Abstract
Several authors 1 - 4 have reported beneficial effects from the oral and intravenous exhibition of the fluorides in the treatment of hyperthyroidism, rationalizing the procedure, in some instances at least, upon the well-known enzyme inhibiting action of this halogen. Laboratory findings offer a scientific basis for this treatment, since moderate doses of the fluorides produce (a) a diminished tissue respiration 5 and anaerobic glycolysis 6 in excised organs, (b) a decreased oxygen consumption and lactic acid production in muscle, 7 and (c) a sharp decrease in the oxygen consumption 2 and the carbon dioxide 8 production in the intact animal. Goldemberg 2 states that thyroxine is precipitated in vitro by fluorides in alkaline medium. He attributes the beneficial effects of the drug in toxic goiter to an in vivo inactivation of thyroxine and an inhibition of oxidases and other tissue ferments.
If this depression of metabolism results from an inactivation of thyroxine and its precursors in the body, it seems logical to postulate that the administration of a fluoride should protect an experimental animal from the toxic action of orally administered desiccated thyroid glands.
The accompanying data (Table I), obtained from the daily intravenous administration of 1% sodium fluoride to 21 adult rabbits which were also poisoned with 100 mg. per kg. per diem of desiccated thyroid glands, given orally in capsule, show no significant variation in the rapidity of weight loss or the life span of the fluoride treated animals from the thyroid controls. Histologic examination of the thyroid glands of both groups likewise showed that fluoride did not prevent the characteristic flattening of the acinal cells produced by thyroid feeding. The quantity of sodium fluoride used (5 to 10 mg. per kg.) was slightly larger than the 1 to 4 mg. per kg. dosage recommended by the clinician.
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