Conclusion: Accumulation of vitamin deficiencies was related to incident fractures.

Background: Anaemia in pregnancy is a common medical condition managed by general practitioners (GPs) in Australia., Objective: The aim of this article is to raise awareness of anaemia that occurs in pregnancy, understand its increasing complexities with an expanding migrant population, identify at-risk groups and promote appropriate management., Discussion: With anaemia reportedly occurring in 25% of women in pregnancy and GPs managing the majority of preconception and early pregnancy care, it is important to have a sound understanding of the aetiology, risks and management options. While iron deficiency anaemia is most commonly seen, a more complex understanding in regard to other causes and haemoglobinopathy screening is required.

As microbiological diagnostic techniques improve and the frequency of nontuberculous mycobacterial pulmonary disease (NTM-PD) infection increases worldwide, NTM-PD is becoming increasingly important to clinicians and researchers. Vitamin activity has been associated with the host immune response in tuberculosis; however, such information is very limited in NTM-PD. We performed a case-control study in 150 patients with NTM-PD and 150 healthy controls to investigate serum vitamin status. We measured concentrations of vitamins A, D, and E along with homocysteine and methylmalonic acid (MMA) as indicators of vitamin B 12 deficiency, using high-performance liquid chromatography (HPLC) or HPLC-tandem mass spectrometry. The serum concentrations of vitamins A and E were significantly lower in patients with NTM-PD than in healthy controls (1.5 vs. 2.1 µmol/L, p < 0.01 for vitamin A; and 27.3 vs. 33.1 µmol/L, p < 0.01 for vitamin E). In contrast, the serum concentrations of vitamin D and homocysteine were not significantly different between the two groups. Vitamin A deficiency (< 1.05 µmol/L) was significantly more prevalent in patients with NTM-PD than in healthy controls ( p < 0.01) and was associated with an 11-fold increase in risk of NTM-PD. Multiple vitamin deficiencies were only observed in patients with NTM-PD (7.3% of all NTM-PD patients). Positive correlations were observed among vitamins (vitamins A and D; r = 0.200, p < 0.05; vitamins D and E, r = 0.238, p < 0.05; vitamins A and E, r = 0.352, p < 0.05). Serum vitamin status, demographic variables, and biochemical indicators were not associated with treatment outcomes. Vitamin A deficiency was strongly associated with patients with NTM-PD. Our study suggests that altered vitamin status is associated with mycobacterial disease. Future well-designed prospective studies with large patient cohorts addressing these issues are needed to clarify the significance of vitamins in NTM-PD.

Introduction: Among the 1.4 million blind children in the world, 300,000 live in Africa. The causes of blindness vary from one country to another. The purpose of our study was to report the causes of childhood blindness and visual impairment in children attending the only school for the blind in Mali (National Institute for the Blind in Mali, INAM)., Materials and Methods: All children attending the INAM were examined. Blindness was defined as visual acuity less than 3/60 (20/400 or 0.05). Visual impairment was moderate when the visual acuity was less than 6/18 (20/70 or 0.30), but greater than or equal to 6/60 (20/200 or 0.1), and severe when visual acuity was less than 6/60 (20/200 or 0.1), but greater than or equal to 3/60 (20/400 or 0.05)., Results: The study included a total of 104 children. The average age of our patients was 12 years with a M/F sex-ratio of 1.12. In all, 85.6 % of the children were blind and 14.4 % visually impaired. The main causes of blindness were corneal opacities (26 %), and whole globe lesions and conditions (19.2 %). Ametropia accounted for 60 % of visual impairment., Discussion: According to WHO, corneal and retinal damage are the leading cause of blindness (50.6 %) in children. In our series, corneal diseases were the leading cause, following by damage to the whole globe., Conclusion: The results of our study indicate that avoidable and treatable causes of childhood blindness are the leading causes of blindness of children at INAM.

