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Inhibition by iodine of the release of thyroxine from the thyroid glands of patients with thyrotoxicosis
Open accessAbstract
A method has been devised which is free of many of the shortcomings of serial epithyroid counting techniques as an index of the rate of thyroid hormone secretion. By means of this method, the effect of treatment with Lugol's iodine on the rate of thyroidal secretion of thyroxine (T(4)) has been assessed in eight patients with thyrotoxicosis due to diffuse or multinodular goiter. The technique involves administration of a tracer dose of inorganic (125)I followed several days later by an intravenous tracer dose of (131)I-labeled T(4). Serial observations of serum protein-bound (PB) (125)I and (131)I are accompanied by frequent measurements of endogenous serum T(4) (T(4)-(127)I) concentration. Regardless of whether or not its administration was anteceded and accompanied by the administration of large doses of methimazole, iodine induced a rapid decrease in serum T(4)-(127)I concentration which could not be explained by an increase in the peripheral turnover of T(4), as judged from the metabolism of the (131)I-labeled hormone. Hence, the decreased serum T(4) concentration could only have resulted from decreased secretion of the hormone by the gland. Analyses of specific activity relationships between PB(125)I or T(4)-(127)I and PB(131)I made possible estimations of the extent to which iodine had decreased the rate of secretion of T(4). From such analysis, and in view of other considerations, it is concluded that the rapid decrease in T(4) secretion induced by iodine is not the result of an acute, sustained inhibition of T(4) synthesis, but rather results from an abrupt decrease in the fractional rate of thyroidal T(4) release.
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“Iodine acutely lowers thyroid hormone concentrations by reducing hormone secretion (238,239), and inhibits its own organification (the Wolff-Chaikoff effect) (240).”
From 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis (2016) · cites this paper as [239]
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Metadata
- Authors
- Wartofsky, L., Ransii, B. J., & Ingbar, S. H.
- Affiliations
- Harvard University (US)
- ORCID
- Wartofsky, Leonard
- Venue
- Journal of Clinical Investigation
- Published
- 1970-01-01
- Volume
- 49
- Issue
- 1
- Pages
- 78-86
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC322446
- OpenAlex
- W2158995119
- Cited by
- 141
- References
- 17
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 5 · 2023: 2 · 2022: 5 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 4 · 2016: 3 · 2015: 3 · 2014: 7 · 2013: 3 · 2012: 2
- FWCI
- 9.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Surgery › Thyroid and Parathyroid Surgery
- Keywords
- thyrotoxicosis, thyroxine release, Lugol's iodine, thyroid hormone secretion, multinodular goiter, diffuse goiter, iodine-125 tracer, methimazole, serum thyroxine, protein-bound iodine, thyroid hormone synthesis
- MeSH terms
- Adult, Aged, Blood Proteins, Female, Goiter, Humans, Hyperthyroidism, Iodine, Iodine Radioisotopes, Male, Mathematics, Methimazole, Methods, Middle Aged, Protein Binding, Thyroid Gland, Thyroxine
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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