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November 1940


Author Affiliations

From the Western Reserve University School of Medicine and the University Hospitals of Cleveland, Department of Surgery, Ophthalmologic Service (Dr. Johnson).
Fellow in biochemistry and recipient of the George Angell and the S. M. A. stipends for research in ophthalmology.

Arch Ophthalmol. 1940;24(5):1001-1005. doi:10.1001/archopht.1940.00870050151015

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."

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