ABSTRACT
A number of studies have demonstrated that deficiency of riboflavin occurs frequently in patients with chronic alcoholism in the context of multiple nutrient deficits. In one study, Fennelly et al. reported that 17% of alcoholic patients with peripheral neuropathy had lower than normal serum levels of riboflavin, as well as reduced serum levels of other B vitamins. The major site of action of the thyroid hormones, thyroxine and triiodothyronine, on riboflavin metabolism is on flavokinase, which converts riboflavin to flavin mononucleotide (FMN), the initial reaction in the two-step biosynthesis of flavin adenine dinucleotide (FAD). Physiological doses of thyroxine increase flavokinase activity. FAD pyrophbsphorylase activity is also stimulated to some degree by thyroid hormones. A number of drugs have significant effects on riboflavin nutriture, by decreasing intestinal absorption, by increasing excretion, or by interfering with its conversion to FMN and FAD. The manifestations of boric acid toxicity in experimental animals can be lessened by the administration of riboflavin.
