Plummer effect
The Plummer effect is one of several feedforward mechanisms taking place in follicular cells of the thyroid gland and preventing the development of thyrotoxicosis in situations of extremely high supply with iodine.
History
In 1923 the American physician Henry Stanley Plummer discovered that high-dose iodine may be effective in the treatment of Graves’ disease [1][2]. Today, “Plummering”, i.e. therapy with Lugol's iodine solution, is one of several emergency measures in the management of severe thyrotoxicosis[3].
Mechanism
In the Plummer effect, a high iodine concentration inhibits the proteolysis of thyroglobulin and the release of pre-formed thyroid hormones from thyroid follicles[4]. Therefore, its mechanism differs from that of the Wolff–Chaikoff effect, where iodine inhibits the uptake of iodine in thyroid cells and the formation of thyroid hormones, and of the dehalogenase inhibition effect, where high iodine levels block deiodinases and other dehalogenases[5]).
Clinical implications
Unlike the Wolff–Chaikoff effect, the Plummer effect does not prevent the thyroid from taking up radioactive iodine in the case of nuclear emergencies. Therefore, "plummering" with high-dose iodine is only effective in a short time window after the release of radionuclides[6]. Wrong timing of iodine use may even increase the risk by triggering the Plummer effect[7].
The Plummer effect is, however, helpful in the management of thyrotoxicosis, where the usage of Lugol’s solution helps to limit the release of thyroid hormones into the bloodstream[3].
See also
References
- ^ Plummer HS 1923 Results of administering iodine to patients having exophthalmic goiter. Journal of the American Medical Association 80 1955–1965
- ^ Loriaux, D. Lynn (March 2016). "A Biographical History of Endocrinology". doi:10.1002/9781119205791.ch58.
{{cite journal}}: Cite journal requires|journal=(help) - ^ a b Reyes-Castano, John J.; Burman, Kenneth (2014). "Thyrotoxic Crisis: Thyroid Storm". Endocrine Emergencies: 77–97. doi:10.1007/978-1-62703-697-9_9.
- ^ Saller, B; Fink, H; Mann, K (1998). "Kinetics of acute and chronic iodine excess". Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association. 106 Suppl 3: S34-8. doi:10.1055/s-0029-1212044. PMID 9865552.
- ^ Solis-S, JC; Villalobos, P; Orozco, A; Delgado, G; Quintanar-Stephano, A; Garcia-Solis, P; Hernandez-Montiel, HL; Robles-Osorio, L; Valverde-R, C (January 2011). "Inhibition of intrathyroidal dehalogenation by iodide". The Journal of endocrinology. 208 (1): 89–96. doi:10.1677/JOE-10-0300. PMID 20974636.
- ^ Zanzonico, PB; Becker, DV (June 2000). "Effects of time of administration and dietary iodine levels on potassium iodide (KI) blockade of thyroid irradiation by 131I from radioactive fallout". Health physics. 78 (6): 660–7. doi:10.1097/00004032-200006000-00008. PMID 10832925.
- ^ Meristoudis, G; Ilias, I (June 2022). "Caveats in the use of potassium iodide for thyroid blocking". European journal of nuclear medicine and molecular imaging. 49 (7): 2120–2121. doi:10.1007/s00259-022-05797-7. PMID 35403862.