riboflavin

Riboflavin is converted into two key coenzymes: flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), which act as cofactors in numerous oxidation-reduction reactions, including those in the electron transport chain (Complex I and II), the citric acid cycle (succinate dehydrogenase), and fatty acid oxidation. It is also required for the activity of glutathione reductase, which regenerates reduced glutathione, an important antioxidant.

Dietary sources include dairy products, eggs, meat, and green leafy vegetables. Riboflavin deficiency (ariboflavinosis) is rare in isolation but commonly occurs alongside other B-vitamin deficiencies in malnourished patients, alcoholics, or those with malabsorption syndromes. Classic clinical findings include: - Angular stomatitis (fissures at corners of mouth) - Cheilosis (cracking/scaling of lips) - Glossitis (magenta-colored tongue) - Corneal vascularization/keratitis - Seborrheic dermatitis

Riboflavin deficiency can also impair the metabolism of other B vitamins, particularly pyridoxine (B6) and niacin (B3), since FAD is required for the conversion of tryptophan to niacin and for pyridoxine activation.

Clinically, riboflavin is relevant in the diagnosis of organic acidurias (glutaric acidemia type II) since FAD is a cofactor for multiple acyl-CoA dehydrogenases. It's also used therapeutically in some mitochondrial disorders and has been studied for migraine prophylaxis at high doses.

On USMLE, riboflavin deficiency is often tested with a vignette describing angular stomatitis/cheilosis/glossitis in a patient with poor nutrition or alcoholism, sometimes as a distractor alongside other B-vitamin deficiencies (niacin causing pellagra, B12 causing megaloblastic anemia, etc.).