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生理性黄疸持续患者的“母婴”碘状态

"Maternal/Neonatal" iodine status in patients with prolonged physiological jaundice.

作者信息

Siklar Z, Oçal G, Bilir P, Ergur A, Berberoğlu M

机构信息

Department of Pediatric Endocrinology, Ankara University School of Medicine, Ankara, Turkey.

出版信息

Exp Clin Endocrinol Diabetes. 2009 Jul;117(7):312-5. doi: 10.1055/s-0028-1086001. Epub 2008 Sep 30.

DOI:10.1055/s-0028-1086001
PMID:19085704
Abstract

BACKGROUND

The increasing knowledge indicated that borderline hypothyroidism may cause neurodevelopmental disorders. Borderline compensated congenital hypothyroidism could caused by iodine deficiency or iodine overload. One of the most important etiological factors causing prolonged jaundice in the neonatal period is congenital hypothyroidism. Aimed of this study is to investigate the frequency of borderline or overt hypothyroidism in a group of newborn with prolonged physiological jaundice, and to evaluate iodine status of these babies and their mothers.

METHODS

Fifty-five apparently healthy newborn were evaluated. Twenty-five of them showed borderline thyroid dysfunctions. Remained 30 babies had normal thyroid function, considered as euthyroid group. Iodine status was evaluated by measuring urinary iodine excretion.

RESULTS

According to UIE, maternal iodine deficiency (55%) associated with neonatal iodine overload (65%) had came to attention. Although mean urinary iodine levels in both mother groups were similar, the mean urinary levels of borderline hypothyroidic and euthyroid groups were 432+/-129 microg/l and 271.5+/-137 microg/l, respectively. Iodine overload was also presence in newborn with normal thyroid function tests.

CONCLUSION

We considered that individual sensitivity to iodine overload could make the differentiation on thyroid function. Iodine overload in important degree seen in borderline hypothyroidic babies emphasize the harmful effect of topical antiseptic iodine application that given to mothers during labor. This application could also mask possible prenatal iodine deficiency.

摘要

背景

越来越多的知识表明,亚临床甲状腺功能减退可能导致神经发育障碍。亚临床代偿性先天性甲状腺功能减退可能由碘缺乏或碘过载引起。先天性甲状腺功能减退是新生儿期导致黄疸持续时间延长的最重要病因之一。本研究旨在调查一组生理性黄疸持续时间延长的新生儿中亚临床或显性甲状腺功能减退的发生率,并评估这些婴儿及其母亲的碘状态。

方法

对55名看似健康的新生儿进行评估。其中25名显示亚临床甲状腺功能障碍。其余30名婴儿甲状腺功能正常,被视为甲状腺功能正常组。通过测量尿碘排泄来评估碘状态。

结果

根据尿碘排泄情况,母亲碘缺乏(55%)与新生儿碘过载(65%)引起了关注。虽然两组母亲的平均尿碘水平相似,但亚临床甲状腺功能减退组和甲状腺功能正常组的平均尿碘水平分别为432±129微克/升和271.5±137微克/升。甲状腺功能测试正常的新生儿中也存在碘过载情况。

结论

我们认为个体对碘过载的敏感性可能会导致甲状腺功能的差异。在亚临床甲状腺功能减退婴儿中明显存在的碘过载强调了分娩期间给母亲使用局部消毒碘的有害影响。这种应用也可能掩盖产前可能存在的碘缺乏。

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