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Effects of fever and hyperthermia on thyroid function

R B Shafer, M M Oken, M K Elson

    Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine
    |December 1, 1980
    PubMed
    Summary

    Fever from E. coli endotoxin rapidly alters thyroid hormones, decreasing T3 and increasing rT3. These changes in triiodothyronine (T3), reverse triiodothyronine (rT3), and thyroxine (T4) occur faster than previously known.

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    Area of Science:

    • Endocrinology
    • Physiology
    • Immunology

    Background:

    • Febrile states significantly impact thyroid hormone levels in humans.
    • Understanding acute febrile changes in thyroid hormones is crucial for clinical management.
    • Rabbit models offer a controlled environment to study rapid physiological responses.

    Purpose of the Study:

    • To investigate the acute effects of endotoxin-induced fever on thyroid hormone levels in a rabbit model.
    • To compare thyroid hormone alterations during endotoxin fever versus heat-induced hyperthermia.
    • To elucidate the temporal dynamics of thyroid hormone changes during acute fever.

    Main Methods:

    • Administered E. coli endotoxin to rabbits and monitored body temperature and serum thyroid hormone levels (T3, rT3, T4) over 24 hours.
    • Induced hyperthermia in rabbits using external heat and measured corresponding thyroid hormone changes.
    • Analyzed serum samples at 0, 2, 4, 6, and 24 hours post-intervention.

    Main Results:

    • Endotoxin injection caused a rapid fever, with peak temperature increases of 1.1°C and 1.4°C at 1 and 3 hours, respectively.
    • Serum T3 levels decreased promptly, while rT3 levels increased reciprocally following endotoxin administration.
    • T4 levels initially decreased then rebounded above basal levels; heat-induced hyperthermia had minimal impact on thyroid hormones.

    Conclusions:

    • Endotoxin-induced fever rapidly alters thyroid hormone metabolism, mirroring changes seen in human infections.
    • The observed changes suggest potential mechanisms including suppressed TSH release, altered peripheral T4 monodeiodination, or enhanced T3 clearance.
    • Fever, not just elevated temperature, appears to be the primary driver of these acute thyroid hormone shifts.

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