Section of Endocrinology, Diabetes, and Nutrition, Boston University Medical Center, 88 East Newton Street, Evans 201, Boston, MA 02118, USA.
J Clin Endocrinol Metab. 2010 Jul;95(7):3207-15. doi: 10.1210/jc.2010-0014. Epub 2010 Apr 28.
Thyroid hormone, requiring adequate maternal iodine intake, is critical for fetal neurodevelopment. Perchlorate decreases thyroidal iodine uptake by competitively inhibiting the sodium/iodide symporter. It is unclear whether environmental perchlorate exposure adversely affects thyroid function in pregnant women. Thiocyanate, derived from foods and cigarette smoke, is a less potent competitive sodium/iodide symporter inhibitor than perchlorate.
Our objective was to determine whether environmental perchlorate and/or thiocyanate exposure is associated with alterations in thyroid function in pregnancy.
We conducted a cross-sectional study at health centers in Cardiff, Wales, and Turin, Italy.
During 2002-2006, 22,000 women at less than 16 wk gestation were enrolled in the Controlled Antenatal Thyroid Screening Study. Subsets of 261 hypothyroid/hypothyroxinemic and 526 euthyroid women from Turin and 374 hypothyroid/hypothyroxinemic and 480 euthyroid women from Cardiff were selected based on availability of stored urine samples and thyroid function data.
Urinary iodine, thiocyanate, and perchlorate and serum TSH, free T(4) (FT(4)), and thyroperoxidase antibody were measured.
Urinary iodine was low: median 98 microg/liter in Cardiff and 52 microg/liter in Turin. Urine perchlorate was detectable in all women. The median (range) urinary perchlorate concentration was 5 microg/liter (0.04-168 microg/liter) in Turin and 2 microg/liter (0.02-368 microg/liter) in Cardiff. There were no associations between urine perchlorate concentrations and serum TSH or FT(4) in the individual euthyroid or hypothyroid/hypothyroxinemic cohorts. In multivariable linear analyses, log perchlorate was not a predictor of serum FT(4) or TSH.
Low-level perchlorate exposure is ubiquitous but did not affect thyroid function in this cohort of iodine-deficient pregnant women.
甲状腺激素需要足够的母体碘摄入,对胎儿的神经发育至关重要。高氯酸盐通过竞争性抑制钠/碘转运体来减少甲状腺中的碘摄取。目前尚不清楚环境中高氯酸盐的暴露是否会对孕妇的甲状腺功能产生不良影响。硫氰酸盐来自食物和香烟烟雾,是一种比高氯酸盐效力稍低的竞争性钠/碘转运体抑制剂。
我们旨在确定环境中高氯酸盐和/或硫氰酸盐的暴露是否与妊娠期间甲状腺功能的改变有关。
我们在威尔士加的夫和意大利都灵的健康中心进行了一项横断面研究。
在 2002 年至 2006 年期间,有 22000 名妊娠不到 16 周的妇女参加了对照产前甲状腺筛查研究。根据储存的尿液样本和甲状腺功能数据的可用性,从都灵选择了 261 名甲状腺功能减退/甲状腺素血症和 526 名甲状腺功能正常的妇女亚组,从加的夫选择了 374 名甲状腺功能减退/甲状腺素血症和 480 名甲状腺功能正常的妇女亚组。
检测尿碘、硫氰酸盐和高氯酸盐以及血清促甲状腺激素、游离 T4(FT4)和甲状腺过氧化物酶抗体。
尿碘水平较低:加的夫中位数为 98μg/L,都灵中位数为 52μg/L。所有妇女的尿高氯酸盐均可检测到。都灵中位数(范围)尿高氯酸盐浓度为 5μg/L(0.04-168μg/L),加的夫中位数为 2μg/L(0.02-368μg/L)。在单独的甲状腺功能正常或甲状腺功能减退/甲状腺素血症患者队列中,尿高氯酸盐浓度与血清 TSH 或 FT4 之间均无关联。在多变量线性分析中,高氯酸盐的对数与血清 FT4 或 TSH 无关。
低水平的高氯酸盐暴露普遍存在,但并未影响碘缺乏的这一孕妇队列的甲状腺功能。