Hospital mortality of severe sepsis and septic shock is still around 40 % according to recent studies. In accordance to the current sepsis definition, sepsis is a life-threatening organ dysfunction caused by a dysregulated response of the organism to infection. Septic shock is defined by vasopressor-dependent circulatory failure and lactic acidosis. Patients with sepsis and septic shock are often old and/or characterized by severe comorbidities, e. g. tumor or liver disease. These factors also predispose to malnutrition and hence to a corresponding deficiency of essential nutritional components e. g. vitamins. A number of recent studies and reviews have addressed the question whether deficiencies in certain vitamins may facilitate the transition from infection to septic shock. In addition, studies have investigated the effect of high-dose vitamin therapies on sepsis mortality and sepsis-associated organ dysfunctions. This article would like to summarize this current discussion with a focus on vitamin B 1 (thiamine), vitamin C and vitamin D., Competing Interests: Disclosure The authors report no conflicts of interest in this work., (© Georg Thieme Verlag KG Stuttgart · New York.)

Metabolic syndrome is the name given to a set of risk factors that increases the risk of cardiovascular disease and other health problems, such as diabetes and stroke. There are different cut-off points to establish the definition of metabolic syndrome according to various international organizations, although in all definitions are considered four main data related to: 1) obesity; 2) alteration of glucose metabolism; 3) alteration of lipid metabolism; and 4) hypertension. Strategies for the treatment of the metabolic syndrome include changes in lifestyle (diet and physical activity), along with pharmacological treatment in certain cases. There is little evidence of the effect of different micronutrients in this syndrome, although there are many investigations in this line.

Background: Nutritional deficiencies have been reported in bariatric surgery patients with inconsistent results. However, scarce data exist for Chinese patients. We aimed to assess nutritional deficiencies in Chinese patients undergoing Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG), and to identify predictors of postoperative nutritional status., Methods: A retrospective review of a prospectively collected database was conducted in the patients undergoing RYGB and SG in our hospital between June 2013 and January 2017. Anthropometric data and nutritional data were collected before surgery, at 6 and 12 months postoperatively., Results: This study enrolled 269 patients (120 RYGB, 149 SG). Nutritional deficiencies were common in Chinese bariatric candidates, with vitamin D deficiency the most serious (78.8%), followed by vitamin B1 (39.2%), vitamin B6 (28.0%), folate (26.8%), vitamin C (18.0%) albumin (13.4%), transferrin (11.6%), and phosphorus (11.5%). Despite postoperative routine multivitamin and calcium supplements, nutritional deficiencies were still obvious for RYGB and SG patients. The prevalence of hemoglobin and vitamin B12 deficiencies increased remarkably in the RYGB group; the levels of hemoglobin, globin, vitamin B12, and ferritin decreased significantly (P < 0.05). Preoperative hemoglobin, vitamin B12, and ferritin levels were independently associated with postoperative decrease, respectively. Deficiencies of vitamin D, vitamin B1, vitamin B6, vitamin C, and albumin before surgery were predictors for deficiencies 1 year after surgery, respectively., Conclusion: Nutritional deficiencies are common in Chinese bariatric surgery candidates. Similar deficiencies were also seen after RYGB and SG. Routine evaluation and related corrections of preoperative nutritional abnormity could contribute to postoperative nutrient balance.

Hair loss is a common condition that affects most people at some point in their lives. It can exist as an isolated problem or with other diseases and conditions. Androgenetic alopecia (AGA) and its association with the metabolic syndrome (MetS) have received increasing interest since 1972, when the first link between cardiovascular risk factors and hair loss was raised. We have reviewed studies concerning the relationship between alopecia and MetS. Many studies have investigated the relationship among AGA and MetS and its individual components, particularly in men, where a disproportionately large number of these studies supports this association. AGA has also been associated with other metabolic-related conditions, including coronary artery disease, polycystic ovary syndrome, and Cushing syndrome, as well as several nutritional deficiencies, all of which have led to many clinicians advocating for the screening of MetS and cardiovascular risk factors in patients who present with AGA., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The study's objective was to investigate the association between inadequate dietary consumption of micronutrients and indicators of general and abdominal obesity. Cross-sectional analysis of the second wave of the EpiFloripa Adults longitudinal study, including 1,222 individuals, aged 22-63 years and residing in Florianópolis, Santa Catarina State, Southern Brazil. Food consumption data was obtained from two 24-hour food recalls, and habitual consumption and prevalence rates of inadequate consumption of calcium, iron, zinc, and vitamins A, C, D, and E were estimated according to the Institute of Medicine and National Research Council guidelines. General obesity was defined based on the body mass index (BMI) values and abdominal obesity was based on waist circumference (WC) values. For most of the micronutrients investigated (calcium and vitamins A, C, D, and E), consumption levels were below the recommendations, with high prevalence of inadequate consumption in the sample as a whole. Only inadequate vitamin C intake was higher among obese individuals (general or abdominal). In addition, there was an inverse association between lower consumption of calcium and iron and higher BMI and WC, and between lower consumption of vitamins A and D and higher WC levels (β = -0.92cm; 95%CI: -1.76; -0.08 and β = -0.69 cm; 95%CI: -1.32; -0.06, respectively), especially in young adults. The study showed an inverse association between inadequate dietary consumption of micronutrients and general and abdominal obesity in a sample of adults in Southern Brazil.

