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[Peripheral thyroid hormone resistance]

J Kvetny1

  • 1Medicinsk afdeling, Centralsygehuset i Esbjerg.

Ugeskrift for Laeger
|December 12, 1994
PubMed
Summary
This summary is machine-generated.

Peripheral thyroid hormone resistance (PTHR), identified in 1967, involves elevated thyroid hormones (T4, T3) and TSH. It stems from TR beta gene mutations affecting thyroid hormone action, impacting bone, heart, and brain function.

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Area of Science:

  • Endocrinology
  • Genetics
  • Molecular Biology

Context:

  • Peripheral thyroid hormone resistance (PTHR) is a rare endocrine disorder.
  • First described in 1967, PTHR presents with elevated serum T4 and T3 with inappropriately normal or elevated TSH.
  • The condition arises from genetic defects impacting thyroid hormone signaling.

Purpose:

  • To summarize the key characteristics of peripheral thyroid hormone resistance.
  • To explain the genetic basis and molecular mechanisms of PTHR.
  • To highlight the phenotypic manifestations of the disorder.

Summary:

  • PTHR is characterized by high circulating levels of thyroid hormones (T4, T3) and TSH.
  • The underlying cause is typically a mutation in the TR beta gene, leading to impaired thyroid hormone binding or post-receptor effects.

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  • Affected individuals often exhibit impaired function in bone, heart, and cerebral systems.

    • Impact:

    • Understanding PTHR pathogenesis is crucial for accurate diagnosis and management.
    • Identifying TR beta gene mutations aids in predicting disease severity and progression.
    • Research into PTHR provides insights into thyroid hormone action and its systemic effects.