Testing of nonfasting specimens or the use of dietary vitamin B2 supplementation can result in elevated plasma vitamin B2 concentrations.
There are 3 principal vitamin B2-active flavins found in nature: riboflavin, riboflavin 5-phosphate (flavin mononucleotide: FMN), and riboflavin-5'-adenosyl-diphosphate (flavin adenosine dinucleotide: FAD). In biological tissues, FMN and FAD serve as prosthetic groups for a large variety of flavoproteins, which are hydrogen carriers in oxidation-reduction processes.
Dietary deficiency of riboflavin (ariboflavinosis) is characterized by sore throat, cheilosis (lesions on the lips), angular stomatitis (lesions on the angles of the mouth), glossitis (fissured and magenta-colored tongue), corneal vascularization, dyssebacia (red, scaly, greasy patches on the nose, eyelids, scrotum, and labia), and normocytic, normochromic anemia. Severe riboflavin deficiency may affect the conversion of vitamin B6 to its coenzyme, as well as conversion of tryptophan to niacin.
There is also evidence that more subtle riboflavin deficiency might have negative health consequences.
Finally, in addition to dietary deficiency, there are rare inborn errors of metabolism, primarily involving loss of function of riboflavin transporters, which result in functional vitamin B2 deficiency. Many of these latter cases present with neurodegenerative features.
Riboflavin has a low level of toxicity and no case of riboflavin toxicity in humans has been reported. The limited absorptivity of riboflavin and its ready excretion in the urine normally preclude a health problem due to increased intake of riboflavin.