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Pediatrics in Review Aug 2012• Based on strong research evidence, all infants should receive 400 IU/day of vitamin D beginning in the first few days of age to prevent vitamin D deficiency and... (Review)
Review
• Based on strong research evidence, all infants should receive 400 IU/day of vitamin D beginning in the first few days of age to prevent vitamin D deficiency and rickets. • Based on strong research evidence, children and adolescents age >1 year may require as much as 600IU/day of vitamin D. • Based on strong research evidence, all newborns should receive 1 mg of vitamin K at birth to prevent vitamin K deficiency bleeding. • Based on strong research evidence, preconceptional and pregnant women should be supplemented with folate to decrease the likelihood of neural tube defects.
Topics: Adolescent; Avitaminosis; Child; Child, Preschool; Dietary Supplements; Female; Humans; Infant; Infant, Newborn; Perinatal Care; Pregnancy; Prenatal Care; Prenatal Exposure Delayed Effects; Prenatal Nutritional Physiological Phenomena; Risk Factors; Vitamins
PubMed: 22855926
DOI: 10.1542/pir.33-8-339 -
The Veterinary Clinics of North... Mar 1991Deficiencies of vitamins A, D, K, E and thiamin can cause severe limitations in beef production. In particular, vitamin A and E can be common causes of lost profit,... (Review)
Review
Deficiencies of vitamins A, D, K, E and thiamin can cause severe limitations in beef production. In particular, vitamin A and E can be common causes of lost profit, secondary to limitations of reproductive and growth potential. Prolonged dry periods will reduce available A and E in pasture forage, as can ensiling and prolonged storage of harvested feedstuffs. Polioencephalomalacia is a thiamin responsive disorder, associated with high concentrate feeding and lush pastures. Antimetabolites, such as amprolium, will cause thiamine deficiency when fed in excess. Recent information has shown improved performance with supplemental beta carotene and niacin. The positive responses in reproductive performance, noted with cattle fed supplemental beta carotene, was independent of vitamin A. Supplementation of vitamins above National Research Council recommendations can be justified. However, proper evaluation of feed and animal status, and documentation of a response to supplementation is necessary before diagnosing deficiencies of specific nutrients.
Topics: Animals; Avitaminosis; Cattle; Cattle Diseases; Niacin; Thiamine Deficiency; Vitamin A Deficiency; Vitamin D Deficiency; Vitamin E Deficiency; Vitamin K Deficiency
PubMed: 2049667
DOI: 10.1016/s0749-0720(15)30817-3 -
Salud Publica de Mexico 1995We carried out a review of the studies related to vitamin deficiencies in the Mexican population published since 1950. Forty four studies were published from which we... (Comparative Study)
Comparative Study Review
We carried out a review of the studies related to vitamin deficiencies in the Mexican population published since 1950. Forty four studies were published from which we can conclude that: a) dietary intake data suggest that ascorbic acid, riboflavin and retinol intake are deficient: reported intakes were 40-70%, 35-64% and 20-72% of the recommended daily amounts respectively; niacin intake was also deficient in some studies; b) about 10% of Mexican children in rural areas had deficient values of plasma retinol (< 100 ng/ml) and about 25 to 30% had low values (100-200 ng/ml); this prevalence is reduced in children with a higher socioeconomic level; c) some studies were found that show the existence of marginal deficiencies of vitamin E, riboflavin and vitamin B12 in apparently healthy populations. Further studies are required to identify the magnitude of these and perhaps other vitamin deficiencies and their potential effects on the health and function of the Mexican population.
