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[碘反应性自身免疫性甲状腺疾病]

[Iodine responsive autoimmune thyroid diseases].

作者信息

Yamada T, Sato A

机构信息

Department of Medicine Kashiwa City Hospital.

出版信息

Nihon Rinsho. 1999 Aug;57(8):1788-93.

Abstract

Iodine is an important element for the thyroid and regulates iodine accumulation, thyroid hormone synthesis and hormone release. As a result, dietary iodine deficiency is largely responsible for the production of T3 thyrotoxicosis. Supplemental iodine significantly elevated incidence of iodine induced hyperthyroidism in endemic goiter area. Even in normal iodine area, intake of iodine sometimes accelerates recurrence of hyperthyroid Graves' disease in antithyroid drug treated patients. In contrast, a possible role of iodine on Hashimoto's thyroiditis is not known. As a therapeutic means, excess iodide is used for rapid control of thyrotoxicosis and thyrotoxic crisis. Experimental studies indicated that excess iodide blocks thyroid hormone release by inhibiting thyroid stimulators. This blocking action is ascertained by measuring cAMP, colloid droplets formation and microscopic techniques. Excess iodide does induce hypothyroidism in Hashimoto's thyroiditis.

摘要

碘是甲状腺的重要元素,可调节碘的积累、甲状腺激素的合成及激素释放。因此,饮食中碘缺乏在很大程度上是导致T3甲状腺毒症产生的原因。在地方性甲状腺肿地区,补充碘会显著提高碘诱发的甲状腺功能亢进的发生率。即使在碘正常的地区,摄入碘有时也会加速接受抗甲状腺药物治疗的甲状腺功能亢进Graves病患者的复发。相比之下,碘在桥本甲状腺炎中可能发挥的作用尚不清楚。作为一种治疗手段,过量碘化物用于快速控制甲状腺毒症和甲状腺危象。实验研究表明,过量碘化物通过抑制甲状腺刺激物来阻止甲状腺激素释放。这种阻断作用可通过测量环磷酸腺苷、胶体小滴形成及显微镜技术来确定。过量碘化物确实会在桥本甲状腺炎中诱发甲状腺功能减退。

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