Riboflavin vitamin clinical signs

Today, biochemical deficiency of riboflavin is accepted in the absence of clinical signs of deficiency. Biochemical signs of deficiency include change in the amount of the vitamin which is excreted in the urine, or change in the level of activity of a red blood cell (erythrocyte) enzyme, which is known as the erythrocyte glutathione reductase. Requirements for the vitamin are defined as that amount which will prevent both clinical and biochemical signs of deficiency. 

Clinical signs of riboflavin deficiency are seen at intakes below about 1 mg per day. At intakes below about 1.1 mg per day, there is very little urinary excretion of riboflavin thereafter, as intake increases, there is a sharp increase in excretion. Up to about 2.5 mg per day, there is a linear relationship between intake and excretion. At higher levels of intake, excretion increases sharply, reflecting active renal secretion of excessive vitamin (Section 7.2.5). 

One could more readily explain the clinical signs of scurvy on the basis of the function of vitamin C in collagen formation, than one could explain the development of wet beriberi for thiamine, or of cheilosis for riboflavin function. For instance, why shouldn t riboflavin cause beriberi, and thiamine cause cheilosis—rather than the reverse We cannot explain this. The situation exemplifies that we often cannot explain the clinical findings on the basis of what is known about the biochemical function of the vitamin. There is still much more to be learned about vitamin nutrition, and this is exemplified by vitamin C. 

---