Topics: Adult; Age Factors; Ascorbic Acid Deficiency; Avitaminosis; Child; Child, Preschool; Female; Folic Acid Deficiency; Humans; Infant; Infant, Newborn; Male; Mexico; Niacin; Pregnancy; Riboflavin Deficiency; Rural Population; Thiamine Deficiency; Trace Elements; Urban Population; Vitamin A Deficiency; Vitamin B 12 Deficiency; Vitamin B 6 Deficiency; Vitamin E Deficiency
PubMed: 8600562
DOI: No ID Found -
Pediatric Allergy and Immunology :... Oct 2020Nutritional deficiencies are seen in patients with food allergy. Low vitamin D levels have been found in patients with atopic conditions. Eosinophilic esophagitis (EoE)...
BACKGROUND
Nutritional deficiencies are seen in patients with food allergy. Low vitamin D levels have been found in patients with atopic conditions. Eosinophilic esophagitis (EoE) is a chronic immune antigen-mediated disease found to be highly associated in patients with atopic disease and treated with dietary elimination with recommendations to utilize a dietician to prevent nutritional deficiencies. Nonetheless, the relationship between EoE and vitamin deficiency remains unclear. We aimed to systematically review the evidence to support a possible association between vitamin deficiency and eosinophilic esophagitis.
METHODS
Electronic searches were performed with keywords relating to EoE and vitamins among pediatric patients in MEDLINE, EMBASE, and The Cochrane Library. Summary estimates were calculated. Citations were reviewed against pre-defined criteria. (Inclusion: human subjects, aged 0-18, with eosinophilic esophagitis. Exclusion: adults over 18 years, non-English papers).
RESULTS
The search yielded 1707 studies. Five of these studies with a total of 137 pediatric patients were included in the systematic review. Outcome measures were assessed at different points in EoE treatment across studies. The single common outcome measure across all included studies was vitamin D. Reported prevalence of low vitamin D varied in these studies (0%-52%). Vitamin D levels of children with EoE both pre- and post-intervention were low.
CONCLUSIONS
There is limited published literature on vitamin deficiencies associated with EoE both pre- and post-intervention. The limited data on vitamin D suggest that insufficiency or deficiency may be present in these patients, but it remains unclear whether deficiency is caused by diet. More prospective, well-defined studies, in addition to routine reporting on dietary intake and nutritional status, are needed to make any conclusions or recommendations for screening.
Topics: Adolescent; Avitaminosis; Child; Child, Preschool; Diet; Eosinophilic Esophagitis; Female; Food Hypersensitivity; Humans; Infant; Infant, Newborn; Male; Nutritional Status; Prevalence; Prospective Studies; Vitamin D; Vitamin D Deficiency
PubMed: 32474949
DOI: 10.1111/pai.13297 -
Pharmazie in Unserer Zeit 2009
Review
Topics: Ascorbic Acid; Avitaminosis; Beriberi; History, 17th Century; History, 18th Century; History, 19th Century; History, 20th Century; Humans; Pellagra; Rickets; Scurvy; Vitamins
PubMed: 19248016
DOI: 10.1002/pauz.200800301 -
Lancet (London, England) Jul 2010
Topics: Adolescent; Dietary Supplements; Erythrocytes; Female; Folic Acid Deficiency; Food Preferences; Humans; Hyperhomocysteinemia; Kidney Cortex Necrosis; Thrombosis; Transcobalamins; Vitamin B 12 Deficiency
PubMed: 20638559
DOI: 10.1016/S0140-6736(10)61102-6 -
Survey of Ophthalmology 1979Vitamin deficiency states are important in the genesis of many ocular disorders. Deficiencies may be due to poor dietary intake, or to alterations in metabolism produced... (Review)
Review
Vitamin deficiency states are important in the genesis of many ocular disorders. Deficiencies may be due to poor dietary intake, or to alterations in metabolism produced by some commonly prescribed medications or by certain diseases. Furthermore, some vitamins may exert important pharmacologic effects on the normal eye. The ocular effects of deficiencies and excesses of specific vitamins, and the therapeutic uses of each vitamin, are reviewed.
