Livadas D P, Koutras D A, Souvatzoglou A, Beckers C
Clin Endocrinol (Oxf). 1977 Aug;7(2):121-7. doi: 10.1111/j.1365-2265.1977.tb01303.x.
In sixteen cases of toxic adenoma of the thyroid (autonomous hot nodule with complete suppression of the surrounding normal parenchyma) potassium iodide was given in doses of 100 microgram/day for one week, 200 microgram/day for another and 400 microgram/day for a third week. There was a progressive increase in the serum T4 level. Serum T3 also increased, although this was significant only after the first week. Serum TSH was undetectable throughout the entire period of the study. This metabolic pattern is different from the response seen in cases of nontoxic endemic goitre, where small iodine supplements induce an increase in serum T4 but a decrease in serum T3. Furthermore, the present results may explain the phenomenon of iodine-induced or iodine-precipitated hyperthyroidism (Jod-Basedow) when patients with autonomous thyroid are presented with a high iodine intake. In contrast to the results obtained with small iodide doses, two other cases treated with large pharmacological doses of iodide showed a decrease in both serum T4 and serum T3. It is concluded that the physician should be aware of the possibility of precipitating or aggravating thyrotoxicosis in patients with an autonomous hot nodule by increasing their intake of iodine.
在16例甲状腺毒性腺瘤（自主性热结节伴周围正常实质完全受抑制）患者中，给予碘化钾，剂量为第1周100微克/天，第2周200微克/天，第3周400微克/天。血清T4水平逐渐升高。血清T3也升高，尽管仅在第1周后才显著。在整个研究期间均未检测到血清TSH。这种代谢模式与非毒性地方性甲状腺肿病例的反应不同，在非毒性地方性甲状腺肿病例中，补充少量碘会导致血清T4升高但血清T3降低。此外，目前的结果可能解释了自主性甲状腺患者碘摄入量高时碘诱导或碘引发的甲状腺功能亢进症（约德-巴塞多氏病）现象。与小剂量碘化物的结果相反，另外2例接受大剂量药理碘治疗的患者血清T4和血清T3均降低。结论是，医生应意识到，增加碘摄入量可能会使自主性热结节患者发生或加重甲状腺毒症。
