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Related Experiment Videos

Serum cytokines in thyrotoxicosis.

A Siddiqi1, J P Monson, D F Wood

  • 1Department of Clinical Biochemistry, St. Bartholomew's and Royal London School of Medicine and Dentistry, United Kingdom. a.siddiqi@mds.qmw.ac.uk

The Journal of Clinical Endocrinology and Metabolism
|February 18, 1999
PubMed
Summary

Thyroid hormone excess increases bone resorption by raising interleukin-6 and -8 levels, independent of autoimmune inflammation. Treatment normalizes these cytokine levels, suggesting thyroid hormones directly impact bone metabolism.

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Area of Science:

  • Endocrinology
  • Bone Biology
  • Immunology

Background:

  • Thyroid hormone overproduction is linked to increased bone resorption.
  • Elevated serum interleukin-6 (IL-6) observed in thyrotoxicosis, but its cause (hormone excess vs. inflammation) is unclear.
  • Graves' disease (GD) and toxic nodular goiter (TNG) involve thyroid hormone excess and potential autoimmune inflammation.

Purpose of the Study:

  • To investigate whether osteotropic cytokines, specifically IL-6 and IL-8, mediate bone resorption in hyperthyroidism.
  • To differentiate the effects of thyroid hormone excess from autoimmune inflammation on cytokine levels.
  • To assess changes in IL-6 and IL-8 following treatment for hyperthyroidism.

Main Methods:

  • Longitudinal study of 34 hyperthyroid patients (GD, TNG, thyroid carcinoma on TSH suppression) and 12 controls.

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  • Measurements included serum free T4, T3, IL-6, IL-8, IL-1beta, TNF-alpha, IL-11, bone-specific alkaline phosphatase (b-ALP), and urinary deoxypyridinoline (Udpd).
  • Measurements taken at baseline and for 6 months after carbimazole treatment.
  • Main Results:

    • Untreated GD and TNG patients showed significantly elevated IL-6 and IL-8 compared to controls.
    • These cytokine levels decreased to control levels after treatment.
    • Thyroid carcinoma patients on TSH suppressive therapy also had elevated IL-6 and IL-8.
    • IL-6 and IL-8 levels correlated with serum T3 and free T4, but not with bone resorption markers (Udpd, b-ALP).
    • IL-1beta, IL-11, and TNF-alpha were not elevated.

    Conclusions:

    • Elevated IL-6 and IL-8 in hyperthyroidism are primarily due to thyroid hormone excess, not autoimmune inflammation.
    • These cytokines likely originate from bone osteoblasts, despite lack of correlation with acute bone turnover markers.
    • Thyroid hormone excess directly influences cytokine production, contributing to bone resorption.