Iodine-induced thyrotoxicosis

Clinical applications include preoperative suppression of thyroid secretion according to Plummer with Lugol s solution (5% iodine + 10% potassium iodide, 50-100 mg iodine/d for a maximum of 10 d). In thyrotoxic crisis, LugoTs solution is given together with thioamides and p-blockers. Adverse effects allergies contraindications iodine-induced thyrotoxicosis. 

Lithium ions inhibit thyroxine release. Lithium salts can be used instead of iodine for rapid thyroid suppression in iodine-induced thyrotoxicosis. Regarding administration of lithium in manic-depressive illness, see p. 234. 

The case of a severe iodine-induced thyrotoxicosis in a patient who had been using iodine-containing eye-drops for more than 10 years has been reported (54). 

Martino E, Aghini-Lombardi F, Mariotti S, Bartalena L, Braverman L, Pinchera A. Amiodarone a common source of iodine-induced thyrotoxicosis. Horm Res 1987 26(1 1) 158-71. 

Broussolle C, Ducottet X, Martin C, Barbier Y, Bornet H, Noel G, Orgiazzi J. Rapid effectiveness of prednisone and thionamides combined therapy in severe amiodarone iodine-induced thyrotoxicosis. Comparison of two groups of patients with apparently normal thyroid glands. J Endocrinol Invest 1989 12(1) 37 2. 

Leger AF, Massin JP, Laurent MF, Vincens M, Auriol M, Helal OB, Chomette G, Savoie JC. Iodine-induced thyrotoxicosis analysis of eighty-five consecutive cases. Eur J Qin Invest 1984 14(6) 449-55. 

Hyperthyroidism and toxicity Iodine-induced hyperthyroidism A mild increase in the incidence of hyperthyroidism worldwide has been described following iodized salt programs (Connolly et al. 1970, Stewart et al. 1971, Bauch 1985, Koutras etal. 1999, Joseph 1989, Meng etal. 1989, Lobbers etal. 1989, Pickardt 1989). Joseph et al. (1980) reported that iodine intakes of < 100 xg per day pose no risk for patients with autonomous tissue due to iodine deficiency critical amounts are between 100 and 200 jg I per day. The absence of iodine deficiency in the Japanese population accounts for the absence of iodine-induced thyrotoxicosis (Nagataki 1987). Hyperthyroidism is easily controlled with antithyroid drugs. 

Iodine-induced thyrotoxicosis has been reported from elsewhere in the world, especially when a moderate-to-large increase in iodine ingestion occurred in a short time span. However, no population-based data are available regarding the prevalence of thyrotoxicosis in India. 

No systematic data are available on the change in occurrence of Graves disease, iodine-induced thyrotoxicosis and thyroid cancer with the introduction of iodization in India. 

Iodine-induced thyrotoxicosis in apparently normal thyroid glands has been reported in two patients after exposure to 2—10 mg iodine daily for 2—12 months before thyrotoxicosis was diagnosed. Although the pathogenesis of this kind of IIH remains obscure, the positive family history for thyroid disease in both patients may indicate a latent abnormality of their thyroid glands (Skare and Frey, 1980). Moreover, 10 further cases of iodine-induced thyrotoxicosis in apparently normal thyroid glands have been reported (Savoie et al, 1975). In contrast, a more-than-adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis, as shown in China in areas with more than adequate and excessive iodine consumption (Teng et al., 2006). 

Notes Iodine-induced thyrotoxicosis following intake of seaweed or seaweed-based dietary supplements appears to be rare as reflected by the limited number of case reports found in the literature. 

The chapter includes a section on the metabolism of iodate, since in the case of iodate toxicokinetics plays an important role in the toxicological evaluation. We have scanned the literature and looked at the regulatory status of iodate in the United States, Europe and Switzerland. The chapter will not deal with iodine-induced thyrotoxicosis, since this is a problem of iodine supplementation in general, whether by iodate or iodide. 