Indiscriminate use of multivitamin/mineral supplements in the general population may be misguided, but patients with chronic Inflammatory Bowel Diseases (IBD) should be monitored and compensated for nutritional deficiencies. Mechanistic links between vitamin/mineral deficiencies and IBD pathology has been found for some micronutrients and normalizing their levels is clinically beneficial. Others, like vitamin A, although instinctively desirable, produced disappointing results. Restoring normal levels of the selected micronutrients requires elevated doses to compensate for defects in absorptive or signaling mechanisms. This article describes some aspects of vitamin and mineral deficiencies in IBD, and summarizes pros and cons of supplementation., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Purpose of Review: The purpose of this study is to discuss the role of dietary factors in the etiology and therapy of attention deficit/hyperactivity disorder (ADHD). Relevant literature published from January 2016 to January 2017 was included in this review., Recent Findings: Unhealthy prenatal diet may be associated with ADHD in the offspring through an increase in epigenetic changes. The few-foods diet may have some efficacy, but requires further investigation before firm conclusions can be drawn. The efficacy of the supplementation of polyunsaturated fatty acids in the therapy of ADHD is probably small and may be confined to patient subgroups. It is unclear whether vitamin deficiency plays a role in the etiology of ADHD., Summary: There is no clear evidence supporting a role of food or nutrient-based intervention strategies in the etiology and therapy of ADHD. The investigation of the inter-relationship between diet and other lifestyle interventions may be a promising approach.

Background: Vitamin deficiency is frequently associated with inflammatory bowel disease (IBD). Supplementation of vitamins could thus serve as an adjunctive therapy. The present meta-analysis reviews the deficiencies and alterations in serum fat-soluble vitamins (A, D, E, and K) reported in IBD patients., Materials and Methods: PubMed database search was performed to identify all primary studies up to January 2015 that evaluated the serum concentrations of fat-soluble vitamin levels in IBD patients compared with healthy individuals. We estimated pooled mean differences between groups and estimated their relations with some compounding variables (age, disease duration, C-reactive protein, albumin), using a meta-regression analysis., Results: Nineteen case-control studies met selection criteria. In patients with Crohn's disease (CD), vitamin A, D, E, K status was lower than in controls [D=212 μg/L.92; 95% confidence interval (CI), 95.36-330.48 μg/L, P=0.0002; D=6.97 nmol/L, 95% CI, 1.61-12.32 nmol/L, P=0.01; D=4.72 μmol/L, 95% CI, 1.60-7.84 μmol/L, P=0.003; D=1.46 ng/mL, 95% CI, 0.48-2.43 ng/mL, P=0.003, respectively]. Patients with ulcerative colitis had lower levels of vitamin A than controls (D=223.22 μg/L, 95% CI, 44.32-402.12 μg/L, P=0.01). Patients suffering from CD for a longer time had lower levels of vitamins A (95% CI=7.1-67.58 y, P=0.02) and K (95% CI, 0.09-0.71 y, P=0.02). Meta-regression analysis demonstrated statistically significant associations between the levels of inflammatory biomarkers: C-reactive protein (P=0.03, 95% CI, -9.74 to -0.6 mgl/L) and albumin (P=0.0003, 95% CI, 402.76-1361.98 g/dL), and vitamin A status in CD patients., Conclusion: Our meta-analysis shows that the levels of fat-soluble vitamins are generally lower in patients with inflammatory bowel diseases and their supplementation is undoubtedly indicated.