Riboflavin(Vitamin B2) deficiency

Riboflavin deficiency

Although riboflavin is involved in all areas of metabolism, and deficiency is widespread on a global scale, deficiency is not fatal. There seem to be two reasons for this. One is that, although deficiency is common, the vitamin is widespread in foods and most diets will provide minimally adequate amounts to permit main-tenance of central metabolic pathways. The second, more important, reason is that in deficiency there is extremely efficient reutilization of the riboflavin that is released by the turnover of flavoproteins, so that only a very small amount is metabolized or excreted.

Riboflavin deficiency is characterized by lesions of the margin of the lips (cheilosis) and corners of the mouth (angular stomatitis), a painful desquamation of the tongue, so that it is red, dry, and atrophic (magenta tongue), and a seborrheic dermatitis, with filiform excrescences, affecting especially the nasola-bial folds, eyelids, and ears.

There may also be conjunctivitis with vasculariza-tion of the cornea and opacity of the lens. This last is the only lesion of ariboflavinosis for which the bio-chemical basis is known: glutathione is important in maintaining the normal clarity of crystallin in the lens, and glutathione reductase is a flavoprotein that is particularly sensitive to riboflavin depletion.

The main metabolic effect of riboflavin deficiency is on lipid metabolism. Riboflavin-deficient animals have a lower metabolic rate than controls and require a 15–20% higher food intake to maintain body weight. Feeding a high-fat diet leads to more marked impair-ment of growth and a higher requirement for ribofla-vin to restore growth.

Resistance to malaria in riboflavin deficiency

Several studies have noted that in areas where malaria is endemic, riboflavin-deficient subjects are relatively resistant and have a lower parasite burden than ade-quately nourished subjects. The biochemical basis of this resistance to malaria in riboflavin deficiency is not known, but two possible mechanisms have been proposed.

●      The malarial parasites may have a particularly high requirement for riboflavin. Some flavin analogues have antimalarial action.

●      As a result of impaired antioxidant activity in erythrocytes, there may be increased fragility of erythrocyte membranes or reduced membrane flu-idity. As in sickle cell trait, which also protects against malaria, this may result in exposure of the parasites to the host’s immune system at a vulner-able stage in their development, resulting in the production of protective antibodies.