The Use of Lithium in the Treatment of Thyrotoxicosis

R. Temple; M. Berman; J. Robbins; J. Wolff

doi:10.1172/JCI107094

The Use of Lithium in the Treatment of Thyrotoxicosis

R. Temple, M. Berman, J. Robbins, and J. Wolff

Published October 1, 1972 - More info

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Abstract

Since lithium has been shown to inhibit release of iodine from the thyroid, we have investigated its therapeutic potential in thyrotoxicosis. Eight detailed ¹³¹I kinetic studies were performed on seven thyrotoxic women and data was analyzed using a computer program. Lithium at serum levels of about 1 mEq liter decreased the loss of ¹³¹I from the thyroid, led to a fall in serum ¹³¹I levels and diminished urinary ¹³¹I excretion. Computer simulation of the lithium effect required, in every case, that lithium inhibit hormonal and nonhormonal thyroid iodine release. In five cases a second lithium effect was required for a satisfactory fit of the model soluton with observed data: namely, an inhibition of hormone disappearance from serum.

Neither inhibition of release nor of hormone disappearance seemed to be affected by methimazole (release: 52% decrease without methimazole, 60% with methimazole; hormone disappearance: ∼60% decrease in both). When Li⁺ was discontinued, recovery of the iodine release rate and hormone disappearance rate over the observed time span was variable, ranging from no recovery to rates that exceeded pre-Li⁺ values.

When Li⁺ is used alone its effect on serum hormone levels is diminished due to continued accumulation of iodide by the thyroid. Thus, serum thyroxine-iodine levels fell 21-30% in 6-8 days in patients who did not receive methimazole and 15-67% in the methimazole-treated subjects. For prolonged therapy, therefore, a thiocarbamide drug must be used in conjunction with Li⁺. The similarity of inhibition of iodine release from the thyroid produced by Li⁺ and iodides is discussed.