Aeschimann S, Buergi U, Wagner H E, Kaempf J, Lauber K, Studer H
Department of Internal Medicine, University of Bern, Inselspital, Switzerland.
J Endocrinol. 1994 Jan;140(1):155-64. doi: 10.1677/joe.0.1400155.
Iodine may have an inhibitory and, in some circumstances, a stimulatory effect on thyroid follicular cell growth. Exogenous iodine deficiency causes the growth of endemic goitres and it has been claimed that low intrathyroidal iodine stores stimulate growth. On the other hand, the role of iodine, if any, in regulating the growth of human nodular goitres exposed to an ample supply of iodine has not been studied systematically. Very few data on intrathyroidal iodine concentration in this type of goitre are available. In the present work we have investigated total iodine content in 24 samples from 11 clinically and histomorphologically well-defined fast and autonomously growing human nodular goitres from a non-endemic area. Iodine was fractionated into thyroglobulin-iodine and non-thyroglobulin-iodine. The regional distribution of intrathyroidal iodo-compounds was also assessed in three goitres. Total iodine concentration, as well as its sub-fractions, i.e. thyroglobulin-iodine and non-thyroglobulin-iodine, were significantly lower than in normal thyroids. Furthermore, there was large inter- and intraindividual heterogeneity of all iodo-compounds as well as of thyroglobulin. Total iodine concentration varied by a factor of almost 40 between different goitre samples and by a factor of 20 between samples taken from the same goitre. Total non-thyroglobulin-iodine, the only fraction comprising possible cell growth-regulating iodo-compounds, varied by a factor of > 60 between different goitres and by a factor of > 6 between different samples of the same goitre. The low iodine concentration in all our goitre samples did not differ from values reported in the literature for endemic iodine-deficient goitres. Since all goitres studied here were actively growing while exposed to an ample supply of iodine, iodine shortage cannot be a primary and causal factor for the growth of this type of sporadic goitre. Rather, the low concentration and the large inter- and intraindividual heterogeneity of all iodo-compounds appear to be secondary incidental events well explained by the recently developed concept of autonomous thyroid growth.
碘可能对甲状腺滤泡细胞生长具有抑制作用,在某些情况下也有刺激作用。外源性碘缺乏会导致地方性甲状腺肿的生长,并且有人声称甲状腺内碘储备低会刺激生长。另一方面,碘在调节摄入充足碘的人类结节性甲状腺肿生长中(若有作用)的作用尚未得到系统研究。关于此类甲状腺肿中甲状腺内碘浓度的数据非常少。在本研究中,我们调查了来自非地方性地区的11个临床和组织形态学明确的快速生长和自主生长的人类结节性甲状腺肿的24个样本中的总碘含量。碘被分为甲状腺球蛋白结合碘和非甲状腺球蛋白结合碘。还评估了三个甲状腺肿中甲状腺内碘化合物的区域分布。总碘浓度及其亚组分,即甲状腺球蛋白结合碘和非甲状腺球蛋白结合碘,均显著低于正常甲状腺。此外,所有碘化合物以及甲状腺球蛋白在个体间和个体内均存在很大的异质性。不同甲状腺肿样本之间的总碘浓度相差近40倍,同一甲状腺肿不同样本之间相差20倍。总非甲状腺球蛋白结合碘是唯一可能包含调节细胞生长的碘化合物的组分,不同甲状腺肿之间相差>60倍,同一甲状腺肿不同样本之间相差>6倍。我们所有甲状腺肿样本中的低碘浓度与文献中报道的地方性碘缺乏性甲状腺肿的值没有差异。由于这里研究的所有甲状腺肿在摄入充足碘的情况下均处于活跃生长状态,碘缺乏不可能是这种散发性甲状腺肿生长的主要和因果因素。相反,所有碘化合物的低浓度以及个体间和个体内的巨大异质性似乎是由最近提出的自主甲状腺生长概念很好解释的继发性偶然事件。