Hyperthyroidism thyroid autonomy

Joseph K, Mahlstedt J, Gonneemann R, Herbert K and Welcke U (1980) Early recognition and evaluation of the risk of hyperthyroidism in thyroid autonomy in an endemic goitre area. J Mol Med 4 21-37. 

Over the years, people living with iodine deficiency tend to develop multifocal thyroid autonomy, and multinodular toxic goiter is a common cause of hyperthyroidism. The difference in relative distribution of the four most common causes of hyperthyroidism in Iceland, with high iodine intake, and Judand, Denmark, with mild-to-moderate iodine deficiency, is shown in Figure 47.3. In Iceland, Graves ... 

C. Hyperthyroidism caused by thyroid autonomy C. Hyperthyroidism caused by Graves disease ... 

Functionally, the state may be compensated up to a certain degree of iodine deficiency and for a considerable period of time, described in clinical terms as euthyroid diffuse or nodular goiter. Functional failure follows only in the presence of severe iodine deficiency, and hypothyroidism may then develop. Much more frequently and somewhat paradoxically, hyperthyroidism ensues after many years of iodine depletion. Rarely, hyperthyroidism may be found in cases of diffuse goiter, which are then termed as diffuse thyroid autonomy. Fiowever, hyperthyroidism frequendy occurs in conjunction with uninodular (toxic adenoma) and multinodular goiters (toxic multinodular goiter). 

This huge multicenter trial demonstrated that there was an increase of hyperthyroidism after the elevation of salt iodization with the highest RR in 1992. For oHTA the incidence increased from 30.5/100000/year in 1987 to 41.7/100000/ in 1992 and decreased to baseline incidence in 1995. In contrast, the incidence of oHGD doubled from 1987 (incidence 10.4/100,000/year) to 1993 (20.9/100,000/ year) and was still high in 1995 (18.0/100000/year). From this study, it can be concluded that increase in iodine supply (change from IDA to ISA) leads to a transient increase, followed by a decrease, in thyroid autonomy, but to a permanent increase in Graves disease. 

Abbreviations-. oHTA, overt hyperthyroidism in thyroid autonomy scHTA, subclinical hyperthyroidism in thyroid autonomy oHGD, overt hyperthyroidism in Graves disease scGD, subclinical hyperthyroidism in Graves disease MRR, maximum relative risk Inc, incidence RR, relative risk. 

In the multicenter trial performed from 1987 to 1995 in more than 400000 inhabitants of Austria it could be demonstrated that due to the increase of salt iodization hyperthyroidism increases (Mostbeck et al., 1998). However, there are differences in the cause of increase if we separate thyroid autonomy from Graves disease as a cause of hyperthyroidism. Hyperthyroidism due to thyroid autonomy increases transiently with a MRR 2 years after the increase of salt iodization and decreases thereafter. In contrast, hyperthyroidism due to Graves disease increases with a MRR 3 years after the increase of salt iodization and remains high thereafter. This means that today in Austria thyroid autonomy as cause of hyperthyroidism decreases, whereas Graves disease increases and it can be expected that for the future in Austria Graves disease will become the main cause of hyperthyroidism. 

The improvement of iodine intake in Austria led to a transient increase in hyperthyroidism caused by thyroid autonomy, but decreased thereafter. 

In 1928 Plummer proposed two origins of thyrotoxicosis a diffuse hyperplasia responding to iodine intake, or alternatively arising in nodular goiter. In 1973, it was first suggested by Vidor et al. (1973) that pre-existing thyroid autonomy plays a crucial role in the pathogenesis of iodine-induced hyperthyroidism (IIH). 

Figure 92.3 The evolution of hyperthyroidism due to thyroid autonomy. The steady growth of the small autonomous areas will lead to progressive scintigraphic visibility, progressive TSH suppression, and finally hyperthyroidism with increased fT3 and fT4.

In Austria patients with hyperthyroidism, classified as autoimmune thyroid disorders or thyroid autonomy, were studied before and after increased iodine supply. Toxic multinodular goiter showed an increased incidence in females (30 0%) compared to males (20—30%), whereas... 

In patients with subclinical hyperthyroidism, longstanding goiter, subchnical thyroid autonomy and, in elderly patients, a prophylactic treatment with perchlorate is recommended. 

Thyrotoxicosis is a type of very late adverse reaction seen after iodine-based contrast media. Untreated Graves disease and multinodular goiter and thyroid autonomy are risks for this adverse reaction. Patients with hyperthyroidism are usually advised not to have iodinated contrast media injection. Patients with normal thyroid function are thought to be at low risk for this condition [3 ]. There are few studies that assess the relationship between iodinated contrast media exposure and thyroid function disorders. In a nested case-control study of 4096 patient intervals, iodinated contrast exposure was associated with incident hyperthyroidism (odds ratio or OR = 1.98 95% confidence interval or Cl = 1.08-3.60) but not statistically significantly associated with incident hypothyroidism (OR = 1.58 95% Cl, 0.95-2.62). Also, incident overt hyperthyroidism (follow-up thyrotropin levelsO.l mlU/L OR, 2.50 95% Cl, 1.06-5.93) and incident overt hypothyroidism (follow-up thyrotropin level >10 mlU/L OR, 3.05 95% C3,1.07-8.72) were found to be associated with iodinated contrast media exposxue [4 ]. 

Extensive iodine absorption from povidone-iodine can cause transient hypothyroidism or in patients with latent hypothyroidism the risk of destabilization and thyrotoxic crisis (SEDA-20, 226 SEDA-22, 263). Especially at risk are patients with an autonomous adenoma, localized diffuse autonomy of the thyroid gland, nodular goiter, latent hyperthyroidism of autoimmune origin, or endemic iodine deficiency (51). 

It has been known that excessive iodine intake results in goiter, hypothyroidism, or hyperthyroidism in humans (Institute of Medicine, 2001). The biological basis for iodine-induced hyperthyroidism (IIH) appears most often to be mutational events in thyroid cells that lead to autonomy of function. When the mass of cells with such an event becomes sufficient, and the iodine supply is increased, the subject may become thyrotoxic. These changes may occur in localized foci within the gland or... 

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