PubMed · 5067399
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K Ito. 1972. [Plummer's disease].. https://pubmed.ncbi.nlm.nih.gov/5067399/
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There have been many theories regarding the origin or etiology of the peculiar disorder Robert James Graves first described in 1834. This article is a chronological discussion of the main ideas and the eras in which they were prominent, including the cardiac, neural, thyroid, pituitary, and modern eras.
To clarify the different roles of free radical scavenging systems in various thyroid disorders, we measured the levels of alpha-, beta-, and gamma-tocopherols and coenzyme Q in the thyroid tissues of patients with thyroid tumors and Graves' disease using high-performance liquid chromatography. The levels of alpha-tocopherols and gamma-tocopherols in the thyroid tissue of patients with papillary carcinoma and the level of gamma-tocopherol in the thyroid tissue of patients with malignant lymphoma were elevated compared with those in normal thyroid tissues. The level of coenzyme Q was reduced in the thyroid tissue of patients with Graves' disease and follicular and papillary thyroid carcinomas. These findings imply that vitamin E and coenzyme Q as scavengers play some role in thyroid follicular cell hyperfunction or dysfunction.
UNLABELLED: Persistent or recurrent Graves' hyperthyroidism after an initial treatment dose of radioactive iodine (RAI) is not uncommon and usually necessitates additional administrations. The radiation sensitivity of the previously irradiated thyroid gland is unknown but is of importance in selecting the retreatment dose. METHODS: A retrospective analysis of patients receiving RAI for Graves' hyperthyroidism was undertaken. A first treatment dose was given to 1076 patients, and 168 of these patients subsequently required a second dose for persistent or recurrent hyperthyroidism (interval between RAI treatments, 8.5 +/- 17.1 mo). RESULTS: Paired comparisons for retreated patients showed similar RAI doses (291 +/- 95 MBq and 283 +/- 129 MBq; p = ns) and treatment intensities (3.26 +/- 1.87 MBq g(-1) and 3.48 +/- 1.88 MBq g(-1); p = ns) for first and second treatments. Hypothyroidism occurred significantly earlier and more frequently after the first RAI dose (p = 0.002), but there was no difference for persistent or recurrent hyperthyroid events (p = 0.14). Multivariate regression established that the RAI treatment number (first or second) was a significant independent determinant of hypothyroid (p = 0.008) and combined (p = 0.001) events, whereas RAI dose and dose intensity were not. CONCLUSION: We conclude that previous RAI treatment failure does not lessen the chance of successfully eradicating Graves' hyperthyroidism with additional RAI treatment. Furthermore, the previously irradiated thyroid gland may be less susceptible to early hypothyroidism than the RAI-naive thyroid gland.