LaFranchi Stephen H, Haddow James E, Hollowell Joseph G
Department of Pediatrics, Oregon Health and Sciences University, Portland, Oregon, USA.
Thyroid. 2005 Jan;15(1):60-71. doi: 10.1089/thy.2005.15.60.
A workshop entitled, "The Impact of Maternal Thyroid Diseases on the Developing Fetus: Implications for Diagnosis, Treatment, and Screening," was held in Atlanta, Georgia, January 12-13, 2004. This paper reports on the individual session that examined thyroid inadequacy during gestation as a risk factor for adverse pregnancy and developmental outcomes. For this session the following papers were presented: "Adverse Pregnancy Outcomes"; "Thyroid Physiology in the Fetus"; "New England Data: Cretinism Revisited-Preventing Fetal Brain Damage when Mothers Have Subclinical Hypothyroidism"; "Dutch Data: Pregnancy, Maternal Thyroid (Dys)function and Outcome of the Offspring"; and "Report on the Wales Controlled Antenatal Thyroid Screening Study (CATS); A Prospective RCT." These presentations were formally discussed by invited respondents well as others in attendance. Salient points from this session about which there was agreement include the following. Maternal hypothyroidism is associated with complications of pregnancy and adverse effects on the fetus. These risks are greater in women with overt hypothyroidism compared to subclinical hypothyroidism, and also appear to be increased in women with euthyroid autoimmune thyroid disease. If maternal hypothyroidism is treated adequately, this appears to reduce the risk for adverse outcomes. The demonstration of a pattern of ontogeny of fetal cerebral cortex deiodinases and thyroid hormone receptors, beginning by 7-8 weeks' gestation, is circumstantial evidence that thyroid hormone plays an important role in fetal neurodevelopment. Significant fetal thyroid hormone production and secretion does not begin until approximately 20 weeks' gestation. If there is a significant role for thyroid hormone in fetal neurodevelopment before 20 weeks' gestation, it likely is of maternal origin. Studies demonstrate low levels of thyroxine in the fetal coelomic fluid and blood prior to 12-14 weeks' gestation. Published data consistently document a relationship between maternal thyroid deficiency during pregnancy and problems with neuropsychological development of the offspring.
2004年1月12日至13日,一场名为“母体甲状腺疾病对发育中胎儿的影响:对诊断、治疗和筛查的启示”的研讨会在佐治亚州亚特兰大市举行。本文报告了一场单独的会议,该会议探讨了孕期甲状腺功能不足作为不良妊娠和发育结局风险因素的情况。在本次会议上,发表了以下论文:《不良妊娠结局》;《胎儿的甲状腺生理学》;《新英格兰数据:再谈呆小症——当母亲患有亚临床甲状腺功能减退时预防胎儿脑损伤》;《荷兰数据:妊娠、母体甲状腺(功能)异常与子代结局》;以及《威尔士产前甲状腺筛查对照研究(CATS)报告;一项前瞻性随机对照试验》。受邀的回应者以及其他与会者对这些报告进行了正式讨论。本次会议达成共识的要点如下。母体甲状腺功能减退与妊娠并发症以及对胎儿的不良影响相关。与亚临床甲状腺功能减退的女性相比,明显甲状腺功能减退的女性这些风险更大,并且在患有甲状腺功能正常的自身免疫性甲状腺疾病的女性中这些风险似乎也有所增加。如果母体甲状腺功能减退得到充分治疗,这似乎会降低不良结局的风险。胎儿大脑皮层脱碘酶和甲状腺激素受体在妊娠7 - 8周开始呈现出一种个体发生模式,这间接证明甲状腺激素在胎儿神经发育中起重要作用。胎儿甲状腺激素的显著产生和分泌直到大约妊娠20周才开始。如果甲状腺激素在妊娠20周前对胎儿神经发育起重要作用,那么其来源很可能是母体。研究表明,在妊娠12 - 14周之前,胎儿体腔液和血液中的甲状腺素水平较低。已发表的数据一致证明孕期母体甲状腺缺乏与子代神经心理发育问题之间存在关联。