ARIBOFLAVINOSIS AND CATARACT
In 1931 the occurrence of cataract as a result of a deficiency of riboflavin in the diet of young rats was described.1 Many significant papers have followed this observation without making close correlation between the type of change observed in the rat eyes and the changes seen with the slit lamp in any type of human cataract. It should be emphasized, however, that structural differences between the human and the rat lens not observed with the slit lamp may exist. It is not permissible to deprive infant human beings of riboflavin so completely as is necessary to produce cataracts in young rats. It is equally improbable that one will ever see patients deficient in riboflavin alone to the extent necessary to produce cataracts in young rats. Fundamental as these studies have been, no specific changes in the human lens have yet been described as "ariboflavinosis opacities."
JOHNSON LV, ECKARDT RE. OCULAR CONDITIONS ASSOCIATED WITH CLINICAL RIBOFLAVIN DEFICIENCY. Arch Ophthalmol. 1940;24(5):1001–1005. doi:10.1001/archopht.1940.00870050151015
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