Postnatal thyroid hormones for respiratory distress syndrome in preterm infants

D A Osborn1, R W Hunt

  • 1Royal Prince Alfred Hospital, RPA Newborn Care, Missenden Road, Camperdown, New South Wales, Australia, 2050. david.osborn@email.cs.nsw.gov.au

Insights

Postnatal thyroid hormone therapy does not improve respiratory distress syndrome outcomes in preterm infants. Studies found no significant benefits in neonatal morbidity or mortality for infants treated with thyroid hormones.

Area of Science:

  • Neonatology
  • Pediatric Respiratory Medicine
  • Endocrinology

Background:

  • Preterm infants with respiratory distress syndrome (RDS) face risks of adverse neonatal and developmental outcomes.
  • Antenatal thyroid hormone administration in animal models stimulates surfactant production and reduces RDS severity.

Purpose of the Study:

  • To evaluate the efficacy of postnatal thyroid hormone therapy in preterm infants with suspected RDS.
  • To determine if this therapy improves respiratory morbidity and subsequent neonatal/long-term outcomes.

Main Methods:

  • Searched CENTRAL, MEDLINE, PREMEDLINE, EMBASE, and other sources up to March 2006.
  • Included trials of preterm infants with suspected RDS, comparing thyroid hormone treatment to control within 48 hours of birth.
  • Conducted independent quality assessment and data extraction, synthesizing data using standard meta-analysis methods.

Main Results:

  • Two studies (80 infants) with methodological concerns were analyzed.
  • No significant benefits were observed in neonatal morbidity or mortality.
  • Meta-analysis showed no significant difference in mortality to discharge or need for mechanical ventilation.

Conclusions:

  • Controlled clinical trials provide no evidence that postnatal thyroid hormone treatment benefits preterm infants with RDS.
  • The therapy did not reduce RDS severity, neonatal morbidity, or mortality.
Abstract

Related Concept Videos

Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Upper Respiratory Drugs: Antitussives, Expectorants, and Mucolytics01:23

Upper Respiratory Drugs: Antitussives, Expectorants, and Mucolytics

Respiratory symptoms, such as congestion and cough, commonly accompany respiratory tract conditions. Various medications, such as antitussives, expectorants, and mucolytics, play crucial roles in providing relief.
Antitussives include codeine, dextromethorphan (Robitussin), and benzonatate (Tessalon). Codeine and dextromethorphan exert their effects centrally by suppressing the cough reflex center in the medulla.  Benzonatate operates peripherally within the respiratory tract by anesthetizing...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...