Tsatsoulis Agathocles
Department of Endocrinology, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece.
J Clin Med. 2018 Feb 26;7(3):37. doi: 10.3390/jcm7030037.
Thyroid follicular cells, as well as adrenocortical cells, are endowed by an intrinsic heterogeneity regarding their growth potential, in response to various stimuli. This heterogeneity appears to constitute the underlying cause for the focal cell hyperplasia and eventually the formation of thyroid and adrenal nodules, under the influence of growth stimulatory factors. Among the main stimulatory factors are the pituitary tropic hormones, thyroid-stimulating hormone (TSH) or thyrotropin and adrenocorticotropic hormone (ACTH), which regulate the growth and function of their respective target cells, and the insulin/insulin-like growth factor system, that, through its mitogenic effects, can stimulate the proliferation of these cells. The predominance of one or the other of these growth stimulatory factors appears to determine the natural history of thyroid and adrenal nodular disease. Thus, iodine deficiency was, in the past, the main pathogenic factor responsible, through a transient rise in TSH secretion, for the endemic nodular goiter with the characteristic colloid thyroid nodules among the inhabitants in iodine deficient areas. The correction of iodine deficiency was followed by the elimination of endemic colloid goiter and the emergence of thyroid autoimmunity. The recent epidemic of obesity and metabolic syndrome (MS), or insulin resistance syndrome, has been associated with the re-emergence of nodular thyroid disease. A parallel rise in the incidence of benign, nonfunctional adrenocortical tumors, known as adrenal incidentalomas, has also been reported in association with the manifestations of the MS. It is likely that the compensatory to insulin resistance hyperinsulinemia may be responsible for the rising trend of thyroid and adrenal nodular disease in the current environment.
甲状腺滤泡细胞以及肾上腺皮质细胞在生长潜力方面具有内在异质性，以响应各种刺激。在生长刺激因子的影响下，这种异质性似乎构成了局灶性细胞增生以及最终形成甲状腺和肾上腺结节的根本原因。主要的刺激因子包括垂体促激素，即甲状腺刺激激素（TSH）或促甲状腺激素以及促肾上腺皮质激素（ACTH），它们调节各自靶细胞的生长和功能；还有胰岛素/胰岛素样生长因子系统，该系统通过其促有丝分裂作用可刺激这些细胞的增殖。这些生长刺激因子中一种或另一种的优势似乎决定了甲状腺和肾上腺结节性疾病的自然病程。因此，过去碘缺乏是主要的致病因素，它通过促甲状腺激素分泌的短暂增加，导致碘缺乏地区居民出现具有特征性胶样甲状腺结节的地方性结节性甲状腺肿。碘缺乏得到纠正后，地方性胶样甲状腺肿消失，甲状腺自身免疫性疾病出现。最近肥胖和代谢综合征（MS）或胰岛素抵抗综合征的流行与结节性甲状腺疾病的再次出现有关。据报道，良性、无功能的肾上腺皮质肿瘤（称为肾上腺偶发瘤）的发病率也与MS的表现同时出现上升。在当前环境下，对胰岛素抵抗的代偿性高胰岛素血症可能是甲状腺和肾上腺结节性疾病上升趋势的原因。
