Anemia vitamin

Naturally occurring compounds with carbon-metal bonds are very rare The best example of such an organometallic compound is coenzyme Bi2 which has a carbon-cobalt ct bond (Figure 14 4) Pernicious anemia results from a coenzyme B12 deficiency and can be treated by adding sources of cobalt to the diet One source of cobalt IS vitamin B12 a compound structurally related to but not identical with coen zyme B12... 

Derivatives of ubiquiaones are antioxidants for foodstuffs and vitamins (qv) (217,218). Ubichromenol phosphates show antiinflammatory activity (219). Chroman o1 compounds inhibit oxidation of fats and can be used ia treatment of macrocytic anemias (220). Monosulfate salts of 2,3-dimethoxy-5-methyl-6-substitutedhydroquiaone have been reported to be inhibitors of Hpid oxidation ia rats (221). Polymers based on chloranilic and bromanilic acid have been prepared and contain oxygenated quiaones (63), which are derived from 1,2,3,4-benzenetetrol (222). 

Fohc acid is a precursor of several important enzyme cofactors required for the synthesis of nucleic acids (qv) and the metaboHsm of certain amino acids. Fohc acid deficiency results in an inabiUty to produce deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and certain proteins (qv). Megaloblastic anemia is a common symptom of folate deficiency owing to rapid red blood cell turnover and the high metaboHc requirement of hematopoietic tissue. One of the clinical signs of acute folate deficiency includes a red and painhil tongue. Vitamin B 2 folate share a common metaboHc pathway, the methionine synthase reaction. Therefore a differential diagnosis is required to measure foHc acid deficiency because both foHc acid and vitamin B 2 deficiency cause... 

Fohc acid is safe, even at levels of daily oral supplementation up to 5—10 mg (97). Gastrointestinal upset and an altered sleep pattern have been reported at 15 mg/day (98). A high intake of foHc acid can mask the clinical signs of pernicious anemia which results from vitamin deficiency and recurrence of epilepsy in epileptics treated with dmgs with antifolate activity (99). The acute toxicity (LD q) is approximately 500 and 600 mg per kg body weight for rats and mice, respectively (100). 

In 1929, Castie (7) tied the work of Combe and Addison with that of Whipple, Miaot, and Murphy by ptoposiag that both an extrinsic factor and an intrinsic factor ate iavolved ia the coatrol of pernicious anemia. The extrinsic factor, from food, is vitamin 2- Th intrinsic factor is a specific B22-biading protein secreted by the stomach. This protein is requited for vitamin B 2 absorption. 

Parallel to the activities in the treatment of pernicious anemia were observations in the 1930s that most farm animals had a requirement for an unknown factor beyond the vitamins then known. The lack of this factor became apparent, eg, when chicks or pigs fed a diet with only vegetable protein evidenced slow growth rate and high mortahty. It became apparent that the requited factor, termed animal protein factor, was present in animal sources such as meat and tissue extracts, milk whey, and cow manure. Subsequent to its isolation, it was rapidly shown that vitamin B 2 is the same as animal protein factor. 

Deficiency. Macrocytic anemia, megaloblastic anemia, and neurological symptoms characterize vitamin B 2 deficiency. Alterations in hematopoiesis occur because of the high requirement for vitamin B 2 for normal DNA repHcation necessary to sustain the rapid turnover of the erythrocytes. Abnormal DNA repHcation secondary to vitamin B 2 deficiency produces a defect in the nuclear maturational process of committed hematopoietic stem cells. As a result, the erythrocytes are either morphologically abnormal or die during development. 

Neurological symptoms result from demyelination of the spinal cord and are potentially irreversible. The symptoms and signs characteristic of a vitamin B 2 deficiency include paresthesis of the hands and feet, decreased deep-tendon reflexes, unsteadiness, and potential psychiatric problems such as moodiness, hallucinations, delusions, and psychosis. Neuropsychiatric disorders sometimes develop independently of the anemia, particularly in elderly patients. Visual loss may develop as a result of optic atrophy. 

Smaller pool sizes with normal semm B 2 levels may be maintained with dietary intakes below 1 pg. However, more substantial pool sizes are considered advantageous as protection against the development of pernicious anemia, which may occur in advanced age achlorhydria becomes more common after age 60, resulting in compromised absorption of vitamin 2-... 