Topics: Animals; Ascorbic Acid Deficiency; Avitaminosis; Child; Child, Preschool; Eye Diseases; Female; Folic Acid Deficiency; Humans; Infant; Infant, Newborn; Nicotinic Acids; Optic Nerve Diseases; Pregnancy; Riboflavin Deficiency; Thiamine Deficiency; Vitamin A Deficiency; Vitamin B 12 Deficiency; Vitamin B 6 Deficiency; Vitamin B Deficiency; Vitamin D Deficiency; Vitamin E Deficiency; Vitamin K Deficiency; Vitamins
PubMed: 396681
DOI: 10.1016/0039-6257(79)90021-3 -
Handbook of Clinical Neurology 2010This historical review addresses major neurological disorders associated with deficiencies of water-soluble B vitamins: beriberi, Wernicke-Korsakoff syndrome, pellagra,... (Review)
Review
This historical review addresses major neurological disorders associated with deficiencies of water-soluble B vitamins: beriberi, Wernicke-Korsakoff syndrome, pellagra, neural tube defects, and subacute combined degeneration of the spinal cord. Beriberi: Beriberi was known for millennia in Asia, but was not described by a European until the 17th century when Brontius in the Dutch East Indies reported the progressive sensorimotor polyneuropathy. The prevalence of beriberi increased greatly in Asia with a change in the milling process for rice in the late 19th century. In the 1880s, Takaki demonstrated the benefits of dietary modification in sailors, and later instituted dietary reforms in the Japanese Navy, which largely eradicated beriberi from the Japanese Navy by 1887. In 1889 Eijkman in Java serendipitously identified dietary factors as a major contributor to "chicken polyneuritis," which he took to be an animal model for beriberi; the polyneuritis could be cured or prevented by feeding the chickens either unpolished rice or rice polishings. By 1901, Grijns, while continuing studies of beriberi in Java, suggested a dietary deficiency explanation for beriberi after systematically eliminating deficiencies of known dietary components and excluding a toxic effect. Wernicke-Korsakoff syndrome: In the late 1870s, Wernicke identified a clinicopathological condition with ophthalmoparesis, nystagmus, ataxia, and encephalopathy, associated with punctate hemorrhages symmetrically arranged in the grey matter around the third and fourth ventricles and the aqueduct of Sylvius. In the late 1880s, Korsakoff described a spectrum of cognitive disorders, including a confabulatory amnestic state following an agitated delirium, occurring in conjunction with peripheral polyneuropathy. Beginning around 1900, investigators recognized the close relationship between Korsakoff's psychosis, delirium tremens, and Wernicke's encephalopathy, but not until several decades later were Wernicke's encephalopathy, Korsakoff's psychosis, and beriberi all linked to the deficiency of a specific dietary factor, i.e. thiamin. Thiamin: Thiamin was crystallized from rice polishings by Jansen and Donath in 1926, and synthesized by Williams and Cline in 1936. In the late 1930s and early 1940s, characteristic pathological changes of Wernicke-Korsakoff syndrome were produced in animal models, the biochemical roles of thiamin in intermediary carbohydrate metabolism were elaborated by Peters and others, and the therapeutic benefits of thiamin for Wernicke-Korsakoff syndrome and beriberi were demonstrated. By the 1950s synthetic forms of the vitamin were produced cheaply, allowing both therapeutic administration and prevention with food enrichment. Pellagra and niacin: Pellagra was unknown prior to the introduction of maize into Europe from the New World. In the 18th century, Casàl and Frapolli described the clinical features of pellagra in Europe, and linked it with poverty and subsistence on nutritionally marginal corn-based diets. In the United States, pellagra became epidemic among poor Southerners in the early 20th century, in part because of economically-driven reliance on monotonous, nutritionally inadequate diets, combined with new manufacturing methods that removed vitamins from processed grain. From 1914-1929, Goldberger completed well-designed epidemiologic investigations, tested theories with human experiments, and utilized an animal model ("black tongue" in dogs) - all strongly supporting a dietary deficiency explanation for pellagra over prevailing toxic and infectious theories. Initial prevention and treatment approaches proved inadequate because of complex social issues linked to poverty, even after Goldberger and colleagues established that dried brewer's yeast could cure or prevent pellagra less expensively than dietary modification. During the depression, the collapse of cotton as an economically viable