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Ariboflavinosis (pronounced "AY-rybo-flayvin-OH-sis") is the medical condition caused by deficiency of riboflavin (vitamin B2). Ariboflavinosis is most often seen in association with protein-energy malnutrition, and also in cases of alcoholism.
The most common cause of ariboflavin deficiency is an inadequate diet; thus, it occurs most frequently in populations consuming limited quantities of riboflavin-containing foods such as meats, eggs, milk, cheese, yogurt, leafy green vegetables and whole grains. Riboflavin deficiency can also occur in those with impaired liver function, which prevents proper use of the vitamin. Borderline riboflavin deficiency as a consequence of certain anti-retroviral medications has also been known to cause acute lactic acidosis.
The signs and symptoms of riboflavin deficiency typically include sore throat with redness and swelling of the mouth and throat mucosa, cheilosis and angular stomatitis (cracking of the lips and corners of the mouth), glossitis (magenta tongue with atrophy), seborrheic dermatitis or pseudo-syphilis (moist, scaly skin particularly affecting the scrotum or labia majora and the nasolabial folds), and a decreased red blood cell count with normal cell size and hemoglobin content (normochromic normocytic anemia).
Riboflavin deficiency is usually found together with other nutrient deficiencies, particularly of the other water-soluble vitamins. Phototherapy to treat jaundice in infants can cause increased degradation of riboflavin, leading to deficiency if not monitored closely. Persons with chronic alcoholism can have impaired absorption of riboflavin and other vitamins such as thiamine (see Wernicke's encephalopathy).
Studies of the Turkoman people of Iran, who have a significantly increased incidence of esophageal cancer, have shown some relationship between chronic riboflavin deficiency and the onset of esophageal malignancies.
Treatment involves a diet which includes an adequate amount of riboflavin. In cases related to weakened liver function, intravenous supplementation may be required.
- Yazdanpanah B, Wiegmann K, Tchikov V et al. (August 2009). "Riboflavin kinase couples TNF receptor 1 to NADPH oxidase". Nature 460 (7259): 1159–1163. doi:10.1038/nature08206. PMID 19641494.
- Wacker J, Frühauf J, Schulz M, Chiwora FM, Volz J, Becker K (2000). "Riboflavin deficiency and preeclampsia". Obstetrics and gynecology 96 (1): 38–44. doi:10.1016/S0029-7844(00)00847-4. PMID 10862839.
- Riboflavin at the Linus Pauling Institute