The treatment of type 1 AIT is more difficult than that of other forms of iodine-induced thyrotoxicosis. Discontinuation of amiodarone therapy is usually recommended in patients with type 1 AIT, as long as other anti-arrhythmic drugs are available. However, withdrawal of amiodarone is often difficult because of underlying severe heart disease. High doses of antithyroid drugs have been used to treat type 1 AIT. Combined therapy with antithyroid drugs and potassium perchlorate is recommended in patients who fail to respond to antithyroid drugs alone after 2—3 months of treatment (Basaria and Cooper,... 

C. Iodine-induced thyrotoxicosis, hypothyroidism, and goiter may occur, but incidence is likely less than 2% even if therapy is used for longer duration. 

Mussig, K., C. Thamer, R. Bares, et al. 2006. Iodine-induced thyrotoxicosis after ingestion of kelp-containing tea.. Gen. Intern. Med. 21(6) C11-14. 

Iodine-Induced Thyrotoxicosis in Northern Tasmania.. New Zealand Med.J.8l 25-26. 

Figure 11 Spontaneous cure of a case of iodine induced thyrotoxicosis (after lymphography). Times courses changes in thyroid iodine content and thyroid hormone blood levels.

All these data support the hypothesis that iodine induced thyrotoxicosis is the consequence of 1) inflated thyroid content 2) absence of impairment of organic binding and hormonal synthesis despite the increased iodine content. 

From a practical standpoint, the measurement of iodine content is of interest in hyperthyroid patients without radioactive uptake. A value above 30 mg, excludes a subacute thyroiditis and suggests an iodine induced thyrotoxicosis (Fig. 13). 

Figure 13 Interest of measurement of iodine content in hyperthyroidism with radioactive uptake (GR 49 Grave diseases) or without radioactive uptake (I.I.T. 28 iodine induced thyrotoxicosis S.T. 15 subacute thyroiditis)...

Vidor GI, Stewart JC, Wall JR, Wangel A, Hetzel BS. 1973. Pathogenesis of iodine-induced thyrotoxicosis studies in northern Tasmania. J Clin Endocrionl Metab 37, 901-909. 

Vagenakis AG, Wang C, Burger A, Maloof F, Braverman LE, Ingbar SM. 1972. Iodine-induced thyrotoxicosis in Boston. N Engl J Med 287, 523-527... 

Savoie JC, Massin JP, Thomopoulos P, Leger F. 1975. Iodine-induced thyrotoxicosis in apparently normal thyroid glands. J Clin Endocrinol Metab 41, 685-691. 

Dr. Braverman told us that iodine-induced thyrotoxicosis could be diagnosed by measuring urinary iodine excretion levels. I would like to comment on this point. If the iodine contamination is of recent onset, urinary iodine will of course be elevated. However, several studies have indicated that after coronary arteriography for instance, iodine in urine will be elevated up to two weeks later. After that period it will rapidly come down to normal excretion levels. My other comment concerns the lowering of thjn-oidal radioactive iodine uptake in patients contaminated with iodine. In some patients with iodine-induced thyrotoxicosis, the radioactive iodine uptake remains elevated. Therefore, a high uptake does not exclude the diagnosis of iodine-induced thyrotoxicosis. 

I think Dr. Jonckheer is correct. However, if you take 100 patients with iodine-induced hyperthyroidism, at least in the US, I would guess that 95 % of them have a suppressed radioactive iodine uptake. As a matter of fact, in a joint study with Dr. Pinchera on iodine-induced thyrotoxicosis in patients treated with amiodarone, we showed that the condition could be associated with normal or elevated uptakes. Those cases represent, however, a minority. The majority of patients with Jod-Basedow in the US will have an elevated urinary iodine excretion and a low radioactive iodine uptake. 

In the presence of thyroid disease, and in areas with endemic iodine deficiency, suddenly raising daily iodine intake may precipitate hyperthyroidism, and this has been the subject of some concern as salt iodization efforts proceed with fledgling quality assurance. This effect is felt to be related in part to autonomous nodules in the gland that synthesize and release excess thyroid hormone. The exact prevalence of iodine-induced hyperthyroidism in deficient areas is not clear. Many coim-tries initiating salt iodization programs have reported increases in the incidence of toxic nodular goitre and iodine-induced thyrotoxicosis, usually in older people. While this may be a significant clinical problem, the risk is estimated to be between 0.01 and 0.06% and must be... 

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