A patient with chronic alcohol use develops Wernicke's encephalopathy. He is given IV dextrose before thiamine. This worsens his neurological status. The biochemical explanation is:
- A Glucose competes with thiamine for intestinal absorption, reducing available thiamine
- B Glucose stimulates insulin release which drives thiamine into adipose tissue away from brain
- C Glucose infusion increases the demand for thiamine pyrophosphate (TPP) in pyruvate dehydrogenase and transketolase reactions, precipitating acute TPP depletion in already marginal stores ✓
- D Glucose increases cerebral blood flow causing haemorrhagic transformation of thiamine-deficient mammillary bodies
Explanation
Thiamine pyrophosphate (TPP) is an essential cofactor for pyruvate dehydrogenase (PDH), alpha-ketoglutarate dehydrogenase, and transketolase (HMP shunt). In thiamine-deficient patients with marginal TPP stores, administering glucose without thiamine dramatically increases the requirement for TPP: PDH must convert the glucose-derived pyruvate to acetyl-CoA for energy. This sudden increased demand depletes remaining TPP stores, precipitating acute thiamine deficiency. The result is PDH failure, pyruvate accumulation, lactic acidosis, and acute Wernicke's encephalopathy. This is why clinical guidelines mandate IV thiamine (at least 100-200 mg) before or simultaneously with glucose administration in any patient with suspected thiamine deficiency.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.