Author:
Yoon Shin Ae,Chang Yun Sil,Ahn So Yoon,In Sung Se,Park Won Soon
Abstract
Abstract
Background
To determine the incidence, etiology, and outcomes of thyroid-stimulating hormone (TSH) elevation in extremely low-birth-weight infants (ELBWIs).
Methods
Newborn thyroid screening data of 584 ELBWIs (birth weight, < 1000 g; gestational age, ≥ 23 weeks) were retrospectively analyzed to identify initial (≤ 2 postnatal weeks) and delayed (> 2 weeks) TSH elevations. Growth and neurodevelopmental outcomes at 2 years’ corrected age (CA) were assessed according to levothyroxine replacement.
Results
Initial and delayed TSH elevations were detected at CAs of 27 and 30 weeks, respectively, with incidence rates of 0.9 and 7.2%, respectively. All infants with initial TSH elevations had perinatal asphyxia, and 95% of those with delayed TSH elevation were exposed to various stressors, including respiratory support, drugs, and surgery within 2 weeks before diagnosis of TSH elevation. Free thyroxine (T4) levels were simultaneously reduced in 80 and 57% of infants with initial and delayed TSH elevations, respectively. Both initial and delayed TSH elevations were transient, regardless of levothyroxine replacement. Infants receiving levothyroxine replacement therapy had significantly higher TSH elevations, significantly lower free T4 levels, and significantly reduced mortality, compared to untreated infants. However, levothyroxine replacement had no significant effect on long-term growth and neurodevelopmental outcomes.
Conclusions
The timing of insult superimposition on hypothalamic–pituitary–thyroid axis maturation is a major determinant of initial or delayed TSH elevation in ELBWIs. Levothyroxine replacement did not affect growth or neurodevelopmental outcomes in this population.
Publisher
Springer Science and Business Media LLC
Subject
Pediatrics, Perinatology, and Child Health
Reference48 articles.
1. Leger J, Olivieri A, Donaldson M, Torresani T, Krude H, van Vliet G, et al. European Society for Paediatric Endocrinology consensus guidelines on screening, diagnosis, and management of congenital hypothyroidism. Horm Res Paediatr. 2014;81(2):80–103.
2. Williams FL, Visser TJ, Hume R. Transient hypothyroxinaemia in preterm infants. Early Hum Dev. 2006;82(12):797–802.
3. Calvo RM, Jauniaux E, Gulbis B, Asuncion M, Gervy C, Contempre B, et al. Fetal tissues are exposed to biologically relevant free thyroxine concentrations during early phases of development. J Clin Endocrinol Metab. 2002;87(4):1768–77.
4. Vulsma T, Gons MH, de Vijlder JJ. Maternal-fetal transfer of thyroxine in congenital hypothyroidism due to a total organification defect or thyroid agenesis. N Engl J Med. 1989;321(1):13–6.
5. Fisher DA, Dussault JH, Sack J, Chopra IJ. Ontogenesis of hypothalamic--pituitary--thyroid function and metabolism in man, sheep, and rat. Recent Prog Horm Res. 1976;33:59–116.
Cited by
12 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献