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环境碘摄入量会影响非恶性甲状腺疾病的类型。

Environmental iodine intake affects the type of nonmalignant thyroid disease.

作者信息

Laurberg P, Bülow Pedersen I, Knudsen N, Ovesen L, Andersen S

机构信息

Department of Endocrinology and Medicine, Aalborg Hospital, Denmark.

出版信息

Thyroid. 2001 May;11(5):457-69. doi: 10.1089/105072501300176417.

DOI:10.1089/105072501300176417
PMID:11396704
Abstract

The relationship between the iodine intake level of a population and the occurrence of thyroid diseases is U-shaped with an increase in risk from both low and high iodine intakes. Developmental brain disorders and endemic goiter caused by severe iodine deficiency may seriously deteriorate overall health status and economic performance of a population. Severe iodine deficiency with a median 24-hour urinary iodine excretion of the population below 25 microg needs immediate attention and correction. Less severe iodine deficiency with median urinary iodine excretion below 120 microg per 24 hours is associated with multinodular autonomous growth and function of the thyroid gland leading to goiter and hyperthyroidism in middle aged and elderly subjects. The lower the iodine intake, the earlier and more prominent are the abnormalities. At the other end of the spectrum, severely excessive iodine intake starting at median urinary iodine excretion levels around 800 microg per 24 hours is associated with a higher prevalence of thyroid hypofunction and goiter in children. A number of studies indicate that moderate and mild iodine excess (median urinary iodine >220 microg per 24 hours) are associated with a more frequent occurrence of hypothyroidism, especially in elderly subjects. The exact mechanism leading to this has not been clarified, and more studies are needed to define the limits of excessive iodine intake precisely. Due to the frequent occurrence of thyroid disorders, proper monitoring and control of the population iodine intake level is a cost-effective alternative to diagnosing, therapy and control of the many individual cases of thyroid diseases that might have been prevented.

摘要

人群碘摄入量与甲状腺疾病发生之间的关系呈U形,碘摄入量过低或过高都会增加患病风险。严重碘缺乏导致的发育性脑障碍和地方性甲状腺肿可能会严重恶化人群的整体健康状况和经济表现。当人群24小时尿碘排泄中位数低于25微克时,严重碘缺乏需要立即引起关注并加以纠正。尿碘排泄中位数低于每24小时120微克的轻度碘缺乏与甲状腺多结节自主性生长和功能有关,会导致中老年人群患甲状腺肿和甲状腺功能亢进。碘摄入量越低,异常情况出现得越早且越明显。在另一个极端,当尿碘排泄中位数水平开始达到每24小时约800微克时,严重碘摄入过量与儿童甲状腺功能减退和甲状腺肿的较高患病率相关。多项研究表明,中度和轻度碘过量(尿碘中位数>每24小时220微克)与甲状腺功能减退的更频繁发生有关,尤其是在老年人群中。导致这种情况的确切机制尚未阐明,需要更多研究来精确界定碘摄入过量的界限。由于甲状腺疾病频繁发生,对人群碘摄入水平进行适当监测和控制是一种具有成本效益的替代方法,可替代对许多可能已预防的甲状腺疾病个体病例进行诊断、治疗和控制。

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