crop facilitated crop diversification, which contributed to an abrupt decline in pellagra mortality in the early 1930s. In 1937 Elvehjem isolated the P-P (pellagra preventive) factor, identified it as nicotinic acid (niacin), and demonstrated that nicotinic acid and nicotinic acid amide cure black tongue in dogs. Although clinical trials soon confirmed dramatic therapeutic effects in individual people, therapeutic administration of niacin had relatively little impact on population-level morbidity and mortality. Vitamin fortification of foodstuffs during World War II ultimately eradicated endemic pellagra in the United States. In the 1940s and 1950s, with expanded biochemical knowledge, pellagra was reformulated as a deficiency disease due to inadequate niacin and its amino acid precursor tryptophan. Neural tube defects and folate: Folate deficiency was initially recognized clinically as a macrocytic anemia in the 1920s, and only clearly separated from pernicious anemia by the mid-20th century. When folic acid was isolated and synthesized in the 1940s, it was shown to correct the macrocytic anemia associated with pernicious anemia, while the neurological manifestations progressed. In the 1950s and 1960s, the biochemical role of folates in transferring single carbon units was elucidated. Beginning in the 1960s, folate deficiency was increasingly recognized as the major cause of preventable neural tube defects. In the early 1990s well-designed randomized trials established that folate supplementation could prevent neural tube defects. Trial data, collectively indicating that periconceptual folate administration reduces both the occurrence and recurrence risks of neural tube defects by at least 70%, helped establish governmental recommendations concerning folic acid intake and health policy concerning vitamin fortification of foodstuffs. When dietary modification and supplementation strategies proved inadequate, folic acid food fortification was legally mandated in the US in the late 1990s, which significantly improved population folate status and produced an abrupt decline (20%-27%) in the prevalence of neural tube defects at birth. Recent studies have established genetic predispositions for neural tube defects, including both infant and maternal gene polymorphisms for enzymes involved in folate-dependent homocysteine metabolism, which help explain how the genotype of the mother, the genotype of the unborn child, and environmental factors (e.g. folate intake) can all impact on the risk of neural tube defects. Subacute combined degeneration and B(12) deficiency: Pernicious anemia was recognized clinically in the mid-19th century by Addison, but the most important neurological manifestation - subacute combined degeneration of the spinal cord - was not recognized clinically and linked with pernicious anemia until the end of the 19th century, particularly by Lichtheim, Putnam, and Dana. At the beginning of the 20th century, pernicious anemia and the associated subacute combined degeneration of the spinal cord were considered, by many investigators, to result from infectious or toxic causes. During the first quarter of the 20th century, various therapies were employed, but, with the possible exception of transfusion, were largely ineffective. In the 1920s, Minot and Murphy showed that large quantities of ingested liver could be used to effectively treat pernicious anemia, and specifically could improve or prevent progression of neurological manifestations, and could extend life expectancy beyond 2 years. Beginning in the late 1920s, Castle demonstrated that a substance elaborated by the gastric mucosa ("intrinsic factor") was essential for the absorption of a dietary factor ("extrinsic factor," later shown to be vitamin B(12)) needed to prevent pernicious anemia. Over two decades, from the late 1920s until the late 1940s, increasingly potent liver extracts were manufactured that could be given either intramuscularly or intravenously. In 1947, vitamin B(12) was isolated by Folkers and colleagues, and nearly simultaneously by Smith. Shortly thereafter the therapeutic efficacy of vitamin B(12) on subacute combined degeneration was demonstrated by West and Reisner and others. By 1955, Hodgkin determined the molecular structure of cyanocobalamin using computer-assisted x-ray crystallography, allowing complete chemical synthesis of vitamin B(12) in 1960 by an international consortium. Beginning in the late 1950s, the absorption and biochemistry of vitamin B(12) were elaborated, and several lines of evidence converged to support an autoimmune basis for pernicious anemia.
