Vitamin deficiency, symptoms

Cobalt Meat, Uver, dairy foods Component of vitamin B12 Pernicious anemia (vitamin-deficiency symptom)... 

In addition to avoiding explicit vitamin deficiency symptoms (see below) or a general depression in production due to a subclinical deficiency, some vitamins are added to the diet at higher levels in order to (1) enhance the quality of the animal product, e.g. vitamin D for eggshell strength and vitamin E for prolonging the shelf... 

Table 6. Vitamin Functions, Clinical Deficiency Symptoms, and Potential Health Benefits...

Cobalt is one of twenty-seven known elements essential to humans (28) (see Mineral NUTRIENTS). It is an integral part of the cyanocobalamin [68-19-9] molecule, ie, vitamin B 2> only documented biochemically active cobalt component in humans (29,30) (see Vitamins, VITAMIN Vitamin B 2 is not synthesized by animals or higher plants, rather the primary source is bacterial flora in the digestive system of sheep and cattle (8). Except for humans, nonmminants do not appear to requite cobalt. Humans have between 2 and 5 mg of vitamin B22, and deficiency results in the development of pernicious anemia. The wasting disease in sheep and cattle is known as bush sickness in New Zealand, salt sickness in Florida, pine sickness in Scotland, and coast disease in AustraUa. These are essentially the same symptomatically, and are caused by cobalt deficiency. Symptoms include initial lack of appetite followed by scaliness of skin, lack of coordination, loss of flesh, pale mucous membranes, and retarded growth. The total laboratory synthesis of vitamin B 2 was completed in 65—70 steps over a period of eleven years (31). The complex stmcture was reported by Dorothy Crowfoot-Hodgkin in 1961 (32) for which she was awarded a Nobel prize in 1964. 

Alimentary biotin deficiency is rare. It may, however, occur in patients on long-term parenteral nutrition lacking biotin or in persons who frequently consume raw egg white. Raw egg white contains a biotin-binding glycoprotein, called avidin, which renders biotin biologically unavailable. Pharmacological doses of the vitamin (1-10 mg/d) are then used to treat deficiency symptoms. There are no reports of toxicity for daily oral doses up to 200 mg and daily intravenous doses of up to 20 mg [2]. 

Vitamins are organic nutrients with essential meta-bohc functions, generally required in small amounts in the diet because they cannot be synthesized by the body. The hpid-soluble vitamins (A, D, E, and K) are hydrophobic molecules requiring normal fat absorption for their efficient absorption and the avoidance of deficiency symptoms. 

As patients lose exocrine function of the pancreas, they have decreased ability to absorb lipids and protein ingested with normal dietary intake. Weight loss from nutritional malabsorption is a common symptom of chronic pancreatitis not often seen in acute pancreatitis. Fatty- or protein-containing stools are also common carbohydrate absorption is usually unaffected. Even though patients with chronic pancreatitis have decreased ability to absorb lipid from the gastrointestinal tract, there does not appear to be an increased incidence of fat-soluble vitamin deficiency in these patients.34... 

The chemistry, metabolism, and clinical importance of folic acid have been the subject of many excellent reviews (A7, Gil, H14, H20, Rl). Folic acid deficiency leads to a macrocytic anemia and leucopenia. These symptoms are due to inadequate synthesis of nucleic acid. The synthesis of purine bases and of thymine, required for nucleic acid synthesis, is impaired in folic acid deficiency. Detection of folic acid activity in biologic fluids and tissues is of the utmost importance it distinguishes between the various anemias, e.g., those due to vitamin Bi2 or folic acid deficiency. Because morphology of the abnormal red cell does not help in diagnosing vitamin deficiency, one must rely on assay methods for differential diagnosis. Treatment of pernicious anemia with folic acid has led to subacute combined degeneration of the spinal cord despite... 

