Vitamin B 2 (Riboflavin), Whole Blood

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Turnaround Time: 3 - 5 days
CPT Code:


Test Type: 1.5 mL Whole blood, frozen, protected from light
Reference Range:

137−370 µg/L. Note: Reference interval reflects flavinadeninedinucleotide (FAD), that accounts for approximately 90% of the total riboflavin in whole blood.


Riboflavin deficiency is known as pellagra, usually found in those who do not consume a diet rich in organ meats, leafy greens, and whole grains. It is seen in elderly, alcoholics, those with chronic liver disease, and those on total parenteral nutrition. Deficiency may be associated with severe lactic acidosis, especially in HIV patients on triple antibiotics. It also functions as an antioxidant. Riboflavin adsorption is decreased in hyperthyroidism.

Vitamin B2 is one of the water-soluble vitamins. It is synthesized in plants and microörganisms and occurs naturally in three forms: the physiologically inactive riboflavin and the physiologically active coenzymes flavinmononucleotide (FMN) and flavinadeninedinucleotide (FAD). The latter accounts for about 90% of the total riboflavin in whole blood. Because of their capacity to transfer electrons, FAD and FMN are essential for proton transfer in the respiratory chain, for the dehydration of fatty acids, the oxidative deamination of amino acids, and for other redox processes.

Exogenous flavin derivatives ingested with the diet (FAD, FMN) are dissociated by gastric acid from their protein binding, transformed by phosphatases to riboflavin, and absorbed in the small intestine. The reconversion of riboflavin to the coenzyme FMN and FAD occurs in the cytoplasm in many different tissues (liver, kidney, small intestine, and heart). Very little riboflavin is stored in the small intestine and it is excreted in the urine. Riboflavin deficiency in humans occurs, if at all, only in combination with deficiency of the entire B2 complex (the other components are nicotinamide and folic and pantothenic acids).

Riboflavin deficiency symptoms are manifest mainly in changes to the skin and mucous membranes (fissures of tongue and mouth angle, pruritus, seborrheic dermatitis, anogenital inflammation), corneal damage, thrombosis and atherosclerotic changes. These symptoms are a consequence of the accumulation of lipid peroxides. As a causative factor, apart from oxidative stress, the strongly oxidizing amino acid homocysteine is a consideration. B2 deficiency leads to reduced activity of the flavin-containing enzymes (glutathione reductase and glutathione peroxidase) which, in turn, allows these peroxides to express their deleterious effects.

Collection Details:

Collection Instructions:

This assay is currently not available in New York state.

Lavender-top (EDTA) tube. Use amber plastic transport tube with amber stopper. (If amber tubes are unavailable, cover standard transport tube completely, top and bottom, with aluminum foil. Identify specimen with patient's name directly on the container and the outside of the aluminum foil. Secure with tape.) For amber plastic transport tube and amber stopper, order LabCorp Nº 23598.

Draw blood. Do not separate. Protect specimen from light. Collect sample before breakfast in the morning prior to any medications. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.

Transfer whole blood to a plastic transport tube and freeze. Protect from light. Samples are only stable for one day at 2°C to 8°C.