Topics: Animals; Avitaminosis; History, 16th Century; History, 17th Century; History, 18th Century; History, 19th Century; History, 20th Century; Humans; Nervous System Diseases; Vitamin B Complex
PubMed: 19892133
DOI: 10.1016/S0072-9752(08)02130-1 -
Annales de Medecine Interne 1994Eight patients with vitamin deficiency pancytopenia were admitted, within a year, in a department of internal medicine. Folic acid and vitamin B12 metabolism and the...
Eight patients with vitamin deficiency pancytopenia were admitted, within a year, in a department of internal medicine. Folic acid and vitamin B12 metabolism and the clinical and haematological symptoms are discussed. These vitamin deficiencies are frequent in underdeveloped countries and are responsible of megaloblastic anaemia. Such deficiencies may also influence the granulocyte and platelet lines and may be mistaken for leukaemia. A therapeutic test may be undertaken, giving rapid diagnosis and avoiding high mortality.
Topics: Adult; Blood Cell Count; Bone Marrow Examination; Developing Countries; Female; Folic Acid Deficiency; Humans; Male; Middle Aged; Pancytopenia; Time Factors; Vitamin B 12; Vitamin B 12 Deficiency
PubMed: 8092628
DOI: No ID Found -
Cellular and Molecular Biology... Jul 2022Ulcerative colitis (UC) is a chronic inflammatory disease. Studies in China and foreign countries have shown that vitamins have anti-inflammation and immunoregulation...
Correlations of Inflammatory Cytokines in the Intestinal Mucosa, Serum Inflammation, Oxidative Stresses and Immune Changes with Vitamin Deficiency in Ulcerative Colitis Patients.
Ulcerative colitis (UC) is a chronic inflammatory disease. Studies in China and foreign countries have shown that vitamins have anti-inflammation and immunoregulation functions in patients with UC, but the specific mechanism is not yet clear. In this study, the levels of inflammatory cytokines in the intestinal mucosa, serum inflammatory indexes, oxidative stress indexes and immune-related indexes were detected, and their correlations with vitamin deficiency and clinical significance were discussed. Enzyme-linked immunosorbent assay (ELISA) was adopted to detect the serum level of 25-hydroxyvitamin D3, immunohistochemistry was applied to examine the expression of inflammatory cytokines in the intestinal mucosa, serum inflammatory indexes, oxidative stress indexes and immune-related indexes were measured, and their correlations were analyzed. Inflammatory and oxidative stress indexes in the UC group were notably higher than in the control group. The Vitamin deficiency group had more inflammatory cytokines than the normal vitamin group. Oxidative stress indexes such as superoxide dismutase (SOD) and malondialdehyde (MDA) in the vitamin deficiency group were significantly different from those in the normal vitamin group, but no difference was found in myeloperoxidase (MPO). Immune-related indexes, complement 3 (C3) and interferon-gamma (IFN-γ), in the normal vitamin group were higher than those in the vitamin deficiency group. Besides, interleukin-4 (IL-4) (r=-0.37, p=0.04) and IL-1β (r=-0.31, p=0.04) had significant correlations with vitamins. Vitamins in patients with UC have significant correlations with inflammatory responses in vivo, which can be used to predict inflammatory responses in vivo and have strong clinical significance. Vitamins are also related to oxidative stresses to some extent but have little effect on immune-related indexes.
Topics: Humans; Cytokines; Colitis, Ulcerative; Intestinal Mucosa; Oxidative Stress; Inflammation; Avitaminosis; Vitamins
PubMed: 36495511
DOI: 10.14715/cmb/2022.68.7.17