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Inhibited hypothalamic-pituitary-thyroid axis in type I pseudohypoparathyroidism.

U M Kabadi1, R P Cech

  • 1Veterans Affairs Medical Center, Des Moines, Iowa, and the University of Iowa School of Medicine, Iowa City, Iowa.

Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
|July 15, 2004
PubMed
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Patients with pseudohypoparathyroidism show inhibited thyroid function. This may be due to impaired cyclic adenosine monophosphate (cAMP) signaling, affecting thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH) responses.

Area of Science:

  • Endocrinology
  • Molecular Endocrinology

Background:

  • Pseudohypoparathyroidism (PHP) is a rare genetic disorder characterized by resistance to parathyroid hormone (PTH).
  • Patients typically present with hypocalcemia, hyperphosphatemia, and elevated PTH levels.
  • The hypothalamic-pituitary-thyroid (HPT) axis function in PHP is not fully understood.

Purpose of the Study:

  • To evaluate the hypothalamic-pituitary-thyroid axis in two patients diagnosed with type I pseudohypoparathyroidism.
  • To investigate the impact of pseudohypoparathyroidism on the response to thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH).

Main Methods:

  • Assessed serum levels of thyroxine (T4) and triiodothyronine (T3), T3 resin uptake, and 24-hour thyroidal uptake of radioactive iodine (123I).
  • Measured responses to subcutaneous TSH administration and intravenous TRH stimulation.

Related Experiment Videos

  • Compared results with 10 healthy control subjects.

    • Main Results:

    • Thyroid hormone levels and iodine uptake were within normal ranges in patients with pseudohypoparathyroidism.
    • Patients exhibited significantly blunted responses to both TSH and TRH compared to controls.
    • Basal TSH levels were elevated, and TRH-induced TSH responses were blunted relative to basal concentrations.

    Conclusions:

    • Pituitary thyrotroph response to TRH and thyroid gland response to TSH are significantly inhibited in pseudohypoparathyroidism.
    • This inhibition may stem from inadequate cyclic adenosine monophosphate (cAMP) generation, a crucial second messenger for hormone action.
    • Impaired cAMP signaling could underlie the observed HPT axis dysfunction in this syndrome.