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Adrenocortical function in hyperprolactinemic women.

J N Carter, J E Tyson, G L Warne

    The Journal of Clinical Endocrinology and Metabolism
    |November 1, 1977
    PubMed
    Summary
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    High prolactin levels in women with hyperprolactinemia appear to stimulate adrenal androgen production, specifically dehydroepiandrosterone sulfate (DHAS) and dehydroepiandrosterone (DHA). Treatment with bromocriptine normalized prolactin and reduced these androgens.

    Area of Science:

    • Endocrinology
    • Reproductive Medicine
    • Androgen Metabolism

    Background:

    • Hyperprolactinemia, characterized by elevated prolactin (PRL) levels, is often associated with reproductive dysfunction, including amenorrhea and galactorrhea.
    • The precise effects of hyperprolactinemia on the human adrenal cortex remain incompletely understood.

    Purpose of the Study:

    • To investigate the influence of prolactin on human adrenocortical function, particularly androgen production.
    • To assess changes in specific adrenal androgens following normalization of prolactin levels.

    Main Methods:

    • Serum levels of dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHAS), androstenedione (delta), and testosterone (T) were measured in 35 women with hyperprolactinemia.
    • Hormone levels were assessed before and after treatment with bromocriptine, which lowered prolactin levels.

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  • Adrenocorticotropic hormone (ACTH) stimulation tests were performed in a subset of women before and after prolactin normalization.

    • Main Results:

    • Bromocriptine treatment significantly reduced mean prolactin levels.
    • Following prolactin reduction, serum levels of DHAS and DHA significantly decreased, while androstenedione and testosterone levels remained unchanged.
    • ACTH stimulation tests did not reveal significant differences in the adrenal response between hyperprolactinemic and normalized prolactin states, despite lower baseline DHAS levels when prolactin was normalized.

    Conclusions:

    • Hyperprolactinemia selectively stimulates the production of adrenal androgens, specifically DHAS and DHA.
    • The findings suggest a direct stimulatory effect of prolactin on the adrenal cortex, independent of ACTH stimulation, in the context of hyperprolactinemia.