Reuss M L, Paneth N, Pinto-Martin J A, Lorenz J M, Susser M
Sergievsky Center, Columbia University, New York, USA.
N Engl J Med. 1996 Mar 28;334(13):821-7. doi: 10.1056/NEJM199603283341303.
Transient hypothyroxinemia, a common finding in premature infants, is not thought to have long-term sequelae or to require treatment. We investigated whether hypothyroxinemia in premature infants is a cause of subsequent motor and cognitive abnormalities.
In this historical cohort study, we retrieved blood thyroxine values, obtained on routine screening in the first week of life, from state screening records on children who weighted 2000 g or less at birth, who were born at 33 weeks' gestation or earlier, and who were enrolled in a population-based study of the late sequelae of neonatal brain hemorrhage. We investigated the relation of these values to the odds for disabling cerebral palsy among 463 subjects for whom data were available and to the mental-development score on the Bayley Scales of Infant Development or the Stanford-Binet Intelligence Scales for Children at the age of two years in 400 subjects. The effects of severe hypothyroxinemia, defined as a blood thyroxine value more than 2.6 SD below the mean for New Jersey newborns, were assessed before and after adjustment for gestational age and potentially confounding variables.
In analyses adjusted for gestational age, infants with severe hypothyroxinemia had a risk of disabling cerebral palsy that was nearly 11 times that of infants without hypothyroxinemia (odds ratio, 10.8; 95 percent confidence interval, 3.0 to 39.3) and a mean mental-development score at the age of two that was 15.4 points lower (95 percent confidence interval, 8.1 to 22.6 points) than the mean score of children with normal neonatal blood thyroxine concentrations. After adjustment for gestational age and multiple prenatal, perinatal, and early and last neonatal variables, severe hypothyroxinemia was still associated with an increased risk of disabling cerebral palsy (odds ratio, 4.4; 95 percent confidence interval, 1.0 to 18.6) and a reduction of nearly 7 points (95 percent confidence interval, 0.3 to 13.2 points) in the mental-development score.
Severe hypothyroxinemia in preterm infants may be an important cause of problems in neurologic and mental development detected at the age of two years.
短暂性甲状腺素血症在早产儿中很常见，一般认为不会产生长期后遗症，也无需治疗。我们调查了早产儿甲状腺素血症是否是随后运动和认知异常的一个原因。
在这项历史性队列研究中，我们从出生体重2000g或更低、孕33周或更早出生且参加了一项基于人群的新生儿脑出血远期后遗症研究的儿童的州筛查记录中，获取了出生第一周常规筛查时的血甲状腺素值。我们调查了这些值与463名有可用数据的受试者中致残性脑瘫的几率，以及与400名受试者两岁时贝利婴儿发育量表或斯坦福-比奈儿童智力量表上的智力发育得分之间的关系。在对胎龄和潜在混杂变量进行调整前后，评估了定义为血甲状腺素值比新泽西州新生儿均值低2.6个标准差以上的严重甲状腺素血症的影响。
在对胎龄进行调整的分析中，患有严重甲状腺素血症的婴儿发生致残性脑瘫的风险几乎是没有甲状腺素血症婴儿的11倍（比值比，10.8；95%置信区间，3.0至39.3），两岁时的平均智力发育得分比新生儿血甲状腺素浓度正常的儿童的平均得分低15.4分（95%置信区间，8.1至22.6分）。在对胎龄以及多个产前、围产期、早期和晚期新生儿变量进行调整后，严重甲状腺素血症仍与致残性脑瘫风险增加（比值比，4.4；95%置信区间，1.0至18.6）以及智力发育得分降低近7分（95%置信区间，0.3至13.2分）相关。
早产儿严重甲状腺素血症可能是两岁时发现的神经和智力发育问题的一个重要原因。
