Transport Storage and Excretion

Thiamin with some TMP (19-75 nmol/l) circulates in the blood bound to albumin. When the binding capacity of plasma albumin is exceeded, or thiamin is in excess of tissue needs, it is rapidly excreted in the urine. Most thiamin in erythrocytes is present as TDP principally bound to the enzyme transketolase. Likewise, in most other tissues, there is very little free thiamin and it is mostly present as TDP (90%) in coenzymes bound to respective enzymes and a smaller amount of TTP (10%) in nervous tissues. The concentration of thiamin in specific tissues is on the order of 2-3 mg/g for heart muscle; 1 mg/g for brain, liver, and kidney; and 0.5 mg/g in skeletal muscle. Thiamin supplements can increase these concentrations slightly and prolonged febrile illnesses are likely to reduce them. Thiamin is mainly excreted intact in the urine but there are small amounts of thiochrome (Figure 2) and other thiazole and pyrimidine metabolites. A linear relationship exists between intake and excretion of thiamin until intake falls to an amount approaching minimum requirements when excretion decreases rapidly indicating a renal conservation mechanism.

There is concern that the long-term use of diuretics in the management of chronic congestive heart failure (CHF) may impair thiamin status and, as a consequence, impair myocardial function. The diuretic drug furosemide has been the subject of much attention. In healthy volunteers, a dose-dependent increase in urine flow accompanied by an increase in the urinary thiamin excretion rate have been demonstrated. In furosemide-treated patients, the concomitant presence of thiamin in the urine and biochemical deficiency of thiamin from measurements in blood has been shown. These results suggest that furosemide treatment can override the renal conservation mechanism. In one study, 23 patients with chronic CHF receiving 80-240 mg furosemide daily for 3-14 months were studied along with 16 age-matched controls without heart failure and not taking diuretics. No subjects in either group were identified as consuming inadequate thia-min intake or having increased thiamin requirements. However, biochemically, 21 of the 23 CHF patients and 2 of the controls were thiamin deficient. Furthermore, 5 of the CHF patients were treated with intravenous thiamin (100 mg thiamin HCl twice daily for 7 days). Biochemical thiamin status normalized and echocardiographic assessment of left ventricular ejection fraction increased in 4 of the 5 patients. Because no other changes were made in the patients' therapeutic regimen, the results suggest that the improvement in cardiac contractility was due to the correction of the thiamin deficiency.

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