The establishment of quantitative methods for the determination of vitamins in body fluids and tissues by microbiological assay techniques should stimulate the search for the significance of vitamins in disease, not only in nutritional deficiency, but in the much wider field of all metabolic disturbances. Functional vitamin deficiencies are produced by malabsorption, by inhibitors of the vitamin function through products of the body, and particularly through drugs and other toxic substances. Vitamin deficiencies may be relative deficiencies whenever an individual s metabolism is deranged so as to require enhanced quantities of a given vitamin to cure or to counteract certain symptoms as, e.g., in Darier s disease (keratosis follicularis) (P2a). 

Since only a few vitamins can be stored (A, D, E, Bi2), a lack of vitamins quickly leads to deficiency diseases. These often affect the skin, blood cells, and nervous system. The causes of vitamin deficiencies can be treated by improving nutrition and by administering vitamins in tablet form. An overdose of vitamins only leads to hypervita mi noses, with toxic symptoms, in the case of vitamins A and D. Normally, excess vitamins are rapidly excreted with the urine. 

The deficiency state scurvy is characterized by degenerative changes in the capillaries, bone, and connective tissues. Mild vitamin C deficiency symptoms may include faulty bone and tooth development, gingivitis, bleeding gums, and loosened teeth. 

The answer is D. Several vitamin deficiencies can cause anemia due to reduced DNA synthesis in the erythropoietic cells of the bone marrow, especially folic acid and vitamin Bj2 (cobalamin), which are particularly prevalent among elderly patients due to poor diet and reduced absorption. In addition, deficiencies of either folic acid or vitamin Bj2 could produce the megaloblastic anemia seen in this patient. However, the absence of neurologic symptoms, a hallmark of vitamin Bj2 deficiency, makes that diagnosis less likely than folic acid deficiency. 

Medical personnel who work in affluent areas are unlikely to see large numbers of people with vitamin deficiency diseases. However, certain groups of the population are particularly at risk, such as low-income families and chronically ill patients. The classic symptoms of any vitamin deficiency disease as observed in laboratory animals are often blurred in humans. The clinical picture is often complicated by deficiencies of other vitamins, minerals, calories, and protein and by infections and parasite infestations, which usually accompany longstanding malnutrition. Biochemical, physiological, and behavioral changes can occur in the marginal deficiency state without or before the appearance of more specific symptoms. Since the nonspecificity of these changes makes them difficult to detail, this section focuses on the symptoms associated with individual vitamin deficiency diseases. 

Pyridoxine vitamin Bf) deficiency symptoms are generally expressed as alterations in the skin, blood, and central nervous system. Symptoms include sensory neuritis, mental depression, and convulsions. Hypochromic, sideroblastic anemia also may result. Since pyridoxine is required for the conversion of tryptophan to diphos-phopyridine and triphosphopyridine nucleotides, pellagralike symptoms can occur with vitamin Bg deficiency. This deficiency is found most often in conjunction with other B complex deficiencies. 

Folic acid deficiency symptoms include megaloblastic anemia, glossitis, diarrhea, and weight loss. The requirement for this vitamin increases during pregnancy and lactation. 

L B. Supplement with vitamin A. Vitamin A deficiency symptoms include night blindness that can lead to corneal ulceration. This deficiency can occur in patients with impaired liver storage or fat malabsorption. Dairy products, such as milk, are a good source of vitamin A. (3-Carotene, a vitamin A precursor, is found in pigmented vegetables, such as carrots. When a deficiency is diagnosed, it is appropriate to treat the patient with a supplement rather than to rely on increased consumption of vitamin A-rich foods. A patient with pancreatic disease and malabsorption syndrome will need parenteral supplementation. 

Vitamin deficiency is seldom seen, and its symptoms of leg ulceration (cheilosis), skin symptoms, a purplish tongue, eye disturbances, and photophobia are vague. 

Vitamins are vital for normal metabolism in body. They vary in their chemical structure and are supplied in very small quantity in diet, because they are not synthesized in body or their rate of production is not sufficient for maintenance of health. Vitamin deficiency leads to development of deficiency symptoms. Different vitamin preparations are available for treatment and prophylaxis. Most of the vitamins are nontoxic but on chronic administration can cause toxicity especially vitamin A and D. 

