Riboflavin deficiency
The early studies of human vitamin deficiencies were complicated by the presence in the subjects of multiple deficiencies. Only recently have the symptoms of a frank ariboflavinosis in man been noted, and it must be said that considerable controversy exists regarding the relation of certain of the symptoms to riboflavin deficiency. In general, however, the deficiency is associated in man with abnormal ectodermal tissue maintenance. The usual signs of this are (a) inflammation of the tongue (glossitis)-the tongue assumes a magenta color, and there is flattening of the papillae; (b) cheilosis, or fissuring at the corners of the mouth and of the lips; and (c) a seborrheic dermatitis, often manifested by a sharklike appearance of the skin in the nasolabial folds and elsewhere.
One of the early experimental studies on human riboflavin deficiency was reported in 1938.
The diet was deficient in niacin as well as riboflavin. The cheilosis and seborrheic lesions that developed did not respond to niacin treatment, but disappeared following riboflavin therapy.
Another manifestation of deficiency according to some workers is corneal vascularization.
It is known that a similar clinical picture can be produced by a variety of deficiencies and even by certain toxic substances. The value of such findings in diagnosing ariboflavinosis is indeed limited. Attempts have been made to establish criteria for differentiating between ocular disturbances of ariboflavinosis and other types of corneal vascularization, and between glossitis of riboflavin deficiency and that found in other diseases. The situation is still complicated, however, and many reports indicate that observers have difficulty .in attaching a specific symptom to a specific avitaminosis.
In many instances one of these symptoms in humans has responded to some other member of the B complex but not to riboflavin. For instance, Cayer and others made a rather intensive biochemical study of a number of patients with glossitis and cheilosis. Excretion and load tests of various B complex vitamins were studied in these patients and it normal individuals.
Interesting among their fmdings are (a) similar riboflavin levels in some patients with and some without cheilosis, indicating the possibility that riboflavin deficiency may not have been responsible for the eheilosis; (b) frequent failure in response to riboflavin and (c) frequent response in patients with cheilosis to niacin (nicotinic acid, another member of the B complex). Some patients responded only after the administration of yeast or liver extract, sources of many B complex vitamins. In man on controlled low intake of riboflavin over extended periods, Horwitt and co-workers observed erythema of the tongue, angular stomatitis, and scrotal dermatitis as prevalent symptoms. Bessey and co-workers studied the riboflavin content (and the coenzymes containing the vitamin: see further) in blood of men on restricted intakes and of men on liberal intakes of the vitamin.
The content in red blood cells was found to be a reasonably sensitive and practical index for the evaluation of nutritional status with respect to riboflavin. A critical review of pathological changes in riboflavin deficiency can be found in the book by Follis. An informative history of pellagra covering the recognition of the nutritional aspect and the conquest of the disease was published by Sydenstricker. With animals long-continued and well-controlled deficiency experiments are practical.
Rats exhibit decreased growth rate; eye. changes, including a keratitis rather typical cataracts; dermatitis; possibly a type of anemia; some nerve degeneration; and poor reproduction. Congenital malformation and a cessa~ion of the estrous cycle have been reported. Definite symptoms of ariboflavinosis in calves have been reported. Wertman and various coworkers have studied a number of vitamins in relation to deficiency and factors in resistance to infection in rats. Paper No. IV of the series concerns a riboflavin deficiency.
