Intra-amniotic injection of thyroxine (T4) to a human fetus

Lightner, Elmer S.; Fismer, Delbert A.; Giles, Harlan R.; Woolfenden, James M.

doi:10.1016/0002-9378(77)90440-9

Cited by 31 publications

(9 citation statements)

References 13 publications

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“…The T4 level during the neonatal period was 21.8 pg/dl, and there was elevated amniotic fluid reverse T3, indi cating a hyperthyroid state. This case clearly established human fetal absorption of intra-amniotically administered lévothy roxine and conversion of T4 to reverse T3 [10]. In the present case, intra-amniotic ad ministration of 500 pg of lévothyroxine more closely approximated the required daily dose, and this conclusion is supported by the blood levels which were obtained subsequently.…”

Section: Discussionsupporting

confidence: 75%

“…The elevated cord TSH and undetectable T4 lev els at birth in the case of Van Herle et al [9] would support this conclusion. Lightner et al [10] treated a euthyroid fetus (which was suspected of being hypothyroid) weekly be tween he 33rd and the 39th week of gesta tion with intra-amniotic injections of 500 pg of levothyroxine. The T4 level during the neonatal period was 21.8 pg/dl, and there was elevated amniotic fluid reverse T3, indi cating a hyperthyroid state.…”

Section: Discussionmentioning

confidence: 99%

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Fetal Goitrous Hypothyroidism

Johnson¹,

Finberg²,

Perelman³

et al. 1989

Fetal Diagn Ther

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We present a first case in whom fetal hypothyroidism with goiter was both successfully diagnosed and treated in utero. An obstetrical sonogram at 33 weeks revealed a bilobed fetal neck mass, compatible with enlarged thyroid gland, associated with neck hyperextension, reduced gastric fluid, and polyhydramnios. Umbilical blood sampling after volume reduction amniocentesis confirmed fetal hypothyroidism with a euthyroid mother. Fetal T₄ measured 1.3 μg/dl, free T₄ 0.3 ng/dl, and thyroidstimulating hormone 186 μU. Intra-amniotic levothyroxine, 500 μg, was given twice with a 14-day interval. The head flexed, gastric fluid increased, and amniotic fluid levels returned to normal. Prenatal (36 weeks) and neonatal blood sampling demonstrated return to euthyroid indices. Ultrasonic estimates of thyroid volume decreased by over 50%. Vaginal delivery at 39 weeks was incomplicated. The newborn appeared normal and is being maintained on thyroid replacement therapy.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Fetal Goitrous Hypothyroidism

Johnson¹,

Finberg²,

Perelman³

et al. 1989

Fetal Diagn Ther

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“…A handful of cases of the prenatal treatment of fetal hypothyroidism, either congenital or as a consequence of maternal treatment with antithyroid drugs, have already been reported (Van Herle et al, 1975;Lightner et al, 1977;Weiner et al, 1980;Perelman et al, 1990;Davidson et al, 1991;Van Loon et al, 1995). In all, infusion of L-thyroxine into the amniotic cavity was the selected therapy, but the regimen varied, the dosage ranging from 120 to 500,ug and the interval between intra-amniotic injections from 1 to 2 weeks.…”

Section: Discussionmentioning

confidence: 97%

Prenatal Treatment of Fetal Hypothyroidism: Is There More Than One Option?

et al. 1996

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“…Lightneretal. treated a similar patient with weekly intraamniotic injections of 500 µg of thyroxine (16). This infant did not have hypothyroidism.…”

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confidence: 88%

The Fetus in Maternal Hyperthyroidism

Perelman¹,

Clemons²

1992

Thyroid

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A recent article in the New England Journal of Medicine reported the successful diagnosis and treatment of fetal goitrous hypothyroidism in a mother with Graves' disease. The fetus is being recognized as an important patient in its own right in terms of thyroid disease. The fetal thyroid system develops independently of the normal maternal thyroid axis. Presence of feedback suppression of TSH by T4 has been demonstrated in a 35-week fetus. Information learned from congenital hypothyroidism suggests that lack of fetal thyroid hormones may have a negative impact on the developing fetal brain with lack of normal myelination. It is uncertain at what gestational age the fetus and the developing central nervous system become adversely affected by thyroid hormone deficiency. Since congenital hypothyroidism is sporadic and since there is no current method for easily screening all pregnancies for hypothyroidism, the thrust in fetal diagnosis and therapy has been in those pregnancies suspected of having a hypothyroid fetus when a fetal goiter is detected by ultrasonography or in a hyperthyroid mother who may be on antithyroid therapy. Intraamniotic injections of L-thyroxine have proven successful for fetal therapy. Amniotic fluid TSH may prove useful in the diagnosis and treatment of a hypothyroid fetus. Previous studies have suggested that the period of thyroxine dependency of the fetal central nervous system is limited predominantly to the last 4-8 weeks of gestation. Fetal hyperthyroidism due to transplacental transmission of thyroid-stimulating immunoglobulins may occur in a mother with a history of hyperthyroidism due to Graves' disease.(ABSTRACT TRUNCATED AT 250 WORDS)

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Intra-amniotic injection of thyroxine (T4) to a human fetus

Cited by 31 publications

References 13 publications

Fetal Goitrous Hypothyroidism

Fetal Goitrous Hypothyroidism

Prenatal Treatment of Fetal Hypothyroidism: Is There More Than One Option?

The Fetus in Maternal Hyperthyroidism

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