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Thyroid-pituitary function in eight anencephalic infants.

S Grasso, S Filetti, D Mazzone

    Acta Endocrinologica
    |April 1, 1980
    PubMed
    Summary
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    Anencephaly does not prevent thyroid-pituitary axis development. The pituitary and thyroid function normally in anencephalic infants when stimulated, despite the absence of a hypothalamus.

    Area of Science:

    • Endocrinology
    • Developmental Biology
    • Neonatal Physiology

    Background:

    • The hypothalamus is crucial for regulating the thyroid-pituitary axis.
    • Anencephaly involves the absence of a developed hypothalamus and cerebral cortex.
    • The impact of hypothalamic absence on fetal thyroid-pituitary axis development is not fully understood.

    Purpose of the Study:

    • To investigate the functional capacity of the thyroid-pituitary axis in anencephalic infants.
    • To determine if pituitary thyrotroph cells and the thyroid gland develop and function without hypothalamic influence.

    Main Methods:

    • Measurement of thyroid-stimulating hormone (TSH), thyroxine (T4), triiodothyronine (T3), and reverse T3 (rT3) in cord blood and early neonatal samples from 8 anencephalic infants.
    • Assessment of TSH response to thyrotropin-releasing hormone (TRH) administration.

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  • Evaluation of thyroid hormone response to bovine TSH stimulation.

    • Main Results:

    • Pituitary glands and thyroids were anatomically normal in all anencephalic infants.
    • Normal TSH, T4, and T3 levels were observed at birth, with no spontaneous T3 surge post-delivery.
    • TRH administration induced a significant TSH release, and thyroid hormones responded normally to TSH stimulation.

    Conclusions:

    • The pituitary gland's TSH-secreting cells and the thyroid gland can develop and function in anencephalic fetuses.
    • Adequate stimulation, such as by TRH and TSH, can elicit responses from the thyroid-pituitary axis even without hypothalamic input.
    • These findings highlight the potential for thyroid-pituitary axis function independent of hypothalamic regulation during fetal development.