Reinhardt M J, Högerle S, Trupkovic T, Krause T M, Moser E
Department of Nuclear Medicine, Hospital of the Albert-Ludwigs-Universität, Freiburg i. Br., Germany.
Eur J Nucl Med. 1998 Nov;25(11):1475-81. doi: 10.1007/s002590050324.
This study examines how thyroid pertechnetate uptake with and without thyroid-stimulating hormone (TSH) suppression changes as a function of increasing iodine supply. This is of special interest in countries at the threshold of sufficient iodine supply, where thyroid scintigraphy plays a key role in thyroid examination, especially for the diagnosis of Plummer's disease. From 1995 to 1997, a total of 1069 patients with euthyroid goitre, Plummer's disease or Graves' disease were included in the study. All patients underwent thyroid examination including sonography, scintigraphy with technetium-99m pertechnetate, and determination of free triiodothyronine, free thyroxine, TSH and urinary iodine excretion. Iodine excretion in the range from 0 to 500 microg iodine/g creatinine showed an inverse correlation with thyroid pertechnetate uptake, but no correlation with TSH was observed. There was no correlation between thyroid pertechnetate uptake and iodine excretion when TSH stimulation was eliminated, with two exceptions: thyroid pertechnetate uptake was significantly increased for iodine excretion values below 50 and 100 microg iodine/g creatinine in patients with Graves' and Plummer's disease, respectively. When iodine excretion exceeded 500 microg iodine/g creatinine, pertechnetate uptake was reduced to a basal level independent of the TSH. In conclusion, the influence of TSH on the thyroid pertechnetate uptake seems to be secondary compared with the influence of the iodine supply. It can be concluded further that the reference range of thyroid pertechnetate uptake under TSH suppression will not change significantly when the iodine supply increases from conditions of mild iodine deficiency to iodine sufficiency. Thyroid pertechnetate uptake with and without TSH suppression cannot be reliably interpreted beyond an iodine excretion of 500 microg iodine/g creatinine.
本研究考察了在有或无促甲状腺激素（TSH）抑制的情况下，甲状腺高锝酸盐摄取量如何随碘供应增加而变化。这在碘供应处于充足阈值的国家尤为重要，在这些国家，甲状腺闪烁扫描在甲状腺检查中起着关键作用，特别是对于诊断普卢默病。1995年至1997年，共有1069例甲状腺功能正常的甲状腺肿、普卢默病或格雷夫斯病患者纳入本研究。所有患者均接受了甲状腺检查，包括超声检查、用高锝[99mTc]酸盐进行闪烁扫描，以及测定游离三碘甲状腺原氨酸、游离甲状腺素、TSH和尿碘排泄量。碘排泄量在0至500微克碘/克肌酐范围内与甲状腺高锝酸盐摄取量呈负相关，但未观察到与TSH相关。在消除TSH刺激后，甲状腺高锝酸盐摄取量与碘排泄量之间无相关性，但有两个例外：在格雷夫斯病和普卢默病患者中，当碘排泄量分别低于50和100微克碘/克肌酐时，甲状腺高锝酸盐摄取量显著增加。当碘排泄量超过500微克碘/克肌酐时，高锝酸盐摄取量降至与TSH无关的基础水平。总之，与碘供应的影响相比，TSH对甲状腺高锝酸盐摄取量的影响似乎是次要的。进一步可以得出结论，当碘供应从轻度碘缺乏状态增加到碘充足状态时，TSH抑制下甲状腺高锝酸盐摄取量的参考范围不会显著变化。当碘排泄量超过500微克碘/克肌酐时，有或无TSH抑制的甲状腺高锝酸盐摄取量都无法得到可靠解释。
