Thiamine mononitrateThiamine pyrophosphate (TPP)
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Thiamine

Thiamine or thiamin, also known as vitamin B1, is a colorless compound with chemical formula C12H17N4OS. It is soluble in water and insoluble in alcohol. Thiamine decomposes if heated. more...

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Thiamine pyrophosphate (TPP) is a coenzyme for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase. The first two of these enzymes function in the metabolism of carbohydrates, while transketolase functions in the pentose phosphate pathway to synthesize NADPH and the pentose sugars deoxyribose and ribose. Systemic thiamine deficiency can lead to myriad problems including neurodegeneration, wasting, and death. Well-known syndromes caused by lack of thiamine due to malnutrition or a diet high in thiaminase-rich foods include Wernicke-Korsakoff syndrome and beriberi, diseases also common in chronic abusers of alcohol.

Genetic diseases of thiamine transport are rare but serious. Thiamine Responsive Megaloblastic Anemia with diabetes mellitus and sensorineural deafness (TRMA) is an autosomal recessive disorder caused by mutations in the gene SLC19A2, a high affinity thiamine transporter. TRMA patients do not show signs of systemic thiamine deficiency, suggesting redundancy in the thiamine transport system. This has led to the discovery of a second high affinity thiamine transporter, SLC19A3.

Thiamine was first discovered by Umetaro Suzuki in Japan when researching how rice bran cured patients of Beriberi. He named it aberic acid.

The only known cases of thiamine overdose occurred with thiamine injections.


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Thiamine deficiency in congestive heart failure patients receiving long term furosemide therapy
From Alternative Medicine Review, 3/1/04 by C. Zenuk

Zenuk C, Healey, J, Donnelly J, et al. Can J Clin Pharmacol 2003;10:184-188.

OBJECTIVE: To assess the presence of thiamine deficiency in congestive heart failure patients receiving furosemide therapy. DESIGN: Prospective, biochemical analysis of thiamine status was performed in outpatients and inpatients of the University of Ottawa Heart Institute. SUBJECTS: Thirty-two patients with congestive heart failure who received at least 40 mg/day of furosemide were included. Patients were then separated into two groups depending on whether the dose of furosemide was greater than or equal to 80 mg/day. METHODS: The primary measure was actual thiamine status as assessed by the erythrocyte transketolase enzyme activity and the degree of thiamine pyrophosphate effect. RESULTS: Biochemical evidence of severe thiamine deficiency was found in 98% (24 of 25) patients receiving at least 80 mg/day of furosemide and in 57% (four of seven) of patients taking 40 mg Furosemide daily, odds ratio (OR) 19.0 (1.13<OR<601.29). Thiamine status was not associated with any other clinical variables. CONCLUSIONS: These findings suggest that thiamine deficiency occurs in a substantial proportion of congestive heart failure patients being treated with furosemide.

COPYRIGHT 2004 Thorne Research Inc.
COPYRIGHT 2004 Gale Group

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