Goichot B, Sapin R, Schlienger J L
Service de médecine interne, hôpital de Hautepierre, Strasbourg, France.
Rev Med Interne. 1998 Sep;19(9):640-8. doi: 10.1016/s0248-8663(99)80043-5.
Patients with nonthyroidal disease frequently exhibit abnormal thyroid function tests; this is referred to as euthyroid sick syndrome. The clinical significance of this syndrome is unknown: abnormal endocrine reaction with reduced triiodothyronine (T3) at the tissue level, or adaptation to stress protecting the body against exaggerated catabolism.
Recent advances in the underlying mechanisms concern the role of deiodinase and of the transport of thyroid hormone in tissues. Various factors acting on deiodinase or on transport system, such as medications and nutritional factors, have been implicated. Considerable interest has raised concerning the role of cytokines. Some cytokines may act at every level of the thyrotropic axis, but their real action in vivo remains unclear. Nutritional factors have a great impact on thyroid hormone metabolism, but the mechanism of the decrease in T3 induced by starvation is not identified. The role of the decrease in type I hepatic deiodinase has been recently challenged.
Despite its complexity, euthyroid sick syndrome is a model for the study of thyroid hormone metabolism regulation. Characterisation of the thyroid hormone transport proteins will lead to significant advances in the understanding of the syndrome.
非甲状腺疾病患者常出现甲状腺功能检查异常；这被称为正常甲状腺病态综合征。该综合征的临床意义尚不清楚：是组织水平上三碘甲状腺原氨酸（T3）降低的异常内分泌反应，还是为保护身体免受过度分解代谢而对压力的适应性反应。
潜在机制的最新进展涉及脱碘酶的作用以及甲状腺激素在组织中的转运。已经发现了各种作用于脱碘酶或转运系统的因素，如药物和营养因素。细胞因子的作用引起了相当大的关注。一些细胞因子可能在促甲状腺轴的各个水平起作用，但其在体内的实际作用仍不清楚。营养因素对甲状腺激素代谢有很大影响，但饥饿导致T3降低的机制尚未明确。最近，I型肝脱碘酶降低的作用受到了挑战。
尽管正常甲状腺病态综合征很复杂，但它是研究甲状腺激素代谢调节的一个模型。甲状腺激素转运蛋白的特性将有助于在理解该综合征方面取得重大进展。