The symptoms of vitamin E deficiency in animals are numerous and vary from species to species (13). Although the deficiency of the vitamin can affect different tissue types such as reproductive, gastrointestinal, vascular, neural, hepatic, and optic in a variety of species such as pigs, rats, mice, dogs, cats, chickens, turkeys, monkeys, and sheep, it is generally found that necrotizing myopathy is relatively common to most species. In humans, vitamin E deficiency can result from poor fat absorption in adults and children. Infants, especially those with low birth weights, typically have a vitamin E deficiency which can easily be corrected by supplements. This deficiency can lead to symptoms such as hemolytic anemia, reduction in red blood cell lifetimes, retinopathy, and neuromuscular disorders. 

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. 

The nutritional requirement for vitamin Bjg is low. Adult humans require only about 3 micrograms per day, an amount easily acquired with normal eating habits. However, because plants do not synthesize vitamin Bjg, pernicious anemia symptoms are sometimes observed in strict vegetarians. 

Macrocytic or magaloblastic anemia is caused by disturbances of DNA synthesis. It occurs, for example, in both folic acid and vitamin B12 deficiencies. Hematopoesis is slowed down due to reduced DNA synthesis and a reduced number of abnormally large (macrocytic) and hemaglobin-rich (hyperchromic) erythrocytes is released. 

It is recommended that women of childbearing age take 400 pg/d synthetic folic acid as a supplement in order to reduce the risk of neural tube defects of the embryo when they later become pregnant (periconcep-tional folic acid supplementation) [2]. When supplementing folic acid, it should be considered that this vitamin can mask the simultaneous presence of vitamin B12 deficiency. The typical symptom of vitamin B12 deficiency, megaloblastic (= macrocytic) anemia, will be reduced by high doses of folic acid, yet the nervous system will - in the long run - be irreversibly damaged (= funicular myelitis) when vitamin B12 is not provided as well. 

As the above mentioned studies with high supplementation dosages exemplarily show, there is no known toxicity for phylloquinone (vitamin Kl), although allergic reactions are possible. This is NOT true for menadione (vitamin K3) that can interfere with glutathione, a natural antioxidant, resulting in oxidative stress and cell membrane damage. Injections of menadione in infants led to jaundice and hemolytic anemia and therefore should not be used for the treatment of vitamin K deficiency. 

Pernicious anemia Anemia resulting from lack of secretions by the gastric mucosa of the intrinsic fador essential to the formation of RBCS and the absorption of vitamin B ... 

Vitamin B12 is essential to growth, cell reproduction, the manufacture of myelin (which surrounds some nerve fibers), and blood cell manufacture. The intrinsic factor, which is produced by cells in the stomach, is necessary for the absorption of vitamin B12 in the intestine A deficiency of the intrinsic factor results in abnormal formation of erythrocytes because of the body s failure to absorb vitamin B12, a necessary component for blood cell formation. The resulting anemia is a type of megaloblastic anemia called pernicious anemia. 

Vitamin B12 is also used to perform the Schilling test, which is used to diagnose pernicious anemia. 

Pernicious anemia must be diagnosed and treated as soon as possbte because vitamin B12 deficiency that is allowed to progress for more than 3 months may result in degenerative lesions of the spinal cord. 

VITAMIN S12. Fhtients with pernicious anemia are treated with vitamin B12 by tiie parenteral route (IM) weekly stabilized. The parenteral route is used because tiie vitamin is ineffective orally due to the absence of tiie intrinsic factor in tiie stomach, which is necessary for utilization of vitamin B12. After stabilization, maintenance (usually monthly) injections are necessary for life... 

When teaching a patient about the use of vitamin B12 for pernicious anemia, the nurse would include which of the following statements ... 

A person with pernicious anemia lacks intrinsic factor, a compound required for the absorption of vitamin B12 and its storage in the liver. The diagnosis is confirmed... 

Anemias, reductions in the number of red blood cells or of hemoglobin in the blood, can reflect impaired synthesis of hemoglobin (eg, in iron deficiency Chapter 51) or impaired production of erythrocytes (eg, in folic acid or vitamin Bjj deficiency Chapter 45). Diagnosis of anemias begins with spectroscopic measurement of blood hemoglobin levels. 

Inorganic iron is absorbed only in the (reduced) state, and for that reason the presence of reducing agents will enhance absorption. The most effective compound is vitamin C, and while intakes of 40-60 mg of vitamin C per day are more than adequate to meet requirements, an intake of 25-50 mg per meal will enhance iron absorption, especially when iron salts are used to treat iron deficiency anemia. Ethanol and fructose also enhance iron absorption. Heme iron from meat is absorbed separately and is considerably more available than inorganic iron. However, the absorption of both inorganic and heme iron is impaired by calcium—a glass of milk with a meal significantly reduces availabiUty. 

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