Anemia riboflavin deficiency

Riboflavin deficiency is associated with hypochromic anemia as a result of secondary iron deficiency. The absorption of iron is impaired in riboflavin-deficient animals, with a greater proportion of a test dose retained in the intestinal mucosal cells bound to ferritin, and hence lost in the feces, rather than being absorbed. The mobilization of iron bound to ferritin, in either intestinal mucosal cells or the liver, for transfer to transferrin, requires oxidation of Fe + to Fe +, areaction catalyzed by NAD-riboflavinphosphateoxidoreductase (Powers et al., 1991 Powers, 1995 Williams et al., 1995). 

In addition to the role of flavoproteins in iron metabolism, it is possible that the anemia associated with riboflavin deficiency is a consequence of the impairment of vitamin Be metabolism in riboflavin deficiency. Pyridoxine oxidase is a flavoprotein and, like glutathione reductase, is very sensitive to riboflavin depletion (McCormick, 1989). Vitamin Be deficiency can result in hypochromic anemia as a result of impaired porphyrin synthesis. Although riboflavin depletion decreases the oxidation of dietary vitamin Be to pyridoxal (Section 9.2), it is not clear to what extent there is secondary vitamin Be deficiency in riboflavin deficiency This is partly because vitamin Be nutritional status is commonly... 

Pure red cell aplasia that responded to the administration of riboflavin was reported in patients with protein depletion and complicating infections. Nutritionists induced riboflavin deficiency in human beings and demonstrated that a hypoproliferative anemia resulted within a month. The spontaneous appearance in human beings of red cell aplasia due to riboflavin deficiency undoubtedly is rare, if it occurs at all. It has been described in combination with infection and protein deficiency, both of which are capable of producing a hypoproliferative anemia. However, it seems reasonable to include riboflavin in the nutritional management of patients with gross, generalized malnutrition. 

Giroud and co-workers found that abortion was frequent in riboflavin deficiency and that monsters often were born (Giroud ). Lepkovsky et had previously showed that riboflavin deficiency in the chick embryo produced a degeneration of the mesonephros and the development of edema and anemia. 

Riboflavin enhances the hematological response to iron, and deficiency may account for at least some of the anemia seen in human populations. Unlike iron-deficiency anemia, the anemia of riboflavin deficiency is reported to be normocytic and normochromic. 

The water-soluble vitamins comprise the B complex and vitamin C and function as enzyme cofactors. Fofic acid acts as a carrier of one-carbon units. Deficiency of a single vitamin of the B complex is rare, since poor diets are most often associated with multiple deficiency states. Nevertheless, specific syndromes are characteristic of deficiencies of individual vitamins, eg, beriberi (thiamin) cheilosis, glossitis, seborrhea (riboflavin) pellagra (niacin) peripheral neuritis (pyridoxine) megaloblastic anemia, methyhnalonic aciduria, and pernicious anemia (vitamin Bjj) and megaloblastic anemia (folic acid). Vitamin C deficiency leads to scurvy. 

Hematopoiesis also requires an adequate supply of minerals e.g., iron, cobalt, and copper) and vitamins ie.g., folic acid, vitamin pyiidoxine, ascorbic acid, and riboflavin), and deficiencies generally result in characteristic anemias, or, less frequently, a general failure of hematopoiesis. Therapeutic correction of a specific deficiency state depends on the accurate diagnosis of the anemic state and knowledge about the correct dose, the use of these agents in various combinations, and the expected response. 

Deficiency conditions Thiamine sensory disturbances, retarded growth, fatigue, anorexia Riboflavin visual defects such as blurred vision and photophobia, cheilosis, rash on nose numbness of extremities Niacin or nicotinic acid retarded growth, peiiagra, headache, memory loss, anorexia, insomnia Pyridoxine neuritis, convulsions, dermatitis, anemia, lymphopenia... 

The enrichment of salt with iodine, the fortification of milk with vitamin D, and the start of the thiamin, riboflavin, niacin, and iron, grain enrichment program in 1941, have played a significant role in the practical elimination of the following deficiency diseases simple goiter, rickets, beriberi, ariboflavi-nosis, pellagra and simple iron-deficiency anemia. The average American receives approximately 40% of his thiamin, 25% of his iron, 20% of his niacin and 15% of his riboflavin from enriched foods. 

Other nutrients and their deficiencies that can impact iron status, utilization, or anemia include vitamin A, folate, vitamin B12, riboflavin, and ascorbic acid (vitamin C). Improving iron status can also increase the utilization of iodine and vitamin A from supplements. On the other hand, it is increasingly recognized that simultaneous provision of iron and zinc in supplements may decrease the benefit of one or both of these nutrients. These complex micronutrient interactions and their implications for nutritional interventions are incompletely imderstood but have significant implications for population-based supplementation strategies. 

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