|Clinical Use:||Riboflavin testing is used to diagnose patients who present the signs of ariboflavinosis.|
|Background:||A deficiency of riboflavin can be primary – poor vitamin sources in one’s daily diet – or secondary, which may be a result of conditions that affect absorption in the intestine, the body not being able to use the vitamin, or an increase in the excretion of the vitamin from the body.
Subclinical riboflavin deficiency has also been observed in women taking oral contraceptives, in the elderly, in people with eating disorders, and in disease states such as HIV, inflammatory bowel disease, diabetes and chronic heart disease. The fact that riboflavin deficiency does not immediately lead to gross clinical manifestations indicates that the systemic levels of this essential vitamin are tightly regulated.
Dietary deficiency of riboflavin (ariboflavinosis) is characterised by sore throat, cheilosis (lesions on the lips), angular stomatitis (lesions on the angles of the mouth), glossitis (fissured and magenta-coloured tongue), corneal vascularisation, dyssebacia (red, scaly, greasy patches on the nose, eyelids, scrotum, and labia), and normocytic, normochromic anaemia. Sources of Vitamin B2 include Milk, cheese, leafy green vegetables, liver, kidneys, legumes, tomatoes, yeast, mushrooms, and almonds.
Severe riboflavin deficiency may affect the conversion of Vitamin B6 to its coenzyme, as well as conversion of tryptophan to niacin.
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
|Patient Preparation:||None required|
|Specimen Requirements:||EDTA – Whole Blood|
|Turnaround Time:||4 weeks|
|Referred Test:||Referred test|
|Location:||Rotherham General Hospital NHS Trust|