His initial transketolase level, taken after his course of thiamine treatment but before clinical improvement, was very low, indicating severe thiamine deficiency.
Potentially lethal thiamine deficiency complicating parenteral nutrition in children.
Malabsorption or consumption by the tumor was considered the mechanism of thiamine deficiency.
However, the ability to store thiamine might have been decreased because of liver dysfunction due to liver cirrhosis.
Certainly, the uptake of thiamine is very significant, indicating that some membrane function remains intact.
The resulting ratio includes thiamine from passive and active uptake in live cells.
The level of delirium remained unchanged until administration of thiamine starting on day 7 postoperatively, which resulted in palliation of delirium without brain damage.
It was considered that the predominant etiological factor for acute delirium was thiamine deficiency.
