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Placento-thyroidal relationship in normal pregnancy.

S Kanazawa, A Nakamura, K Saida

    Acta Obstetricia Et Gynecologica Scandinavica
    |January 1, 1976
    PubMed
    Summary
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    Human chorionic thyrotropin (HCT) from the placenta, not elevated TSH, appears to drive thyroid hormone increases during pregnancy. Estrogen-induced increases in thyroxine-binding globulin (TBG) capacity bind excess thyroid hormones.

    Area of Science:

    • Endocrinology
    • Reproductive Biology
    • Thyroid Physiology

    Background:

    • Pregnancy involves significant physiological changes, including alterations in thyroid hormone levels.
    • The role of placental hormones and estrogen in modulating thyroid function during gestation requires clarification.
    • Understanding these changes is crucial for differentiating normal pregnancy adaptations from pathological conditions.

    Purpose of the Study:

    • To investigate the hormonal factors influencing thyroid function during normal pregnancy.
    • To determine the relative contributions of placental human chorionic thyrotropin (HCT) and pituitary thyroid-stimulating hormone (TSH) to thyroid hormone changes.
    • To examine the impact of estrogen-induced thyroxine-binding globulin (TBG) capacity on thyroid hormone transport and availability.

    Main Methods:

    Related Experiment Videos

    • Simultaneous measurement of serum HCT, TSH, T4, T3, PBI, ETR, Triosorb, TBG-binding capacity, BMR, and urinary total estrogen in 160 pregnant women.
    • TRH stimulation tests were performed in 20 women per trimester to assess pituitary TSH secretion.
    • Radio-immunoassay was used for serum TSH measurements.

    Main Results:

    • Serum HCT increased progressively throughout pregnancy, correlating with increased thyroid hormone levels (T3, T4, PBI).
    • Serum TSH levels remained unchanged compared to non-pregnant states, and TRH tests indicated normal pituitary TSH secretion.
    • TBG-binding capacity increased progressively due to estrogen, leading to decreased Triosorb uptake and binding of free thyroxine.

    Conclusions:

    • Thyroid hormone elevation in pregnancy is primarily driven by placental HCT, not by increased pituitary TSH secretion.
    • Increased estrogen levels lead to higher TBG capacity, which binds excess thyroid hormones, preventing clinical hyperthyroidism.
    • A 'placento-thyroidal system' likely exists, where HCT stimulates thyroid function and estrogen-modulated TBG influences thyroid hormone distribution.