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Riboflavin is involved in carbohydrate metabolism as an essential coenzyme in many oxidation-reduction reactions. Riboflavin is essentially nontoxic.
Riboflavin deficiency usually occurs with other B vitamin deficiencies. Symptoms and signs include sore throat, lesions of the lips and mucosa of the mouth, glossitis, conjunctivitis, seborrheic dermatitis, and normochromic-normocytic anemia. Diagnosis is usually clinical. Treatment consists of oral or, if needed, IM riboflavin.
Primary riboflavin deficiency results from inadequate intake of fortified cereals, milk, and other animal products.
Secondary riboflavin deficiency is most commonly caused by chronic diarrhea, malabsorption syndromes, liver disorders, hemodialysis, peritoneal dialysis, long-term use of barbiturates, and chronic alcoholism.
The most common signs 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 can be confirmed by a therapeutic trial or laboratory testing, usually by measuring urinary excretion of riboflavin.
* This is a professional Version *