Strong evidence suggests that ethanol interferes directly with
thiamine uptake in the gastrointestinal tract. Ethanol also disrupts
thiamine storage in the liver and the transformation of thiamine into
its active form. The role of alcohol consumption in the
development of WKS has been experimentally confirmed through studies
in which rats were subjected to alcohol exposure and lower levels
thiamine through a low-thiamine diet. In particular, studies have
demonstrated that clinical signs of the neurological problems that
result from thiamine deficiency develop faster in rats that have
received alcohol and were also deficient in thiamine than rats who did
not receive alcohol. In another study, it was found that rats that
were chronically fed alcohol had significantly lower liver thiamine
stores than control rats. This provides an explanation for why
alcoholics with liver cirrhosis have a higher incidence of both
thiamine deficiency and WKS.
 Todd, K. G., Hazell, A. S., & Butterworth, R. F. (1999). Alcohol thiamine interactions: an update on the pathogenesis of wernicke encephalopathy. Addiction Biology, 4, 261-272.
 He, X., Sullivan, E. V., Stankovic, R. K., Harper, C. G., & Pfefferbaum, A. (2007). Interaction of thiamine deficiency and voluntary alcohol consumption disrupts rat corpus collosum ultrastructure. Neuropsychopharmacology, 32, 2207-2216.
but this is of course over a long period.
for just one instance, there's no scientifical evidence AFAIK