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Related Experiment Videos

Thyroid hormone resistance.

B A Lamberg, K Liewendahl

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

    This study explores generalized resistance to thyroid hormones, a condition with varied symptoms. Research suggests receptor-level or post-receptor issues may cause this hormonal resistance.

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    Area of Science:

    • Endocrinology
    • Molecular Biology
    • Genetics

    Background:

    • Generalized resistance to thyroid hormones (RTH) presents with elevated thyroid hormone levels and normal binding proteins, yet clinical euthyroidism.
    • The condition exhibits a broad clinical spectrum, from congenital goiter and subclinical hypothyroidism to asymptomatic individuals.
    • Specific physical features may be present in more severely affected patients.

    Purpose of the Study:

    • To summarize the characteristics of generalized resistance to thyroid hormones.
    • To explore potential molecular mechanisms underlying RTH.
    • To describe familial cases and inheritance patterns.

    Main Methods:

    • Review of existing literature on generalized resistance to thyroid hormones.

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  • Analysis of clinical presentations, laboratory findings (serum TSH, TRH response), and genetic data.
  • Investigation of cellular mechanisms involving thyroid hormone receptors in lymphocytes and fibroblasts.

    • Main Results:

    • Increased thyroid hormones with normal binding proteins but clinical euthyroidism characterize RTH.
    • TSH and TRH responses are typically normal but can fluctuate.
    • Studies suggest decreased receptor affinity, binding capacity, or post-receptor defects are involved.
    • Six families (24 patients) and seven sporadic cases show dominant inheritance patterns.
    • Selective pituitary thyrotroph refractoriness to thyroid hormones was noted in five hyperthyroid patients.

    Conclusions:

    • Generalized resistance to thyroid hormones is a complex endocrine disorder with variable clinical manifestations.
    • Molecular mechanisms likely involve alterations in thyroid hormone receptor function.
    • Further research is needed to elucidate the precise underlying mechanisms, particularly in cases of selective pituitary resistance.