Lazarus J H
Cardiff University School of Medicine, Centre for Endocrine and Diabetes Sciences, Academic Centre, Llandough Hospital, Llandough, Cardiff, UK.
Minerva Endocrinol. 2005 Jun;30(2):71-87.
The subject of thyroid disease in pregnancy is receiving increasing attention from many scientific disciplines. Thyroid function in pregnancy is characterised by a T4 surge at 12 weeks declining thereafter. Serum thyroid hormone concentrations fall in the second half of pregnancy but there are few data on normal reference ranges. Fetal brain development depends on T4 transport into the fetus which in turn depends on sufficient maternal iodine supply. There is current concern that adequate iodisation is not present in large parts of Europe. There is increasing evidence that thyroid autoimmunity is associated with fetal loss but the mechanism is unclear and therapy requires carefully conducted studies. While hyperthyroidism in pregnancy is uncommon, effects on both mother and child are critical if untreated. The use of propylthiouracil is recommended together with measurement of TSH receptor antibodies at 36 weeks gestation. Women receiving thyroxine therapy for hypothyroidism or as suppressive therapy should have their dose increased by up to 50% during pregnancy. There are now substantial data to show deleterious effects on child IQ resulting from low maternal T4 (or high TSH) during gestation. Major advances in molecular biology have contributed to elucidation of many genetic causes of congenital hypothyroidism. However, the aetiology of the majority of cases is still unclear and further research is required. The presence of TPO antibodies in about 10% of pregnant women in early gestation is a predictor of an increased incidence of subclinical hypothyroidism during pregnancy and also of postpartum thyroid dysfunction. The latter condition occurs in 5-9% of women and 25-30% progress to permanent hypothyroidism. This review suggests that screening for thyroid function in early pregnancy and levothyroxine intervention therapy for maternal subclinical hypothyroidism should be considered but evidence is awaited. Screening for both thyroid dysfunction and thyroid antibodies ideally at a preconception clinic but certainly in early gestation is recommended.
妊娠甲状腺疾病这一主题正受到众多科学学科越来越多的关注。妊娠期间的甲状腺功能特点是在孕12周时T4激增，此后逐渐下降。妊娠后半期血清甲状腺激素浓度会降低，但关于正常参考范围的数据较少。胎儿脑发育依赖于T4转运至胎儿体内，而这又取决于母体充足的碘供应。目前人们担心欧洲大部分地区碘摄入不足。越来越多的证据表明甲状腺自身免疫与胎儿丢失有关，但机制尚不清楚，治疗需要谨慎开展研究。虽然妊娠甲亢并不常见，但如果不治疗，对母婴的影响都很严重。建议使用丙硫氧嘧啶，并在妊娠36周时检测促甲状腺素受体抗体。接受甲状腺素治疗的甲减女性或接受抑制治疗的女性，在妊娠期间其剂量应增加多达50%。现在有大量数据表明，孕期母体T4水平低（或促甲状腺素水平高）会对儿童智商产生有害影响。分子生物学的重大进展有助于阐明先天性甲减的许多遗传病因。然而，大多数病例的病因仍不清楚，需要进一步研究。妊娠早期约10%的孕妇存在甲状腺过氧化物酶抗体，这是妊娠期间亚临床甲减以及产后甲状腺功能障碍发病率增加的一个预测指标。后者在5%至9%的女性中发生，25%至30%会进展为永久性甲减。这篇综述表明，应考虑在妊娠早期筛查甲状腺功能，并对母体亚临床甲减进行左甲状腺素干预治疗，但尚需证据。建议理想情况下在孕前诊所，但肯定要在妊娠早期同时筛查甲状腺功能障碍和甲状腺抗体。
