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Endocrine function in the Prader-Willi syndrome.

W J Jeffcoate, B M Laurance, C R Edwards

    Clinical Endocrinology
    |January 1, 1980
    PubMed
    Summary
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    This study investigated hormonal function in Prader-Willi syndrome patients, finding combined hypothalamic and gonadal issues contribute to hypogonadism. Hormone level analysis revealed impaired responses to stimulation tests in most participants.

    Area of Science:

    • Endocrinology
    • Human Genetics
    • Reproductive Medicine

    Background:

    • Prader-Willi syndrome (PWS) is a complex genetic disorder.
    • Hypogonadism is a common endocrine complication in PWS.
    • The precise mechanisms underlying hypogonadism in PWS remain incompletely understood.

    Purpose of the Study:

    • To evaluate hypothalamic, pituitary, and gonadal function in patients with Prader-Willi syndrome.
    • To investigate the hormonal response to specific stimulation tests in PWS patients.
    • To elucidate the contributing factors to hypogonadism in Prader-Willi syndrome.

    Main Methods:

    • Hormonal assays were performed on five male and three female PWS patients.
    • Patients underwent stimulation tests using clomiphene, human chorionic gonadotrophin (hCG), and human menopausal gonadotrophin (hMG).

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  • Circulating levels of testosterone, oestradiol, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were measured.

    • Main Results:

    • All patients exhibited clinical signs of hypogonadism.
    • Males presented with low circulating testosterone levels.
    • While some females had normal basal oestradiol, gonadotrophin levels were low, with impaired responses to clomiphene and hMG stimulation in tested individuals.
    • Testosterone response to hCG was subnormal in most males, with only transient normalization in one patient.

    Conclusions:

    • The hypogonadism observed in Prader-Willi syndrome appears to result from a combination of hypothalamic dysfunction and primary gonadal abnormalities.
    • These findings highlight the complex endocrine involvement in PWS, necessitating further investigation into targeted therapeutic strategies.