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.
Immediately following collection, mix sample thoroughly by gentle inverting 8 - 10 times to prevent clotting
Refrigerated - 1 days
Ambient - NO
Liquid chromatography/tandem mass spectrometry (LC/MS)
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.