Derwahl M
Medizinische Universitätsklinik Bergmannsheil, Ruhr-Universität, Bochum.
Schweiz Med Wochenschr. 1994 Sep 17;124(37):1613-8.
Recent advances in thyroid research are reviewed which reflect fundamental changes in understanding of the pathogenesis of thyroid adenomas, and of clonal and polyclonal goiter nodules. It is generally accepted that chronic iodine deficiency leads to the development of a diffuse homogeneous goiter. However, low iodine supply does not explain generation and growth of thyroid nodules and the characteristic functional heterogeneity of most nodular goiters. Molecular analyses of recent years have revealed that thyroid adenomas and most nodules in goiters, even if morphologically heterogeneous, are clonal and thus true benign tumors. This has been demonstrated in areas both with iodine deficiency and with sufficient iodine supply. However, in areas with iodine deficiency, chronic stimulation accelerates the genesis of nodules and adenomas. The molecular pathogenesis of these tumors is still unknown. Only in a subgroup of toxic adenomas mutations of the TSH receptor and the Gs-alpha gene have recently been found that may explain the genesis of these tumors and the development of hyperthyroidism in patients with these adenomas.
本文综述了甲状腺研究的最新进展，这些进展反映了对甲状腺腺瘤、克隆性和多克隆性甲状腺肿结节发病机制理解的根本变化。人们普遍认为，慢性碘缺乏会导致弥漫性均匀性甲状腺肿的发生。然而，低碘供应并不能解释甲状腺结节的产生和生长以及大多数结节性甲状腺肿的特征性功能异质性。近年来的分子分析表明，甲状腺腺瘤和甲状腺肿中的大多数结节，即使在形态上具有异质性，也是克隆性的，因此是真正的良性肿瘤。这在碘缺乏地区和碘供应充足的地区均已得到证实。然而，在碘缺乏地区，慢性刺激会加速结节和腺瘤的发生。这些肿瘤的分子发病机制仍然未知。最近仅在一小部分毒性腺瘤中发现了促甲状腺激素受体和Gs-α基因的突变，这可能解释了这些肿瘤的发生以及患有这些腺瘤的患者甲状腺功能亢进的发展。
