An important interaction of riboflavin with iron economy has been suspected for many years, partly because iron-deficient animals failed to respond readily to iron supplements if they were also ribo-flavin deficient, and also because the redox system involving riboflavin and its coenzymes has been shown to interact very readily with the redox system between ferric and ferrous iron.
Some recent studies in experimental animals have shown that not only is there evidence for some impairment of absorption of iron in riboflavin-deficient animals, and of its distribution between discrete compartments within the body, but also, more surprisingly and strikingly, a major increase in rates of iron loss from the intestinal mucosa, resulting in impaired retention of the body iron stores. This enhanced rate of iron loss is accompanied by hyperproliferation of crypt cells, and increased cellular transit along the villi, leading to an excessive proportion of immature villi, and probably also to a reduction in absorptive area. These studies begin to explain how a combination of iron deficiency and riboflavin deficiency, which is frequently encountered in human populations in many developing countries, may lead to a gradual deterioration of iron status, which is often accompanied by other intestinal lesions and by impaired gut function.
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 ribo-flavin deficiency is reported to be normocytic and normochromic.
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