Wolff–Chaikoff effect
The Wolff–Chaikoff effect is a reduction in thyroid hormone levels caused by ingestion of a large amount of iodine.[1]
It is an autoregulatory phenomenon that inhibits organification (oxidation of iodide) in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream.[2] This becomes evident secondary to elevated levels of circulating iodide. The Wolff–Chaikoff effect lasts several days (around 10 days), after which it is followed by an "escape phenomenon",[3] which is described by resumption of normal organification of iodine and normal thyroid peroxidase function. "Escape phenomenon" is believed to occur because of decreased inorganic iodine concentration secondary to down-regulation of sodium-iodide symporter on the basolateral membrane of the thyroid follicular cell.
The Wolff–Chaikoff effect can be used as a treatment principle against hyperthyroidism (especially thyroid storm) by infusion of a large amount of iodine to suppress the thyroid gland. Iodide was used to treat hyperthyroidism before antithyroid drugs such as propylthiouracil and methimazole were developed. Hyperthyroid subjects given iodide may experience a decrease in basal metabolic rate within 24 hours that is comparable to that seen after thyroidectomy.[2] The Wolff–Chaikoff effect also explains the hypothyroidism produced in some patients by several iodine-containing drugs, including amiodarone.
Controversy
Endocrinology. 1999 Aug;140(8):3404-10.
In 1948, Wolff and Chaikoff reported that organic binding of iodide in the thyroid was decreased when plasma iodide levels were elevated (acute Wolff-Chaikoff effect), and that adaptation or escape from the acute effect occurred in approximately 2 days, in the presence of continued high plasma iodide concentrations.
We later demonstrated that the escape is attributable to a decrease in iodide transport into the thyroid, lowering the intrathyroidal iodine content below a critical inhibitory threshold and allowing organification of iodide to resume. We have now measured the rat thyroid sodium/iodide symporter (NIS) messenger RNA (mRNA) and protein levels, in response to both chronic and acute iodide excess, in an attempt to determine the mechanism responsible for the decreased iodide transport. Rats were given 0.05% NaI in their drinking water for 1 and 6 days in the chronic experiments, and a single 2000-microg dose of NaI i.p. in the acute experiments. Serum was collected for iodine and hormone measurements, and thyroids were frozen for subsequent measurement of NIS, TSH receptor, thyroid peroxidase (TPO), thyroglobulin, and cyclophilin mRNAs (by Northern blotting) as well as NIS protein (by Western blotting). Serum T4 and T3 concentrations were significantly decreased at 1 day in the chronic experiments and returned to normal at 6 days, and were unchanged in the acute experiments. Serum TSH levels were unchanged in both paradigms. Both NIS mRNA and protein were decreased at 1 and 6 days after chronic iodide ingestion. NIS mRNA was decreased at 6 and 24 h after acute iodide administration, whereas NIS protein was decreased only at 24 h. TPO mRNA was decreased at 6 days of chronic iodide ingestion and 24 h after acute iodide administration. There were no iodide-induced changes in TSH receptor and thyroglobulin mRNAs. These data suggest that iodide administration decreases both NIS mRNA and protein expression, by a mechanism that is likely to be, at least in part, transcriptional.
Our findings support the hypothesis that the escape from the acute Wolff-Chaikoff effect is caused by a decrease in NIS, with a resultant decreased iodide transport into the thyroid. The observed decrease in TPO mRNA may contribute to the iodine-induced hypothyroidism that is common in patients with Hashimoto's thyroiditis. While initially well received in the 1950s, subsequent attempts to demonstrate the Wolff-Chaikoff effect met largely with failure[4].
Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein. Eng PH, Cardona GR, Fang SL, Previti M, Alex S, Carrasco N, Chin WW, Braverman LE. Source Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. eng@rascal.med.harvard.edu Abstract
[edit] See also
[edit] References
- ^ Physiology at MCG 5/5ch5/s5ch5_6
- ^ a b Goodman, Louis Sanford; Gilman, Alfred Goodman (1996). Goodman and Gilman's the pharmacological basis of therapeutics (9th ed.). McGraw-Hill. p. 1402. ISBN 9780070262669. http://books.google.com/books?id=09h_hZiYXgUC&q=%22the+basal+metabolic+rate+may+fall+at+a+rate+comparable%22&dq=%22the+basal+metabolic+rate+may+fall+at+a+rate+comparable%22.
- ^ Eng P, Cardona G, Fang S, Previti M, Alex S, Carrasco N, Chin W, Braverman L (1999). "Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein". Endocrinology 140 (8): 3404–10. doi:10.1210/en.140.8.3404. PMID 10433193.
- ^ http://www.optimox.com/pics/Iodine/IOD-04/IOD_04.html
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