Riboflavin is involved in carbohydrate metabolism as an essential coenzyme in many oxidation-reduction reactions involved in carbohydrate and protein metabolism (see table Sources, Functions, and Effects of Vitamins). Riboflavin is essentially nontoxic.
Dietary sources include milk, cheese, liver, meat, eggs, and enriched cereal products. (See also Overview of Vitamins.)
Primary riboflavin deficiency results from inadequate intake of the following:
Secondary riboflavin deficiency is most commonly caused by the following:
The most common signs of riboflavin deficiency are pallor and maceration of the mucosa at the angles of the mouth (angular stomatitis) and vermilion surfaces of the lips (cheilosis), eventually replaced by superficial linear fissures. The fissures can become infected with Candida albicans, causing grayish white lesions (perlèche). The tongue may appear magenta.
Seborrheic dermatitis develops, usually affecting the nasolabial folds, ears, eyelids, and scrotum or labia majora. These areas become red, scaly, and greasy.
Rarely, neovascularization and keratitis of the cornea occur, causing lacrimation and photophobia.
The lesions characteristic of riboflavin deficiency are nonspecific. Riboflavin deficiency should be suspected if characteristic signs develop in a patient with other B vitamin deficiencies.
Diagnosis of riboflavin deficiency can be confirmed by a therapeutic trial or laboratory testing, usually by measuring urinary excretion of riboflavin.
Riboflavin deficiency causes various nonspecific skin and mucosal lesions, including maceration of mucosa at the angles of the mouth (angular stomatitis) and surfaces of the lips (cheilosis).
Suspect riboflavin deficiency in patients with characteristic symptoms and other B vitamin deficiencies; confirm it with a therapeutic trial of riboflavin supplements or measurement of urinary excretion of riboflavin.
Treat with supplement of riboflavin and other water-soluble vitamins.