内分泌
词汇介绍
拓展阅读
解析
thyroid 英 /'θaɪrɒɪd/ 美 /'θaɪrɔɪd/
释 义 n. 甲状腺;甲状软骨;甲状腺剂
adj. 甲状腺的;盾状的
例 句 Located near the base of the neck, the thyroid is a large endocrine gland that produces hormones that help control growth and metabolism. 甲状腺位于颈部的底部附近,是一个很大的内分泌腺体,它产生激素,协助控制生长和新陈代谢。
stimulating 英 /'stɪmjʊleɪtɪŋ/ 美 /'stɪmjuletɪŋ/
释 义 adj. 刺激的;有刺激性的
v. 刺激;激励;促进(stimulate的ing形式)
例 句 This hints that the vagus nerve is involved because it is responsible for stimulating the throat and neck muscles. 这暗示着振奋情绪牵扯到交感神经,因为交感神经负责刺激咽喉和脖颈肌肉。
hormone 英/'hɔːməʊn/ 美 /'hɔrmon/
释 义 n. [生理] 激素,荷尔蒙
例 句 But the hormone has its drawbacks. 但荷尔蒙也有它的缺点。
概述
概述
促甲状腺激素是一种垂体激素,刺激甲状腺产生甲状腺素,然后是三碘甲状腺原氨酸,刺激体内几乎所有组织的新陈代谢。它是由垂体前叶中的甲状腺细胞产生的糖蛋白激素,调节甲状腺的内分泌功能。
血液检查
TSH血液测试是评估甲状腺症状和/或功能的首选测试。它经常在T4测试之前或与T4测试一起。
正常范围
2003年,美国临床内分泌学家协会(AACE)发布了一份新闻稿,以更新TSH正常值的变化。从0.5 mI/L到5.0 mI/L的范围,它们将目标TSH水平范围缩小到0.3 mI/L到3.0 mI/L。但是,许多传统医生仍然没有意识到这个新的更新,并坚持旧的范围。
TSH值的意义
正常TSH:成人中正常的TSH激素水平范围为0.5 mI/L至5.0 mI/L,这表明来自脑下垂体的信号与甲状腺的活动相符。医生可能会根据TSH水平,以确定是否有其他问题需要关注。
低TSH:甲状腺功能亢进,脑垂体受损,无法释放TSH(继发性甲状腺功能减退症)。
高TSH:甲状腺功能减退症,由于垂体中的肿瘤导致TSH产生过多(罕见)。
无论是低还是高,都应该及时解决超出正常范围的TSH结果。为了进一步调查,还需要进行额外的测试以确定异常值的原因。
母亲和脐带血中全氟烷基物质暴露与甲状腺激素/甲状腺抗体水平的相关性: 北海道研究
发表时间:2019-09-10
影响指数:7.9
作者: Sachiko Itoh
期刊:Environ Int
In maternal TH analysis, current study found that significant positive associations between PFASs and FT3 in both TA groups. On the contrary to the postulation, our result did not find that TA-positive mothers were more susceptible than TA-negative mothers. Reardon et al. (2019) suggested the susceptibility for PFAS effect on THs in TA-positive mothers might be different depending on the gestational stage. The timing of blood collection for TH measurements may be an important factor, since circulating TH levels during pregnancy change dramatically during gestational weeks (Webster et al., 2014; between gestational weeks 15–18, Preston et al., 2018; median, 9.6 weeks of gestation, and current study; 11.35 weeks of gestation). Fetal thyroid glands begin to secrete hormones after the second trimester of gestation (de Escobar et al., 2004; Obregon et al., 2007). During early pregnancy, fetuses rely on maternal THs, and the disruption of maternal TH homeostasis can affect both maternal and fetal health. Deficiencies or imbalances in maternal THs likely disrupt the normal neurological development of fetuses; therefore, we investigated the effect of maternal THs on fetuses in their early gestational stages. The current analyses of the associations between maternal PFAS levels and maternal THs were designed as a cross-sectional study. PFASs have long half elimination time as reported in Olsen et al. (2007). Therefore, we believe that PFAS levels at later gestational stage could also reflect the PFAS levels at early gestational stage. Additionally, we included TgAb-positive mothers in TA-positive group, while previous studies measured only TPOAb. We included TgAb-positive women because TgAb status was considered to be important as effect modifier to explore “multiple hit hypothesis”. Unfortunately, we are unable to further speculate the differences as those previous studies did not measure TgAb. Webster et al. (2016) reported the joint effect of high TPOAb and low iodine exposure in the PFAS-TH relationships. Other factors should be considered as one of the effect modifier as well as TA status in the further study. There are some potential mechanisms of thyroid disruption by PFAS; competitive binding to TH binding proteins (Weiss et al., 2009) and the change of hepatic clearance (Yu et al., 2009), leading to decrease of T4 and Possible mechanism of the positive association between PFAS and FT3 have been proposed to be the up-regulation of the deiodinase enzyme which converts T4 to T3 (Yu et al., 2009). In our study, PFHxS associated with higher FT3 with and higher FT4 (p < 0.010), while PFNA associated with higher FT3 and lower FT4 (not significant). The current results suggest the possibility of different mechanism between PFHxS and PFNA, and different susceptibility between TA-positive and negative group. Regarding neonatal TH analysis, Kim et al. (2011) found a negative correlation between maternal PFOS and fetal total T3, and between maternal PFTrDA and total T3 and T4 levels in fetuses; moreover, maternal PFOA positively correlated with fetal TSH among 44 South Korean participants. A Dutch study (n = 83) found that a high level of PFOA in cord blood was associated with increased total T4 levels in heel prick blood among girls (de Cock et al., 2014). Furthermore, we previously reported the positive association between maternal PFOS and boy's heel prick TSH (Kato et al., 2016), which was also seen among all boys in the current study. Current results support the hypothesis that maternal PFAS exposure disrupt neonatal TH levels as shown in previous studies, though our results cannot be compared directly to others because previous studies did not take stratification of maternal TA status into account as mentioned above. In addition, current study suggests that maternal TA status might affect neonatal susceptibility of TH disruption; in particular, p-interaction was significant in the associations between maternal PFTrDA and girl's FT3 shown in Table 6. However, the directions of B in linear regression analysis are almost the same between in TA-positive and TA-negative group (Supplemental Tables 4 and 5). Ultimately, it remains unclear how maternal TA status might modify the relationships between PFASs and neonatal THs. The relationships should be evaluated repeatedly in other cohorts.
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