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Neonatal Thyroid Stimulating Hormone and Subsequent Diagnosis of Autism Spectrum Disorders and Intellectual Disability.
Autism Research ( IF 4.7 ) Pub Date : 2019-12-10 , DOI: 10.1002/aur.2247
Jennifer L Ames 1 , Gayle C Windham 2 , Kristen Lyall 3 , Michelle Pearl 2 , Martin Kharrazi 2 , Cathleen K Yoshida 1 , Judy Van de Water 4, 5 , Paul Ashwood 5, 6 , Lisa A Croen 1
Affiliation  

Hypothyroid conditions in early life, if left untreated, are associated with adverse neurodevelopmental outcomes, including intellectual disability (ID). However, evidence addressing the role of neonatal thyroid hormone insufficiencies in the altered neurobiology underlying autism spectrum disorders (ASD), particularly among its subphenotypes, is limited. We conducted a population‐based, case–control study among a sample of children born during 2000–2003 in Southern California. We examined neonatal thyroid‐stimulating hormone (TSH) measured during routine newborn screening among children later diagnosed with ASD (n = 518) or ID (n = 145) and general population (GP) controls (n = 399). TSH was further analyzed in relation to ASD subgroups of intellectual ability and onset type (early‐onset ASD vs. ASD with regression) ascertained by expert review of developmental services records. Odds ratios (ORs) of the differences in TSH between groups were obtained from multivariate logistic regression. We examined neonatal TSH as continuous (ln‐transformed) and as quartiles. We found no association between continuous neonatal TSH levels and ASD (adj‐OR: 1.00, 95% CI: 0.79–1.26) nor ID (adj‐OR = 1.01, 95% CI: 0.73–1.40). Among ASD subphenotypes, we observed a suggestive inverse trend between ASD with regression and TSH, though the association only reached statistical significance in the highest TSH quartile (adj‐OR: 0.50, 95% CI: 0.26–0.98). While there was little evidence that neonatal TSH is related to overall ASD risk, more work is needed to understand the influence of thyroid hormones on ASD subphenotypes. Autism Res 2020, 13: 444–455. © 2019 International Society for Autism Research,Wiley Periodicals, Inc.

中文翻译:

新生儿甲状腺刺激激素和自闭症谱系障碍和智力障碍的后续诊断。

如果不及时治疗,甲状腺机能减退会导致不良的神经发育结果,包括智力障碍(ID)。但是,关于新生儿甲状腺激素功能不足在自闭症谱系障碍(ASD)尤其是其亚表型潜在的神经生物学改变中的作用的证据是有限的。我们对南加州2000-2003年间出生的儿童样本进行了基于人群的病例对照研究。我们检查了在常规新生儿筛查期间在后来被确诊为ASD(n = 518)或ID(n = 145)和一般人群(GP)对照(n= 399)。通过对发展服务记录的专家审查确定了与TSH的智力和发病类型(早期ASD对比具有回归的ASD)有关的TSD进一步分析。组间TSH差异的几率(OR)通过多因素logistic回归获得。我们将新生儿TSH检查为连续(转换后)和四分位数。我们发现连续新生儿TSH水平与ASD(adj-OR:1.00,95%CI:0.79-1.26)和ID(adj-OR = 1.01,95%CI:0.73-1.40)之间没有关联。在ASD亚型中,尽管在最高TSH四分位数中(adj-OR:0.50,95%CI:0.26-0.98),相关性仅在统计学上具有显着意义,但我们观察到ASD与回归和TSH之间存在相反的趋势。尽管几乎没有证据表明新生儿TSH与总体ASD风险有关,Autism Res 2020,13:444-455。©2019国际自闭症研究协会,Wiley Periodicals,Inc.
更新日期:2019-12-10
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