LaFranchi S
Department of Pediatrics, Oregon Health Sciences University, Portland 97201, USA.
Thyroid. 1999 Jan;9(1):71-8. doi: 10.1089/thy.1999.9.71.
Thyroid gland function develops and matures during fetal life, with production of serum thyroxine (T4) concentrations beginning around 12 weeks gestation and increasing to term. Infants born prior to term have lower cord serum T4 concentrations that correlate with gestational age or birth weight. This is partially the result of lower thyroxine-binding globulin (TBG) concentrations. The cord serum free thyroxine (FT4) concentrations also correlate with gestational age, but they are not proportionately as low as the cord T4 concentration. Preterm infants have a postnatal thyrotropin (TSH) surge and rise in serum T4 and triiodothyronine (T3), which is qualitatively similar to, but quantitatively smaller than, term infants. In contrast to term infants, preterm infants often experience a fall in serum T4 and T3 in the first week of life to below birth levels. This drop appears to be the result of many factors, including nutritional problems and decreased hepatic TBG production, immaturity of hypothalamic-pituitary control of the thyroid gland, immaturity of the thyroid gland itself, and increased tissue utilization of T4. These changes are impacted by complications of prematurity, such as respiratory distress syndrome (RDS), which result in nonthyroidal illness-like changes. Again, serum FT4 seems less affected, and when measured by equilibrium dialysis may be in the normal range for age. Several studies have correlated different measures of morbidity and mortality in the preterm infant with lower serum T4 concentrations. However, as with adults, it may be that low serum T4 concentrations are a marker of the sickest preemies. Also, as with adults, this has led to speculation that T4 treatment might be beneficial in improving these complications of prematurity, in particular the neurological outcome. While some studies appear to show improvement in some facet of medical complications with T4 treatment, most show no effect. Regarding neurological outcome, the 2 best controlled trials do not show improvement in neuropsychiatric testing outcome assessed up to 2 years of age. One study, however, showed an IQ that was 18 points higher in the T4-treated subgroup less than 27 weeks gestational age. It may be that the most preterm infants, eg, those less than 27 weeks of age, are at a disadvantage compared with their intrauterine counterparts, in that they lack the maternal thyroid hormone contribution and are forced to adapt to extrauterine life before their hypothalamic-pituitary-thyroid axis is mature enough to deal with tissue thyroxine demands. Further controlled studies are needed to determine if this subgroup of infants indeed may benefit from transient thyroid hormone supplementation.
甲状腺功能在胎儿期发育并成熟，血清甲状腺素（T4）浓度在妊娠12周左右开始产生，并持续增加直至足月。早产婴儿的脐血血清T4浓度较低，且与胎龄或出生体重相关。这部分是由于甲状腺素结合球蛋白（TBG）浓度较低所致。脐血血清游离甲状腺素（FT4）浓度也与胎龄相关，但下降幅度不如脐血T4浓度那么大。早产婴儿出生后促甲状腺激素（TSH）激增，血清T4和三碘甲状腺原氨酸（T3）升高，这在性质上与足月婴儿相似，但在数量上较小。与足月婴儿不同，早产婴儿在出生后第一周血清T4和T3常降至出生水平以下。这种下降似乎是多种因素导致的，包括营养问题、肝脏TBG生成减少、下丘脑 - 垂体对甲状腺控制的不成熟、甲状腺本身的不成熟以及T4的组织利用率增加。这些变化会受到早产并发症的影响，如呼吸窘迫综合征（RDS），从而导致类似非甲状腺疾病的变化。同样，血清FT4似乎受影响较小，通过平衡透析测量时可能处于该年龄的正常范围内。多项研究将早产婴儿较低的血清T4浓度与不同的发病率和死亡率指标相关联。然而，与成年人一样，血清T4浓度低可能是病情最严重的早产儿的一个标志。而且，与成年人一样，这引发了一种推测，即T4治疗可能有助于改善这些早产并发症，特别是对神经学结局。虽然一些研究似乎显示T4治疗在某些医学并发症方面有所改善，但大多数研究表明没有效果。关于神经学结局，两项控制最严格的试验并未显示在2岁时评估的神经精神测试结局有所改善。然而，一项研究表明，在胎龄小于27周的T4治疗亚组中，智商高出18分。可能是最早产的婴儿，例如那些胎龄小于27周的婴儿，与其子宫内的同龄人相比处于劣势，因为他们缺乏母体甲状腺激素的供应，并且在其下丘脑 - 垂体 - 甲状腺轴成熟到足以应对组织甲状腺素需求之前就被迫适应宫外生活。需要进一步的对照研究来确定这一亚组婴儿是否确实可能从短暂的甲状腺激素补充中获益。
