Hesch R D
Klin Wochenschr. 1984 Nov 15;62(22):1059-73. doi: 10.1007/BF01711375.
In an attempt to derive diagnostic concepts for thyroid diseases we present pathophysiological models for the prevalent thyroid disorders. 'Euthyroid goiter' is a disease mainly caused by iodine deficiency but an additional immunopathogenesis was recently proposed. The 'immunthyropathy' is the thyroid disease with orbitopathy and other extraglandular immunological manifestations. A complete model of the immunological phenomena which begin with a tolerance defect is given, and both the T-cell, and B-cell-mediated pathways are detailed. The complex interaction of immunoglobulins at the thyroid-stimulating hormone receptor and their dependency on human leukocyte antigen loci are presented. The peripheral metabolism depends ultimately upon a prevalence of thyroid gland stimulation (thyrotoxicosis) or glandular destruction (hypothyroidism) and this is true for overt thyroid disease under antithyroid drug therapy or any other therapy. Euthyroidism during 'immunethyropathy' is presented as an equilibrium between thyroid stimulation and destruction. This concept allows an exact description of the thyroid disease and the resulting clinical situation provided that established laboratory tests are used as suggested by the model. 'Disseminated thyroid autonomy and autononous thyroid adenoma' develops during goitrous thyroid disease as a consequence of uncoupling of thyroid cellular growth stimulation, iodine utilization, and thyroid hormone synthesis. The polyclonal origin seems more frequent than monoclonal foci. The size of autononous tissue and individual iodine supply determines the endocrine function in this disease. The TRH test monitors with great sensitivity subtle increases in T4 or T3 production and indicates critical clinical situations earlier than the scintiscan.(ABSTRACT TRUNCATED AT 250 WORDS)
为了推导甲状腺疾病的诊断概念,我们提出了常见甲状腺疾病的病理生理模型。“甲状腺肿”是一种主要由碘缺乏引起的疾病,但最近有人提出了另一种免疫发病机制。“免疫性甲状腺病”是伴有眼眶病和其他腺外免疫表现的甲状腺疾病。给出了一个从耐受性缺陷开始的免疫现象的完整模型,并详细阐述了T细胞和B细胞介导的途径。介绍了免疫球蛋白在促甲状腺激素受体处的复杂相互作用及其对人类白细胞抗原位点的依赖性。外周代谢最终取决于甲状腺刺激(甲状腺毒症)或腺体破坏(甲状腺功能减退)的普遍程度,这对于接受抗甲状腺药物治疗或任何其他治疗的显性甲状腺疾病来说都是如此。“免疫性甲状腺病”期间的甲状腺功能正常表现为甲状腺刺激与破坏之间的平衡。只要按照模型建议使用既定的实验室检查,这一概念就能准确描述甲状腺疾病及其导致的临床情况。“弥漫性甲状腺自主性和自主性甲状腺腺瘤”在甲状腺肿性甲状腺疾病期间由于甲状腺细胞生长刺激、碘利用和甲状腺激素合成的解偶联而发展。多克隆起源似乎比单克隆病灶更为常见。自主性组织的大小和个体碘供应决定了这种疾病的内分泌功能。促甲状腺激素释放激素试验能高度灵敏地监测T4或T3产生的细微增加,并比闪烁扫描更早地指示危急临床情况。(摘要截短于250字)