Hyperthyroidism iodine/iodides

Blockers are usually used as adjunctive therapy with antithyroid drugs, RAI, or iodides when treating Graves disease or toxic nodules in preparation for surgery or in thyroid storm. /3-Blockers are primary therapy only for thyroiditis and iodine-induced hyperthyroidism. 

The perchlorate ion of potassium perchlorate, KCIO4, is a competitive inhibitor of thyroidal 1 transport via the Sodium Iodide Symporter (NIS).This drug can cause fatal aplastic anemia and gastric ulcers and is now rarely used. If administered with careful supervision, in limited low doses and for only brief periods, serious toxic effects can be avoided. The compound is especially effective in treating iodine-induced hyperthyroidism, which may occur, for example, in patients treated with the antiar-rhythmic compound amiodarone. Perchlorate ion can also be used in a diagnostic test of 1 incorporation into Tg, the so-called perchlorate discharge test. 

The thyroid gland also regulates its uptake of iodide and thyroid hormone synthesis by intrathyroidal mechanisms that are independent of TSH. These mechanisms are primarily related to the level of iodine in the blood. Large doses of iodine inhibit iodide organification (Wolff-Chaikoff block, see Figure 38-1). In certain disease states (eg, Hashimoto s thyroiditis), this can inhibit thyroid hormone synthesis and result in hypothyroidism. Hyperthyroidism can result from the loss of the Wolff-Chaikoff block in susceptible individuals (eg, multinodular goiter). 

It has been suggested that potassium perchlorate should be used in the treatment of type 1 hyperthyroidism and glucocorticoids in the treatment of type 2 (SEDA-21, 199). Since hypothyroidism due to amiodarone tends to occur in areas in which there is sufficient iodine in the diet, it has been hypothesized that an iodinated organic inhibitor of hormone synthesis is formed and that the formation of this inhibitor is inhibited by perchlorate to a greater extent than thyroid hormone iodination is inhibited, since the iodinated lipids that are thought to be inhibitors require about 10 times more iodide than the hormone. However, there is a high risk of recurrence after treatment with potassium perchlorate, and it can cause serious adverse effects (SED-13,1281). 

In euthyroid subjects with normal glands an excess of iodide from any source can cause goitre (with or without hyperthyroidism), e.g. use of iodide-containing cough medicines, iodine-containing radio-contrast media, amiodarone, seaweed eaters. 

Sodium iodide I is a radiopharmaceutical/antithyroid agent. After rapid GI absorption, iodine I is primarily distributed within extracellular fluid. It is trapped and rapidly converted to protein-bound iodine by the thyroid it is concentrated, but not protein bound, by the stomach and salivary glands. It is promptly excreted by kidneys. About 90% of the local irradiation is caused by beta radiation and 10% is caused by gamma radiation. I has a physical half-life of 8.04 days. It is indicated in the treatment of thyroid carcinoma, hyperthyroidism. 

Radioactive iodine finds its widest use in the treatment of hyperthyroidism and in the diagnosis of disorders of thyroid function. Sodium iodide (lodotope Therapeutic) is available as a solution or in capsules containing essentially carrier-free suitable for oral administration. Sodium iodide is available for scanning procedures. Discussion here is limited to the uses of... 

Radioactive iodine is highly useful in the treatment of hyperthyroidism in many circumstances it is regarded as the therapeutic procedure of choice for this condition. The use of stable iodide as treatment for hyperthyroidism, however, may preclude treatment and certain imaging studies with radioactive iodine for weeks after the iodide has been discontinued. 

P-Adrenergic antagonists, antithyroid drugs, or both, or stable iodide, can be used to hasten the control of hyperthyroidism while awaiting the full effects of the radioactive iodine. 

On the other hand, excess iodine intake may also inhibit thyroid function, by either inhibition of iodide organification (Wolff-Charkoff effect) or inhibition of Tg proteolysis with reduction in hormone secretion, and may manifest itself either as a goiter, as hypothyroidism with/without goiter, or as hyperthyroidism (0.01-0.6% in populations on iodine prophylaxis), the outcome depending on the initial and current iodine status and current thyroid dysfunction (European Commission, 2002). The comparison of iodine intake and concentrations of serum Tg at various physiological or pathophysiological conditions is shown in Table 6.1. 

Perchlorate is a competitive inhibitor of the sodium-iodide symporter (NIS) and has been used in pharmacological doses to treat hyperthyroidism, especially iodine-induced hyperthyroidism. Perchlorate appears to be ubiquitous in the environment, and has been detected in trace amounts in the urine in almost all subjects evaluated both in the United States and Europe. In prospective clinical studies and environmental studies, there is no convincing evidence that environmental perchlorate adversely affects thyroid function. 

The beneficial effects of iodine supplementation in the prevention and control of developed thyroid abnormalities due to iodine deficiency have been discussed so far in this chapter. However, supplementation with excess iodine, including the improvement of a previous iodine-deficient state, may cause thyroid dysfunctions, viz., iodine-induced hypothyroidism/iodide goiter in susceptible subjects (Roti and Vagenakis, 2000) and iodine-induced hyperthyroidism (IIH) especially in individuals over 40 years of age and who have been iodine deficient for a long period in the past (Vidor et ai, 1973). It may also increase the ratio of papillary/follicular carcinomas (Slowinska-Klencka et ai, 2002). In other words, both low and excess intake of iodine is related to further risk of thyroid disease. Although a daily intake of up to 1000 pg/day by a normal adult individual is quite safe (WHO, 1994), the upper limit is much lower in a population that has been exposed to iodine deficiency in the past. Therefore, to prevent IDD, the recommended iodine requirement in an adult individual is fixed within a narrow range of 150 rg/day (Knudsen et ai, 2000). Iodine supplementation under certain conditions in certain populations causes adverse effects, e.g., iodide goiter and iodine-induced hypothyroidism, IIH, iodine-induced thyroiditis and thyroid cancer. 

Iodine-induced hyperthyroidism (especially AIT) is often difficult to treat, whereas iodine-induced hypothyroidism usually resolves after iodide withdrawal. Individuals at risk of developing iodine-induced thyroid dysfunction should be observed carefully if they are administered iodine-containing drugs. 

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