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Acute iodine excess

Acute excess iodine ingestion has long been known to result in a transient decrease in iodine organification, termed the Wolff—Chaikoff effect (Wolff and Chaikoff, 1948). With sustained excess iodine exposure, however, most individuals thyroid glands escape from acute Wolff— Chaikoff effect, despite continued excess iodine exposure, and resume synthesis of normal amounts of T4 and T3. The mechanism responsible for this escape or adaptation to the iodine load probably involves a decrease in the Na /H symporter protein, resulting in a decrease in thyroid iodide content (Eng et ai, 1999). In some individuals... [Pg.758]

Consistent with other studies (Bagchi et al., 1985, 1995 Li et al, 1993), excessive iodine not only triggered the onset of autoimmune thyroiditis, but also enhanced the development of inflammation. Our study found that all these effects were in positive correlation with the amount of iodine and exposure duration. The larger the amount and the longer the duration, the higher the incidence of autoimmune thyroiditis and the more acute the inflammation (Figure 91.3). [Pg.883]

Wolfi ChaikofF effect. Raben (1949) showed that this effect was dependent on the amount of iodine in the thyroid gland and not on the plasma concentration of iodine. The acute inhibitory effect of iodine overload is usually transient. Intrathyroidal iodine decreases within a few days despite a high plasma iodine concentration and thyroid hormone synthesis then returns to the previous level. This resumption of the organification of iodine is known as the escape phenomenon (Wolff, 1969), and it means that hypothyroidism will not develop in most individuals despite excessive iodine intake. [Pg.928]

Acute inhibitory effects of excess iodide was first demonstrated in vitro in 1944 by Morton, Chaikoff and Rosenfeld (i) and in vivo in 1948 by Wolff and Chaikoff (Wolff-Chaikoff effect) (2). As shown in Fig. 1, they injected 100 pg of iodide per rat with a tracer dose of and determined pleisma inorganic iodide concentration, total thyroidal iodine uptake and thyroidal organic iodine uptake until 50 hours after the injection of iodide. Thyroidal organic iodine... [Pg.43]

Thyroid hormone synthesis as pg/rat increased 10-20 times to acute excess iodide (Fig.3) and 2-4 times to chronic excess iodide Thyroid hormone concentrations expressed as FBI or iodothyronines were constant regardless of iodide dose, and the degradation rates of thyroxine were not affected by excess iodide. Indeed, increase of organic iodine formation is far more than the increase of thyroidal organic iodine content To release the excessively organified iodine in the form of iodide from the thyroids is another good example of autoregulation by iodide. [Pg.45]


See other pages where Acute iodine excess is mentioned: [Pg.677]    [Pg.901]    [Pg.1033]    [Pg.482]    [Pg.73]    [Pg.73]    [Pg.391]    [Pg.73]    [Pg.121]    [Pg.860]    [Pg.903]    [Pg.937]    [Pg.79]   
See also in sourсe #XX -- [ Pg.52 , Pg.53 ]




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Iodine excess

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