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Growth hormone resistance.

Z Laron, A Kowadlo-Silbergeld, R Eshet

    Annals of Clinical Research
    |October 1, 1980
    PubMed
    Summary
    This summary is machine-generated.

    Growth hormone (GH) resistance, seen in conditions like Laron-type dwarfism, occurs when the body cannot generate active somatomedin (SM) despite normal GH receptor binding. This resistance has various causes, including antibodies or inhibitors.

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    Area of Science:

    • Endocrinology
    • Human Genetics
    • Molecular Biology

    Background:

    • Biological ineffectiveness of growth hormone (GH) is observed in various clinical conditions, often termed GH resistance.
    • Laron-type dwarfism is a hereditary condition characterized by high plasma GH but low somatomedin (SM), presenting similarly to isolated GH deficiency.

    Purpose of the Study:

    • To elucidate the mechanisms underlying growth hormone (GH) resistance in different clinical contexts.
    • To differentiate between GH receptor binding issues and post-receptor defects in GH insensitivity.

    Main Methods:

    • Analysis of plasma GH and somatomedin (SM) levels in patients with GH resistance syndromes.
    • Assessment of GH binding to human liver receptors to confirm GH molecule normalcy.
    • Investigation of factors contributing to GH resistance, such as antibodies and SM inhibitors.

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    Main Results:

    • In Laron-type dwarfism, GH binds normally to liver receptors, indicating the defect lies in the inability to generate active SM.
    • GH resistance can also result from receptor occupancy by endogenous GH (newborns, acromegaly) or end-organ insensitivity (Pygmies).
    • Acquired GH resistance can be induced by anti-GH antibodies or increased levels of SM inhibitors (e.g., in renal failure, corticosteroid excess).

    Conclusions:

    • GH resistance is a complex phenomenon with diverse etiologies, including genetic defects in SM generation, receptor saturation, end-organ unresponsiveness, and acquired factors.
    • Understanding these distinct mechanisms is crucial for diagnosing and potentially managing conditions related to GH insensitivity.
    • The study highlights the critical role of the GH-SM axis and identifies multiple points of potential failure leading to biological ineffectiveness of GH.