Intraamniotic Triidothyronine instillation for prevention of respiratory distress syndrome in pregnancies complicated by hypertension

Schreyer, Peter; Caspi, E; Letko, Y.; Ron-El, Raphaël; Pinto, Nicolau Albuquerque Barbosa; Ziedman, J L

doi:10.1515/jpme.1982.10.1.27

Cited by 11 publications

(6 citation statements)

References 14 publications

(15 reference statements)

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“…The most widely recognized stimulator of pulmonary surfactant production is thyroxine (T4) [5], However, it has been recently observed that triiodothyronine (T3) can directly influence surfactant production and that its cir culating levels are low in premature infants with RDS probably due to a low T4-T3 hepatic conversion mecha nism [6,7]. Considering this state of hypotriiodothyroni nemia at birth, we studied the influence of postnatal intra venous T3 administration on the course of RDS in a group of preterm infants of less than 32 weeks' gestation.…”

Section: Introductionmentioning

confidence: 99%

Postnatal Triiodothyronine Replacement and Respiratory Distress Syndrome of the Preterm Infant

Amato¹,

Guggisberg²,

Schneider³

1989

Horm Res

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Improvements in the management of respiratory distress syndrome (RDS) include pre- and postnatal stimulation of pulmonary maturity, and triiodothyronine (T3) is believed to influence directly surfactant production. Its circulating levels are low in premature infants with RDS probably due to a low thyroxine T4-T3 hepatic conversion mechanism. While a state of hypotriiodothyroninemia exists at birth, we studied the influence of postnatal intravenous T3 administration on the course of RDS in preterm infants of less than 32 weeks’ gestation. Fifty preterm infants with RDS were studied (mean gestational age 30.4 ± 1.2 weeks and birth weight 1,180 ± 220 g). They were at random assigned to treatment with 50 µg L-T3 (Thyrotardin) or to the control group. Mortality rate, peak oxygen concentrations, duration of artificial ventilation and development of major complications of RDS were the criteria to estimate the influence of T3 treatment on RDS. We failed to detect a statistically significant difference between the two groups in all of the mentioned criteria except for Fio₂ concentrations required to maintain Pao₂ between 50 and 60 mm Hg (p < 0.05). These observations suggest a relative beneficial effect of T3 replacement on the course of RDS in preterm infants of less than 32 weeks of gestation.

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Section: Introductionmentioning

confidence: 99%

Postnatal Triiodothyronine Replacement and Respiratory Distress Syndrome of the Preterm Infant

Amato¹,

Guggisberg²,

Schneider³

1989

Horm Res

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“…In the quest for more efficient methods to accelerate lung maturation in the fetus a number of compounds have been investigated in experimental animals [2]. Thyroid hormones [1,12,33,44], bromhexine metabolite VIII (ambroxol) [41,48], carnitine [40] and thyrotropin stimulating hormone (TRH, LIGGINS unpublished) have recently also been used in humans.…”

Section: Introductionmentioning

confidence: 99%

New approaches to hormonal acceleration of fetal lung maturation

Schellenberg¹,

Liggins²

1987

Journal of Perinatal Medicine

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The paper reviews the effects on lung maturation of glucocorticoids in animals and humans and presents relevant recent findings from the author's laboratory. It is now well established that antenatal glucocorticoid treatment reduces the incidence and severity of the respiratory distress syndrome (RDS) in prematurely born infants. The recommended doses of glucocorticoids produce fetal glucocorticoid activity levels similar to those of newborns with RDS or prolonged rupture of the membranes. Extensive follow-up studies have shown that adverse effects on child development are unlikely to occur. It is also evident that a significant number of fetuses do not respond to the treatment, which is of particular consequence in fetuses of less than 28 weeks gestation. These fetuses are less likely to respond to glucocorticoid therapy that fetuses between 28 and 32 weeks gestation and are at a higher risk of developing complications due to their immaturity. In fetal sheep, there is a similar decrease in the efficacy of glucocorticoids on lung maturation with decreasing gestational age. Simultaneous infusion of cortisol, triiodothyronine and prolactin but not of any of these hormones administered singly or in combination of two produced mature lungs in fetal sheep of 125 days gestation. Similar results were obtained with thyrotropin releasing hormone (TRH) and cortisol. It remains to be seen whether the combined administration of glucocorticoids and TRH accelerates lung maturation in human fetuses.

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“…On the contrary, administration of T3 either alone or in combination with beta methasone does not provide additional bene fits on these aspects of fetal lung maturation. Uncontrolled studies in humans are not strongly suggestive of marked or rapid effects of thyroid hormones on fetal lung maturation [26,27]. Recent studies in humans suggest that combined hormonal therapy with beta methasone plus thyrotropin-releasing hor mone (TRH), a tripeptide that crosses the pla centa and increases fetal thyroid hormones, ameliorates respiratory distress syndrome and its consequences [28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Effects of Betamethasone and Thyroid Hormone on Fetal Rat Lung Maturation in vivo

Moya

Sánchez²,

Baudy³

1992

Dev Pharmacol Ther

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We studied the effect of maternal administration at various intervals of betamethasone, triiodothyronine (T3), or both, on fetal rat lung maturation. T(3) alone did not enhance choline incorporation to phosphatidylcholine by 20-day fetal lung expiants, or morphometric lung maturation. Betamethasone, and betamethasone plus T(3), increased both of those parameters over control and T(3) values. However, addition of T(3) offered no advantage over administration of betamethasone alone. Significant enhancement of morphometric lung maturation was already present after only 24 h of exposure to betamethasone, or to the combination of hormones. However, choline incorporation to phosphatidylcholine only increased significantly by 36 h of exposure to betamethasone with or without T(3).

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Intraamniotic Triidothyronine instillation for prevention of respiratory distress syndrome in pregnancies complicated by hypertension

Cited by 11 publications

References 14 publications

Postnatal Triiodothyronine Replacement and Respiratory Distress Syndrome of the Preterm Infant

Postnatal Triiodothyronine Replacement and Respiratory Distress Syndrome of the Preterm Infant

New approaches to hormonal acceleration of fetal lung maturation

Effects of Betamethasone and Thyroid Hormone on Fetal Rat Lung Maturation in vivo

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