however, the cumulative amount excreted is similar to the amount excreted by older infants.
The signs of riboflavin deficiency (ariboflavinosis) in humans are sore throat; hyperemia and edema of the pharyngeal and oral mucous membranes; cheilosis; angular stomatitis; glossitis (magenta tongue); seborrheic dermatitis; and normochromic, normocytic anemia associated with pure erythrocyte cytoplasia of the bone marrow (Wilson, 1983). Riboflavin deficiency is most often accompanied by other nutrient deficiencies. Severe riboflavin deficiency may impair the metabolism of vitamin B6 by limiting the amount of FMN required by pyridoxine (pyridoxamine) 5-phosphate oxidase and the conversion of tryptophan to functional forms of niacin (McCormick, 1989).
Riboflavin deficiency has been documented in industrialized and developing nations and across various demographic groups (Komindr and Nichoalds, 1980; Nichoalds, 1981). Diseases such as cancer (Rivlin, 1975), cardiac disease (Steier et al., 1976), and diabetes mellitus (Cole et al., 1976; Prager et al., 1958) are known to precipitate or exacerbate riboflavin deficiency.
Several indicators have been used to estimate the adequacy of riboflavin status in humans (McCormick, 1994; McCormick and Greene, 1994). Principal among them are erythrocyte glutathione reductase; erythrocyte flavin concentration; and urinary excretion of the vitamin in fasting, random, or 24-hour specimens or by load tests.
Currently, one of the most commonly used methods for assessing riboflavin status involves the determination of erythrocyte glutathione reductase (EGR) activity, as described by Sauberlich and coworkers