Water soluble vitamin that participates in carbohydrate metabolism.
Essential for the oxidative decarboxylation of the multienzyme branch-chain alpha keto acid dehydrogenase complexes of the citric acid cycle.
An important cofactor for key enzymes responsible for the maintenance of cerebral energy homeostasis: alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase and transketolase of the pentose phosphate pathway.
With deficiency of the vitamin. toxic intermediary substances accumulate due to a decrease in the enzyme activity.
Thiamine deficiency is rare in the United States.
Thiamine deficiency is relatively common in sub-Saharan Africa.
Outbreaks of thiamine deficiency have been seen in refugee camps.
Food is fortified with thiamine and other essential vitamins as a preventative measure.
Thiamine deficiency impairs pyruvate conversion to acetyl coenzyme A, which increases lactic acid production.
Intermediates that accumulate induce tissue injury but inhibiting metabolism in the brain in areas with high metabolic requirement and thiamine turnover.
Thiamine in the human body has a half-life of 18 days and is quickly exhausted, particularly when metabolic demands exceed intake.
Deficiency can lead to Wernicke’s encephalopathy, an acute neuropsychiatric disorder with ocular motor disorders, ataxia, and altered mental status.
Thiamine deficiency can be present in other processes besides Wernicke’s s encephalopathy and include beriberi, and Marchiafava-Bignami disease.
Patients with alcoholism and secondary malnutrition are often deficient in magnesium, which is a cofactor for normal functioning of thiamine dependent enzymes and neurochemical transmission.
Alcoholics may have thiamine deficiency because of the following:
Alcoholics tend to intake less than the recommended amount of thiamine.
Active transport of thiamine into enterocytes is disturbe during acute alcohol exposure.
Liver thiamine stores in alcoholics are reduced due to hepatic steatosis or fibrosis.
Magnesium is required for the binding of thiamine to thiamine-using enzymes within the cell, is also deficient due to chronic alcohol consumption.
Ethanol per se inhibits thiamine transport in the gastrointestinal system and blocks phosphorylation of thiamine to its cofactor form.
Should be given to all patients with risk for or symptoms of Wernicke-Korsakoff syndrome.
Poor absorption enterally in alcohol dependent patients and should be given parenterally in high risk patients at a dose of 100-250 mg intravenously, daily for several days.
Rarely associated with anaphylaxis when given parenterally.
Alcoholic patients should receive thiamine when simultaneously treated with intravenous glucose to prevent the Wernicke-Korsakoff syndrome.
Patients with thiamine deficiency can present with beriberi,congestive heart failure with high output, abdominal pain, vomiting, lactic acidosis, and coma.