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Serum Interleukin-6 and Bone Metabolism in Patients with Thyroid Function Disorders¹

1st Department of Medicine (P.L., J.F., C.H., A.T.,I.T.), Semmelweis University Medical School, Budapest, Hungary, H-1083; Hetenyi Geza County Hospital (L.K.), Szolnok, Hungary, H-5000; and Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Medical School (P.L., G.T., P.H.S.) Chicago, Illinois 60611

Address all correspondence and requests for reprints to: Peter Lakatos, 1st Department of Medicine, Semmelweis University Medical School, Koranyi 2/A, Budapest, H-1083, Hungary.

To determine the possible involvement of interleukin-6 (IL-6) in the bone loss of hyperthyroidism, relationships between thyroid status, biochemical and densitometric parameters of bone metabolism, and IL-6 were studied in female subjects. Patients with hyperthyroidism caused by either toxic nodular goiter or Graves’ disease had significantly higher serum IL-6 concentrations than normal controls. Within the control group, serum IL-6 was higher in postmenopausal than in premenopausal women, but this influence of menopausal status was not seen in the hyperthyroid patients. The production of IL-6 by blood mononuclear cells was higher in cells from the hyperthyroid women. Bone turnover was increased in the hyperthyroid patients based on serum osteocalcin and urinary deoxypyridinoline excretion, and the hyperthyroid group also had reduced radius bone mineral content (BMC). A subgroup of hyperthyroid patients who had the lowest BMC (values more than 1 SD below normal age-matched controls) also had serum IL-6 concentrations significantly greater than those of hyperthyroid patients showing less reduction of BMC. The correlations observed in this study support the possibility that IL-6 plays a role in mediating the bone loss that results from excess thyroid hormone.

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