Deficiency symptoms Rickets occurs in patients who are having deficiency of vitamin D. The bones are unusually soft and due to stress and strain of weight bearing produce characteristic deformities. 

Deficiency symptoms In vitamin E deficiency in experimental animals the manifestations are seen in several systems... 

Deficiency symptoms In severe vitamin B deficiency beriberi develops. 

Deficiency symptoms Deficiency of panthothenic acid is unlikely in man because of its widespread distribution in food, though it has been administered by mouth as a nutritional supplement as the calcium salt and usually in conjunction with other vitamins of the B group. 

Deficiency symptoms In vitamin C deficiency scurvy develops. It is characterized by ecchymosis, petechiae, swollen and bleeding gums, subperiosteal haemorrhage, bones are painful to touch, impaired wound healing, anaemia, loosening of teeth and gingivitis. 

Vitamin B12 deficiency normally results from indequate absorption rather than inadequate dietary intake. Pernicious anaemia is caused by vitamin B12 deficiency symptoms include anaemia, glossitis, fatigue and degeneration of the peripheral nervous system and hypersensitivity of the skin. The adult RDA and RNI for B12 are 2 and 1.5 figday- respectively. Unlike other vitamins, B12 is obtained exclusively from animal food sources, such as meat, fish, poultry, eggs, shellfish, milk, cheese and eggs. Vitamin B12 in these foods is protein-bound and released by the action of HC1 and pepsin in the stomach. 

Riboflavin deficiency is not associated with a major human disease, although it frequently accompanies other vitamin deficiencies. Deficiency symptoms include dermatitis, cheilosis (fissuring at the corners of the mouth), and glossitis (the tongue appearing smooth and purplish). 

The nutritional need for accessory food factors was first stated explicitly in 1905-1906, although the influence of diet in preventing or curing some diseases such as scurvy had long been known. The name vitamine was proposed in 1912, but the terminal e was dropped when it was realized that not all these compounds are nitrogenous bases. The vitamins serve as coenzymes in various metabolic processes, and the necessary quantities are usually supplied by an adequate diet or by synthesis by the intestinal flora. Vitamin deficiency can arise from a failure to absorb the compound from the gut. The symptoms of deficiency vary in different animal species, and not all the substances found necessary in other species have been shown to be essential for human nutrition. Vitamins are used for the prevention or cure of deficiency diseases and for some other pathological conditions,... 

WHO Task Force on Oral Contraceptives. Oral and injectable hormonal contraceptive and signs and symptoms of vitamin deficiency and goitre prevalence studies in five 186. centres in the developing and developed world. WHO... 

Observations on deficiency symptoms in the cardiovascular system were also made [29, 30]. In chicks, exudative diathesis, a condition in which plasma moves from the capillaries into surrounding, particularly subcutaneous, tissue, was studied and found to be associated with lipid peroxidation [31]. In cardiac muscle, a necrotizing myopathy was found in vitamin-E-deficient mice [32], rats [33], rabbits [34] and ruminants [35], Blood abnormalities, associated with increased susceptibility of erythrocytes to haemolysis, figure among reports of the effects of vitamin E deficiency [36, 37]. 

Deficiency symptoms in poultry include muscular incoordination, uric acid deposits in the ureters and kidneys and general unthriftiness. Hens receiving insufficient vitamin A produce fewer eggs and the eggs frequently do not hatch. Other deficiency signs in poultry include reduced feed intake, susceptibility to respiratory and other infections and, ultimately, death. 

Although, owing to the wide distribution of vitamin Bg in nature, clinical deficiency symptoms are seldom observed, there is little doubt that pyridoxine is essential in human nutrition. Pyridoxine is absorbed from the gastrointestinal tract and is converted to the active form pyri-doxal phosphate. Absorption is decreased in gastrointestinal diseases and also in subjects taking isoniazid (3). It is excreted in the urine as 4-pyridoxic acid (2). The metabolism of vitamin Bg in human beings has been investigated (56). 

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