Effect of ethanol ingestion on thiamine metabolism: Clinical and experimental studies.

The effect of ethanol ingestion on thiamine metabolism was studies both in man and rats, and in the latter, the effect on the central nervous system was also studied morphologically. Fifty alcoholics who had consumed 120 g of ethanol daily for more than ten years were selected including 7 with delirium tremens. None of them had either Wernicke's encephalopathy or peripheral neuritis. More than half of them had blood thiamine levels within the normal range. With the determination of the hemolysate transketolase (TK) activity and thiamine pyrophosphate (TPP) effect, however, thiamine deficiency was detected in more than half of them and was seen more frequently in the cases with liver damage. All patients with delirium tremens except one had both liver damage and thiamine deficiency. In the animal experiments, when 36% of the daily total calorie of the thiamine-deficient diet was given as ethanol for 35 days, the thiamine content of the liver and brain was not decreased as much as in the rat which received the same but non-ethanol diet. Although the TK activity of the liver was low, TPP effect was also decreased. It seemed that ethanol had a sparing action on the thiamine deprivation, but impaired the TK activity of the liver through involvement of factors other than thiamine deficiency. Bilateral diapedesis and status spongiosus of the neuropile were seem in the lateral vestibular nucleus of the rat fed on thiamine-deficient and non-ethanol diet. This typical lesion for thiamine deficiency was not seen when ethanol was added. Instead, degenerative changes in both Purkinje cells and Bergmann glia were remarkable. The changes were much more severe when the rats were fed for a longer period of time (75 days) with a minimal amount of thiamine added to the diet. When the rats were fed on ethanol and thiamine-replete diet for a longer period of time (135 days), there were most remarkable changes in astroglia in the striatum. It is suggested that the thiamine deficiency could augment the cerebellar lesions induced by ethanol administration, while ethanol administration could decelerate the appearance of the lesions in the vestibular nuclei induced by thiamine deficiency.