Palaniappan Srinivasan, Shanmughavelu Lakshmi, Prasad Hemchand K, Subramaniam Sundari, Krishnamoorthy Nedunchezian, Lakkappa Lakshmi
Department of Pediatric Intensive Care, Sri Ramachandra Medical College, Chennai, Tamil Nadu, India.
Departent of Pediatrics, Stanley Medical College, Chennai, Tamil Nadu, India.
Indian J Endocrinol Metab. 2017 Jan-Feb;21(1):85-89. doi: 10.4103/2230-8210.195996.
The objective of this study is to evaluate the link between excess iodine intake as evidenced by increased urinary iodine excretion (UIE) and autoimmune thyroiditis in children and to assess the correlation between UIE and thyroid microsomal antibody (thyroid peroxidase [TPO]) titers in children.
All children with goiter between age group 6 and 12 years, were subjected to blood tests for free thyroxine, thyroid stimulating hormone, and TPO antibody, fine needle aspiration was advised for all children with goiter. Forty-three children with confirmed autoimmune thyroiditis served as cases, and 43 children with euthyroid goiter with workup negative for autoimmune thyroiditis and iodine deficiency were enrolled as controls. UIE was estimated in spot urine sample for both cases and controls. The levels of urinary iodine were compared between cases and controls.
The levels of urinary iodine were significantly higher in children with autoimmune thyroiditis as compared with control. There was a positive correlation between UIE and antimicrosomal antibody titers among cases. Among cases 65% children had subclinical hypothyroidism, 27.9% had overt hypothyroidism and 7% of cases, and 100% of controls had euthyroid functional status. Excessive (≥300 μg/L) UIE was strongly associated with autoimmune thyroiditis. If the UIE level is ≥ 300 μg/L, then there is 17.94 times higher chance of having amiodarone-induced thyrotoxicosis than those who have UIE level < 300 μg/L ( < 0.001).
A possible association between increased iodine intake and autoimmune thyroiditis was found in this study. Excessive iodine intake may trigger thyroid autoimmunity and eventually thyroid hypofunction.
本研究旨在评估儿童尿碘排泄量增加所证明的碘摄入过量与自身免疫性甲状腺炎之间的联系,并评估儿童尿碘排泄量与甲状腺微粒体抗体(甲状腺过氧化物酶 [TPO])滴度之间的相关性。
所有6至12岁患有甲状腺肿的儿童均接受了游离甲状腺素、促甲状腺激素和TPO抗体的血液检测,建议所有患有甲状腺肿的儿童进行细针穿刺活检。43例确诊为自身免疫性甲状腺炎的儿童作为病例组,43例甲状腺功能正常的甲状腺肿儿童,其自身免疫性甲状腺炎和碘缺乏检查结果为阴性,作为对照组。对病例组和对照组的随机尿样进行尿碘排泄量评估。比较病例组和对照组的尿碘水平。
与对照组相比,自身免疫性甲状腺炎儿童的尿碘水平显著更高。病例组中尿碘排泄量与抗微粒体抗体滴度呈正相关。病例组中65%的儿童患有亚临床甲状腺功能减退,27.9%的儿童患有显性甲状腺功能减退,7%的病例以及100%的对照组甲状腺功能正常。尿碘排泄量过高(≥300μg/L)与自身免疫性甲状腺炎密切相关。如果尿碘排泄量水平≥300μg/L,那么发生胺碘酮所致甲状腺毒症的几率比尿碘排泄量水平<300μg/L的人高17.94倍(<0.001)。
本研究发现碘摄入量增加与自身免疫性甲状腺炎之间可能存在关联。碘摄入过量可能引发甲状腺自身免疫,最终导致甲状腺功能减退。