Quantitative Studies of Iodine Metabolism After Long-Term Treatment of Thyrotoxicosis with Antithyroid Drugs

Rm, Harden; Wd, Alexander; Da, Koutras; Mt, Harrison; Wayne, E. J.

doi:10.1210/jcem-26-4-397

Cited by 18 publications

(9 citation statements)

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“…In a recent study, Harden, Koutras, Alexander, and Wayne (30) found that patients with good clinical and T4 responses to iodide treatment at the end of 2 wk had relapsed by the end of 4 wk despite continued therapy, their T values returning to pretreatment levels. Since iodine accumulates in thyrotoxic glands treated with Lugol's solution (31), we suggest that in patients treated either with iodide (23,30) or lithium alone, increased glandular hormone content permits total hormone release to rise despite a decreased fractional rate of secretion. This eventually leads to escape from control.…”

Section: Resultsmentioning

confidence: 99%

The Use of Lithium in the Treatment of Thyrotoxicosis

Temple¹,

Berman²,

Robbins³

et al. 1972

J. Clin. Invest.

128

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A B S T R A C T Since lithium has been showx%n to inhibit release of iodine from the thyroid, we have investigated its therapeutic potential in thvrotoxicosis. Eight detailed "lI kinetic studies were performed on seven thvrotoxic women and data was analy,zed using a computer program. Lithium at serum levels of about 1 mEq 'liter decreased the loss of '31I from the thyroid, led to a fall in serum "II levels and diminished urinary "'I excretion. Coinputer simulation of the lithium effect required, in every case, that lithium inhibit hormonal and( nonllormonal 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 serunm.Neither inhibition of release nor of hormone disappearance seemled to be affected by mlethimazole (release: 52% decrease without methimilazole, 60,% \w-ith mlethimazole; hormone disappearance: -60% decrease in both). Wlheni Li' was discontinued, recovery of the iodine release rate and hormiione 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 wlho did not receive methimazole and 15-67%C in the methimazoletreated subjects. For prolonged therapy, therefore, a thiocarbamide drug must be used in conjunction witlh Li'. The similarity of inhibition of iodine release from the thvroid produced by Li' and iodides is discussed.

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Section: Resultsmentioning

confidence: 99%

The Use of Lithium in the Treatment of Thyrotoxicosis

Temple¹,

Berman²,

Robbins³

et al. 1972

J. Clin. Invest.

128

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Section: Discussionmentioning

confidence: 99%

“…The ability of iodine acutely to inhibit T4 synthesis (Wolff-Chaikoff effect) is well known and has been demonstrated to occur in patients with thyrotoxicosis (15,16). This effect is usually transient (16), and such transiency might be considered as evidence against its primary role in decreasing T4 secretion. On the other hand, the transient nature of the Wolff-Chaikoff effect could be taken to be responsible for the observation that serum T4 concentration generally did not continue to fall during the entire period of iodine administration.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition by iodine of the release of thyroxine from the thyroid glands of patients with thyrotoxicosis

Wartofsky¹,

Ransii²,

Ingbar³

1970

J. Clin. Invest.

135

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A B S T R A C T A method has been devised which is free of many of the shortcomings of serial epithyroid counting techniques as an index of the rate of thyroid hormone seeretion. By means of this method, the effect of treatment with Lugol's iodine on the rate of thyroidal secretion of thyroxine (T4) has been assessed in eight patients with thyrotoxicosis due to diffuse or multinodular goiter. The technique involves administration of a tracer dose of inorganic 'I followed several days later by an intravenous tracer dose of "'I-labeled T4. Serial observations of serum protein-bound (PB) 'I and 'I are accompanied by frequent measurements of endogenous serum T4 (T4-'I) concentration. Regardless of whether or not its administration was anteceded and accompanied by the administration of large doses of methimazole, iodine induced a rapid decrease in serum T4-RI concentration which could not be explained by an increase in the peripheral turnover of T., as judged from the metabolism of the "I-labeled hormone. Hence, the decreased serum T4 concentration could only have resulted from decreased secretion of the hormone by the gland. Analyses of specific activity relationships between PB'I or T4-1'I and PB1I made possible estimations of the extent to which iodine had decreased the rate of secretion of T4. From such analysis, and in view of other considerations, it is concluded that the rapid decrease in T4 secretion induced by iodine is not the result of an acute, sustained inhibition of T4 synthesis, but rather results from an abrupt decrease in the fractional rate of thyroidal T4 release.

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“…as those found in PTU group within one week, we thus expected that the addition of 1mg iodine to PTU would lead to more pronounced reduction of the serum thyroidhormone levels than PTU or iodide alone. We were also anxious for the possibility that iodide, administered in combination with PTU, might reduce the efficacy of PTU even in a short term treatment, as suggested by Alexander et al, (1964); Alexander et al, (1965) and Harden et al, (1966). The data from the present study suggested strongly that PTU+I-therapy was much more effective than PTU alone therapy to reduce the several thyroid functions.…”

Section: Discussionmentioning

confidence: 53%