Serum Interleukin-6 and Bone Metabolism in Patients with Thyroid Function Disorders1
Peter Lakatos,
Janos Foldes,
Csaba Horvath,
Laszlo Kiss,
Agnes Tatrai,
Istvan Takacs,
Gabor Tarjan2 and
Paula H. Stern
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 thyroidstatus,
biochemical and densitometric parameters of bone metabolism,and IL-6
were studied in female subjects. Patients with hyperthyroidismcaused
by either toxic nodular goiter or Graves’ diseasehad significantly
higher serum IL-6 concentrations than normalcontrols. Within the
control group, serum IL-6 was higher inpostmenopausal than in
premenopausal women, but this influenceof menopausal status was not
seen in the hyperthyroid patients.The production of IL-6 by blood
mononuclear cells was higherin cells from the hyperthyroid women. Bone
turnover was increasedin the hyperthyroid patients based on serum
osteocalcin andurinary deoxypyridinoline excretion, and the
hyperthyroid groupalso had reduced radius bone mineral content (BMC).
A subgroupof hyperthyroid patients who had the lowest BMC (values more
than1 SD below normal age-matched controls) also had serum
IL-6concentrations significantly greater than those of hyperthyroid
patientsshowing less reduction of BMC. The correlations observed in
thisstudy support the possibility that IL-6 plays a role in mediating
thebone loss that results from excess thyroid hormone.
This article has been cited by other articles:
A. Antonelli, C. Ferri, P. Fallahi, S. M. Ferrari, D. Giuggioli, M. Colaci, A. Manfredi, S. Frascerra, F. Franzoni, F. Galetta, et al. CXCL10 ({alpha}) and CCL2 ( ) chemokines in systemic sclerosis a longitudinal study
Rheumatology,
January 1, 2008;
47(1):
45 - 49.
[Abstract][Full Text][PDF]
A. Antonelli, P. Fallahi, M. Rotondi, S. M. Ferrari, P. Romagnani, M. Grosso, E. Ferrannini, and M. Serio Increased serum CXCL10 in Graves' disease or autoimmune thyroiditis is not associated with hyper- or hypothyroidism per se, but is specifically sustained by the autoimmune, inflammatory process.
Eur. J. Endocrinol.,
May 1, 2006;
154(5):
651 - 658.
[Abstract][Full Text][PDF]
H. W. Vesper, L. M. Demers, R. Eastell, P. Garnero, M. Kleerekoper, S. P. Robins, A. K. Srivastava, G. R. Warnick, N. B. Watts, and G. L. Myers Assessment and Recommendations on Factors Contributing to Preanalytical Variability of Urinary Pyridinoline and Deoxypyridinoline
Clin. Chem.,
February 1, 2002;
48(2):
220 - 235.
[Abstract][Full Text][PDF]
P. M. Yen Physiological and Molecular Basis of Thyroid Hormone Action
Physiol Rev,
July 1, 2001;
81(3):
1097 - 1142.
[Abstract][Full Text][PDF]
S. C. Manolagas Birth and Death of Bone Cells: Basic Regulatory Mechanisms and Implications for the Pathogenesis and Treatment of Osteoporosis
Endocr. Rev.,
April 1, 2000;
21(2):
115 - 137.
[Abstract][Full Text]
A. Siddiqi, J. P. Monson, D. F. Wood, G. M. Besser, and J. M. Burrin Serum Cytokines in Thyrotoxicosis
J. Clin. Endocrinol. Metab.,
February 1, 1999;
84(2):
435 - 439.
[Abstract][Full Text]
