Berg V, Nøst T H, Skeie G, Thomassen Y, Berlinger B, Veyhe A S, Jorde R, Odland J Ø, Hansen S
Department of Laboratory Medicine, Diagnostic Clinic, University Hospital of North Norway, Tromsø, Norway.
Department of Community Medicine, UiT, The Arctic University of Norway, Tromsø, Norway.
Eur J Clin Nutr. 2017 Aug;71(8):1002-1007. doi: 10.1038/ejcn.2017.83. Epub 2017 May 24.
BACKGROUND/OBJECTIVES: Iodine deficiency during pregnancy may influence maternal and foetal thyroid function with the risk of causing neurocognitive and psychomotor deficits in the offspring. The objective of this study was to assess iodine status in pregnant women from Northern Norway and to investigate the influence of iodine status on maternal and infant thyroid function.
SUBJECTS/METHODS: Women from the Northern Norway Mother-and-Child contaminant Cohort Study (MISA) donated a blood and urine sample at three visits during their pregnancy and postpartum period (in second trimester, 3 days and 6 weeks after delivery. N=197). Women were assigned to iodine status groups according to urine iodine concentrations (UICs) in second trimester and mixed effects linear models were used to investigate potential associations between iodine status and repeated measurements of thyroid-stimulating hormone (TSH), thyroid hormones (THs), TH-binding proteins and thyroid peroxidase antibodies. Associations between maternal iodine status and TSH in heel prick samples from the infants were investigated with linear regression.
Median UIC in second trimester was 84 μg/l (range 18-522) and 80% had UIC below recommended level (<150 μg/l). Iodine-deficient women had higher concentrations of T3, FT3 and FT4 (estimated differences (confidence intervals) of 0.10 nmol/l (0.01, 0.17), 0.16 pmol/l (0.05, 0.26) and 0.45 pmol/l (0.10, 0.78), respectively) compared with iodine-sufficient women. The concentrations varied within normal reference ranges, but the majority of women with subclinical hypothyroidism were iodine deficient. Maternal iodine status did not influence infant TSH concentrations.
This study indicate iodine deficiency among pregnant women in Norway. Iodine status during pregnancy influences maternal thyroid homeostasis and is therefore a risk factor for foetal and infant development.
背景/目的:孕期碘缺乏可能影响母体和胎儿的甲状腺功能,有导致后代神经认知和精神运动发育缺陷的风险。本研究的目的是评估挪威北部孕妇的碘状况,并调查碘状况对母体和婴儿甲状腺功能的影响。
对象/方法:来自挪威北部母婴污染物队列研究(MISA)的女性在孕期和产后的三次访视时(孕中期、分娩后3天和6周)捐赠了血液和尿液样本(N = 197)。根据孕中期的尿碘浓度(UIC)将女性分为碘状况组,并使用混合效应线性模型研究碘状况与促甲状腺激素(TSH)、甲状腺激素(THs)、TH结合蛋白和甲状腺过氧化物酶抗体重复测量值之间的潜在关联。通过线性回归研究母体碘状况与婴儿足跟血样本中TSH之间的关联。
孕中期UIC的中位数为84μg/l(范围18 - 522),80%的孕妇UIC低于推荐水平(<150μg/l)。与碘充足的女性相比,碘缺乏的女性T3、FT3和FT4浓度更高(估计差异(置信区间)分别为0.10nmol/l(0.01,0.17)、0.16pmol/l(0.05,0.26)和0.45pmol/l(0.10,0.78))。这些浓度在正常参考范围内变化,但大多数亚临床甲状腺功能减退的女性碘缺乏。母体碘状况不影响婴儿TSH浓度。
本研究表明挪威孕妇存在碘缺乏。孕期碘状况影响母体甲状腺内环境稳定,因此是胎儿和婴儿发育的一个风险因素。