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PIERRE M. DREYFUS, MD

Arch Ophthalmol. 1965;74(5):617-620.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

It appears well established that tobaccoalcohol amblyopia has a nutritional rather than a toxic etiology.^1,2 As yet, the metabolic aberration or specific vitamin deficiency responsible for the development of this syndrome has not been defined. A lack of cyanocobalamine (vitamin B₁₂)³, thiamine,⁴ riboflavin,⁵ and pyridoxine⁶ has been implicated in the genesis of amblyopia. Except for low serum cyanocobalamine levels and an abnormal urinary excretion of methylmalonic acid,⁷ no other biochemical abnormalities have been reported in instances of tobacco-alcohol or deficiency amblyopia. Recently, whole blood transketolase assays, which reflect in a sensitive and specific manner the state of thiamine nutrition, have been performed in two alcoholic patients suffering from untreated amblyopia. The results of these assays clearly demonstrate that a deficiency of thiamine is present in some cases of amblyopia.

Transketolase, a thiamine dependent transferase, acts as catalyst in the metabolic step which condenses . . . [Full Text PDF of this Article]

Author Affiliations
BOSTON

From the Department of Neurology and the Joseph P. Kennedy Jr. Memorial Laboratories of the Massachusetts General Hospital, and the Department of Neurology and Psychiatry, Harvard Medical School, Boston.

Footnotes
Submitted for publication April 27, 1965.

Reprint requests to Neurology Service, Massachusetts General Hospital, Boston, Mass 02114.

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