Lavender (EDTA), 4mL

• Immediatley following collection, mix sample thoroughly by gentle inverting 8 - 10 times, to prevent clotting

1. Do not separate
2. Transfer 1.0mL of EDTA whole blood into a Amber screw-cap polypropylene frozen transport tube/vial - 4mL (LabCorp), labelled as EDTA whole blood, to protect from light
   • If amber tubes are unavailable, cover standard transport tube completely, top and bottom, with aluminum foil
3. Freeze

Amber screw-cap polypropylene frozen transport tube/vial - 4mL (LabCorp)

Dk green Lithium heparin (Li hep), no gel

Dk green Sodium heparin (Na hep), no gel

Immediately following collection, mix sample thoroughly by gentle inverting 8 - 10 times to prevent clotting

1. Do not separate
2. Transfer 1.0mL of EDTA whole blood into a Amber screw-cap polypropylene frozen transport tube/vial - 4mL (LabCorp), labelled as the appropriate type of whole blood, to protect from light
   • If amber tubes are unavailable, cover standard transport tube completely, top and bottom, with aluminum foil
3. Freeze

Frozen (preferred)

Refrigerated - 1 days

Ambient - NO

• Specimen not frozen
• Plasma specimen
• Use of anticoagulants other than EDTA
• Specimen not protected from light

Liquid chromatography/tandem mass spectrometry (LC/MS)

137−370 µg/L

Reference interval reflects flavin adenine dinucleotide (FAD), that accounts for approximately 90% of the total riboflavin in whole blood.

Vitamin B2 is one of the water-soluble vitamins. It is synthesized in plants and microorganisms and occurs naturally in three forms: the physiologically inactive riboflavin and the physiologically active coenzymes flavin mononucleotide (FMN) and flavin adenine dinucleotide (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.